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Review for 10.1186/s12876-025-03730-4
|
Reviewed - bmc_gastroenterology
|
Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from
a Retrospective Cohort Study
Version: 1 Date: 01 Dec 2024
Reviewer's report:
In this manuscript entitled “Effect of L-carnitine Supplementation on Muscle Cramps in Liver
Cirrhosis: Results from a Retrospective Cohort Study”, the authors examined the association
between levocarnitine supplementation and muscle cramps in patients with cirrhosis. While this
is an interesting study, there are some concerns which should be clarified.
Major comments
1. Malnutrition is important in the pathogenesis of muscle cramps in patients with liver cirrhosis
(PMID: 35861232). The authors should make an introduction regarding this point.
2. In the result section, the authors should demonstrate the baseline characteristics of the included
patients such as Child-Pugh score, MELD score, other medications, and laboratory data.
3. The molecular mechanism of levocarnitine on muscle cramps needs to be explained in the
discussion session (PMID: 31864971).
4. Levocarnitine also improves mortality in patients with cirrhosis. The authors should add a
discussion in this point (PMID: 35511698).
|
Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from
a Retrospective Cohort Study
Version: 1 Date: 01 Dec 2024
Reviewer's report:
In this manuscript entitled “Effect of L-carnitine Supplementation on Muscle Cramps in Liver
Cirrhosis: Results from a Retrospective Cohort Study”, the authors examined the association
between levocarnitine supplementation and muscle cramps in patients with cirrhosis. While this
is an interesting study, there are some concerns which should be clarified.
Major comments
1. Malnutrition is important in the pathogenesis of muscle cramps in patients with liver cirrhosis
(PMID: 35861232). The authors should make an introduction regarding this point.
2. In the result section, the authors should demonstrate the baseline characteristics of the included
patients such as Child-Pugh score, MELD score, other medications, and laboratory data.
3. The molecular mechanism of levocarnitine on muscle cramps needs to be explained in the
discussion session (PMID: 31864971).
4. Levocarnitine also improves mortality in patients with cirrhosis. The authors should add a
discussion in this point (PMID: 35511698).
|
BMC
|
12876_2025_3730_ReviewerReport_V1_R3.pdf
|
{
"criticism": 0,
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"results_and_discussion": 3,
"suggestion_and_solution": 5,
"total": 12
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"content": "Please review this paper.",
"role": "user"
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{
"content": "Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from\na Retrospective Cohort Study\nVersion: 1 Date: 01 Dec 2024\nReviewer's report:\nIn this manuscript entitled “Effect of L-carnitine Supplementation on Muscle Cramps in Liver\nCirrhosis: Results from a Retrospective Cohort Study”, the authors examined the association\nbetween levocarnitine supplementation and muscle cramps in patients with cirrhosis. While this\nis an interesting study, there are some concerns which should be clarified.\nMajor comments\n1. Malnutrition is important in the pathogenesis of muscle cramps in patients with liver cirrhosis\n(PMID: 35861232). The authors should make an introduction regarding this point.\n2. In the result section, the authors should demonstrate the baseline characteristics of the included\npatients such as Child-Pugh score, MELD score, other medications, and laboratory data.\n3. The molecular mechanism of levocarnitine on muscle cramps needs to be explained in the\ndiscussion session (PMID: 31864971).\n4. Levocarnitine also improves mortality in patients with cirrhosis. The authors should add a\ndiscussion in this point (PMID: 35511698).",
"role": "assistant"
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Review for 10.1186/s12876-025-03730-4
|
Reviewed - bmc_gastroenterology
|
Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from
a Retrospective Cohort Study
Version: 1 Date: 07 Dec 2024
Reviewer's report:
I would like to thank the journal for considering me as a reviewer for this manuscript. After a
thorough review, I have identified several areas where the manuscript could be improved.
Abstract
The abstract does not sufficiently detail the study's quantitative findings, particularly in the
conclusion. Including specific data points, such as the percentage reduction in cramp severity
or duration, would make the findings more impactful and informative for potential readers.
Study Design and Cohort Description
While the retrospective cohort design is acknowledged as a limitation in the discussion, it
should be justified earlier in the methodology section. The rationale for choosing a retrospective
approach over a randomized or prospective design is unclear and could raise questions about
the robustness of the findings. Additionally, the manuscript does not address the potential for
selection bias due to the retrospective nature of the study. For instance, it is not clear if patients
with incomplete records were systematically different from those included in the analysis.
Novelty and Clinical Implications
The manuscript mentions the need for further research but does not adequately position this
study in the context of existing literature. While prior studies on L-carnitine are referenced, the
specific novelty or unique contributions of these findings are not well-highlighted. For example,
the manuscript could discuss in more depth how demographic or response trends in this cohort
contribute to the existing body of knowledge. Additionally, the practical application of the
findings, such as their potential influence on treatment guidelines or clinical practice, is not
sufficiently explored.
Statistical Reporting
Although the statistical analysis is generally robust, key findings would benefit from the
inclusion of confidence intervals alongside p-values to provide a fuller context for the results.
The study also lacks a discussion on its statistical power, which is particularly important given
the relatively small final sample size.
Tables and Figures
The tables, while informative, could be improved for readability and presentation. For example,
tables summarizing cramp indices before and after treatment could combine summary statistics
with graphical elements, such as bar or line charts, to visually demonstrate the changes. Including
a flowchart to clarify the patient selection process would also enhance transparency in the
methodology.
Results Presentation
The results section is clear but could better integrate findings across tables to provide a cohesive
narrative. For instance, the significant correlations between BMI and cramp indices could be
discussed more comprehensively, linking them directly to potential clinical implications.
Language and Clarity
The manuscript is generally well-written but could benefit from simplification of overly complex
sentences, particularly in the discussion of BMI and treatment response. Some technical terms,
such as "relative change in cramp indices," should be explicitly defined to improve accessibility
for readers.
Limitations
The limitations section is too brief and could benefit from further critical reflection. The absence
of a control group is a major limitation that requires a more thorough discussion, particularly
regarding its potential impact on the observed results. Additionally, confounding factors such as
diet, physical activity, or concurrent medications are not addressed and should be considered.
Ethical and Practical Considerations
Although ethical approval and informed consent are mentioned, the manuscript does not
elaborate on how retrospective data collection adhered to ethical guidelines. Clarifying how
patient confidentiality and data security were maintained would strengthen the study's ethical
rigor.
Future Research Directions
The manuscript concludes by mentioning the need for further studies but does not provide
specific recommendations. Suggestions could include conducting randomized controlled trials,
exploring higher doses of L-carnitine, or investigating subgroups with specific characteristics,
such as high BMI or severe cirrhosis, who might benefit differently from supplementation.
|
Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from
a Retrospective Cohort Study
Version: 1 Date: 07 Dec 2024
Reviewer's report:
I would like to thank the journal for considering me as a reviewer for this manuscript. After a
thorough review, I have identified several areas where the manuscript could be improved.
Abstract
The abstract does not sufficiently detail the study's quantitative findings, particularly in the
conclusion. Including specific data points, such as the percentage reduction in cramp severity
or duration, would make the findings more impactful and informative for potential readers.
Study Design and Cohort Description
While the retrospective cohort design is acknowledged as a limitation in the discussion, it
should be justified earlier in the methodology section. The rationale for choosing a retrospective
approach over a randomized or prospective design is unclear and could raise questions about
the robustness of the findings. Additionally, the manuscript does not address the potential for
selection bias due to the retrospective nature of the study. For instance, it is not clear if patients
with incomplete records were systematically different from those included in the analysis.
Novelty and Clinical Implications
The manuscript mentions the need for further research but does not adequately position this
study in the context of existing literature. While prior studies on L-carnitine are referenced, the
specific novelty or unique contributions of these findings are not well-highlighted. For example,
the manuscript could discuss in more depth how demographic or response trends in this cohort
contribute to the existing body of knowledge. Additionally, the practical application of the
findings, such as their potential influence on treatment guidelines or clinical practice, is not
sufficiently explored.
Statistical Reporting
Although the statistical analysis is generally robust, key findings would benefit from the
inclusion of confidence intervals alongside p-values to provide a fuller context for the results.
The study also lacks a discussion on its statistical power, which is particularly important given
the relatively small final sample size.
Tables and Figures
The tables, while informative, could be improved for readability and presentation. For example,
tables summarizing cramp indices before and after treatment could combine summary statistics
with graphical elements, such as bar or line charts, to visually demonstrate the changes. Including
a flowchart to clarify the patient selection process would also enhance transparency in the
methodology.
Results Presentation
The results section is clear but could better integrate findings across tables to provide a cohesive
narrative. For instance, the significant correlations between BMI and cramp indices could be
discussed more comprehensively, linking them directly to potential clinical implications.
Language and Clarity
The manuscript is generally well-written but could benefit from simplification of overly complex
sentences, particularly in the discussion of BMI and treatment response. Some technical terms,
such as "relative change in cramp indices," should be explicitly defined to improve accessibility
for readers.
Limitations
The limitations section is too brief and could benefit from further critical reflection. The absence
of a control group is a major limitation that requires a more thorough discussion, particularly
regarding its potential impact on the observed results. Additionally, confounding factors such as
diet, physical activity, or concurrent medications are not addressed and should be considered.
Ethical and Practical Considerations
Although ethical approval and informed consent are mentioned, the manuscript does not
elaborate on how retrospective data collection adhered to ethical guidelines. Clarifying how
patient confidentiality and data security were maintained would strengthen the study's ethical
rigor.
Future Research Directions
The manuscript concludes by mentioning the need for further studies but does not provide
specific recommendations. Suggestions could include conducting randomized controlled trials,
exploring higher doses of L-carnitine, or investigating subgroups with specific characteristics,
such as high BMI or severe cirrhosis, who might benefit differently from supplementation.
|
BMC
|
12876_2025_3730_ReviewerReport_V1_R4.pdf
|
{
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"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from\na Retrospective Cohort Study\nVersion: 1 Date: 07 Dec 2024\nReviewer's report:\nI would like to thank the journal for considering me as a reviewer for this manuscript. After a\nthorough review, I have identified several areas where the manuscript could be improved.\nAbstract\nThe abstract does not sufficiently detail the study's quantitative findings, particularly in the\nconclusion. Including specific data points, such as the percentage reduction in cramp severity\nor duration, would make the findings more impactful and informative for potential readers.\nStudy Design and Cohort Description\nWhile the retrospective cohort design is acknowledged as a limitation in the discussion, it\nshould be justified earlier in the methodology section. The rationale for choosing a retrospective\napproach over a randomized or prospective design is unclear and could raise questions about\nthe robustness of the findings. Additionally, the manuscript does not address the potential for\nselection bias due to the retrospective nature of the study. For instance, it is not clear if patients\nwith incomplete records were systematically different from those included in the analysis.\nNovelty and Clinical Implications\nThe manuscript mentions the need for further research but does not adequately position this\nstudy in the context of existing literature. While prior studies on L-carnitine are referenced, the\nspecific novelty or unique contributions of these findings are not well-highlighted. For example,\nthe manuscript could discuss in more depth how demographic or response trends in this cohort\ncontribute to the existing body of knowledge. Additionally, the practical application of the\nfindings, such as their potential influence on treatment guidelines or clinical practice, is not\nsufficiently explored.\nStatistical Reporting\nAlthough the statistical analysis is generally robust, key findings would benefit from the\ninclusion of confidence intervals alongside p-values to provide a fuller context for the results.\nThe study also lacks a discussion on its statistical power, which is particularly important given\nthe relatively small final sample size.\nTables and Figures\nThe tables, while informative, could be improved for readability and presentation. For example,\ntables summarizing cramp indices before and after treatment could combine summary statistics\nwith graphical elements, such as bar or line charts, to visually demonstrate the changes. Including\na flowchart to clarify the patient selection process would also enhance transparency in the\nmethodology.\nResults Presentation\nThe results section is clear but could better integrate findings across tables to provide a cohesive\nnarrative. For instance, the significant correlations between BMI and cramp indices could be\ndiscussed more comprehensively, linking them directly to potential clinical implications.\nLanguage and Clarity\nThe manuscript is generally well-written but could benefit from simplification of overly complex\nsentences, particularly in the discussion of BMI and treatment response. Some technical terms,\nsuch as \"relative change in cramp indices,\" should be explicitly defined to improve accessibility\nfor readers.\nLimitations\nThe limitations section is too brief and could benefit from further critical reflection. The absence\nof a control group is a major limitation that requires a more thorough discussion, particularly\nregarding its potential impact on the observed results. Additionally, confounding factors such as\ndiet, physical activity, or concurrent medications are not addressed and should be considered.\nEthical and Practical Considerations\nAlthough ethical approval and informed consent are mentioned, the manuscript does not\nelaborate on how retrospective data collection adhered to ethical guidelines. Clarifying how\npatient confidentiality and data security were maintained would strengthen the study's ethical\nrigor.\nFuture Research Directions\nThe manuscript concludes by mentioning the need for further studies but does not provide\nspecific recommendations. Suggestions could include conducting randomized controlled trials,\nexploring higher doses of L-carnitine, or investigating subgroups with specific characteristics,\nsuch as high BMI or severe cirrhosis, who might benefit differently from supplementation.",
"role": "assistant"
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Review for 10.1186/s12876-025-03730-4
|
Reviewed - bmc_gastroenterology
|
Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from
a Retrospective Cohort Study
Version: 1 Date: 08 Dec 2024
Reviewer's report:
Line 98: Exclusion criteria were other secondary caused of cramps. By authors own submission
causes of cramps in cirrhosis can be AKI, dehydration, dyselectrolytemia. There is no mention
of these confounding factors in the manuscript. Authors should have mentioned in the methods
and methodology the prevalence of such predisposing factors in the study population. Ideally
these factors should be corrected before one can comment on the effectiveness of L-carnitine.
A multivariate analysis to take care of confounding factors would have given a more accurate
results on the effectiveness of L-carnitine
Line 11: 27.8% patients in this retrospective study had cramps. The authors could have studied
the factors as to why these patients had cramps while the remaining 71% screened patients did
not have cramps to make this study more insightful. This could have been a secondary objective
of the study
Table 3: Does not explain clearly the correlation of BMI and severity of cramps. It is not clear
from the table if high BMI is protective, or low BMI is protective against cramps
Line 182, 183: There is mention of complete resolution of cramps in certain percentage of
patients. However, there is no table in the manuscript to substantiate this conclusion.
The numbers in each subgroup especially the group with daily cramps is very small hence
making it difficult to come to a conclusion
If these points could be added to the manuscript, then study will have more impact
|
Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from
a Retrospective Cohort Study
Version: 1 Date: 08 Dec 2024
Reviewer's report:
Line 98: Exclusion criteria were other secondary caused of cramps. By authors own submission
causes of cramps in cirrhosis can be AKI, dehydration, dyselectrolytemia. There is no mention
of these confounding factors in the manuscript. Authors should have mentioned in the methods
and methodology the prevalence of such predisposing factors in the study population. Ideally
these factors should be corrected before one can comment on the effectiveness of L-carnitine.
A multivariate analysis to take care of confounding factors would have given a more accurate
results on the effectiveness of L-carnitine
Line 11: 27.8% patients in this retrospective study had cramps. The authors could have studied
the factors as to why these patients had cramps while the remaining 71% screened patients did
not have cramps to make this study more insightful. This could have been a secondary objective
of the study
Table 3: Does not explain clearly the correlation of BMI and severity of cramps. It is not clear
from the table if high BMI is protective, or low BMI is protective against cramps
Line 182, 183: There is mention of complete resolution of cramps in certain percentage of
patients. However, there is no table in the manuscript to substantiate this conclusion.
The numbers in each subgroup especially the group with daily cramps is very small hence
making it difficult to come to a conclusion
If these points could be added to the manuscript, then study will have more impact
|
BMC
|
12876_2025_3730_ReviewerReport_V1_R2.pdf
|
{
"criticism": 4,
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[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from\na Retrospective Cohort Study\nVersion: 1 Date: 08 Dec 2024\nReviewer's report:\nLine 98: Exclusion criteria were other secondary caused of cramps. By authors own submission\ncauses of cramps in cirrhosis can be AKI, dehydration, dyselectrolytemia. There is no mention\nof these confounding factors in the manuscript. Authors should have mentioned in the methods\nand methodology the prevalence of such predisposing factors in the study population. Ideally\nthese factors should be corrected before one can comment on the effectiveness of L-carnitine.\nA multivariate analysis to take care of confounding factors would have given a more accurate\nresults on the effectiveness of L-carnitine\nLine 11: 27.8% patients in this retrospective study had cramps. The authors could have studied\nthe factors as to why these patients had cramps while the remaining 71% screened patients did\nnot have cramps to make this study more insightful. This could have been a secondary objective\nof the study\nTable 3: Does not explain clearly the correlation of BMI and severity of cramps. It is not clear\nfrom the table if high BMI is protective, or low BMI is protective against cramps\nLine 182, 183: There is mention of complete resolution of cramps in certain percentage of\npatients. However, there is no table in the manuscript to substantiate this conclusion.\nThe numbers in each subgroup especially the group with daily cramps is very small hence\nmaking it difficult to come to a conclusion\nIf these points could be added to the manuscript, then study will have more impact",
"role": "assistant"
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Review for 10.1186/s12876-025-03730-4
|
Reviewed - bmc_gastroenterology
|
Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from
a Retrospective Cohort Study
Version: 2 Date: 29 Dec 2024
Reviewer's report:
The authors have appropriately revised the paper. I have no further comments.
|
Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from
a Retrospective Cohort Study
Version: 2 Date: 29 Dec 2024
Reviewer's report:
The authors have appropriately revised the paper. I have no further comments.
|
BMC
|
12876_2025_3730_ReviewerReport_V2_R3.pdf
|
{
"criticism": 1,
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"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from\na Retrospective Cohort Study\nVersion: 2 Date: 29 Dec 2024\nReviewer's report:\nThe authors have appropriately revised the paper. I have no further comments.",
"role": "assistant"
}
] | 2,025
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||
0
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|
Review for 10.1186/s12876-025-03730-4
|
Reviewed - bmc_gastroenterology
|
Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from
a Retrospective Cohort Study
Version: 2 Date: 11 Jan 2025
Reviewer's report:
Thank you for your response to the comments.
Absence of baseline data like 1.disease severity (CTP/ MELD scores) 2. Nutritional status 3.
severity of sarcopenia makes it difficult to conclude if these are potential confounding factors
for response to L carnitine supplementation.
Perhaps the authors in their conclusion can add a note that this is a pilot study and results of
this study should be validated with a well designed prospective study to avoid all biases and
confounders.
|
Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from
a Retrospective Cohort Study
Version: 2 Date: 11 Jan 2025
Reviewer's report:
Thank you for your response to the comments.
Absence of baseline data like 1.disease severity (CTP/ MELD scores) 2. Nutritional status 3.
severity of sarcopenia makes it difficult to conclude if these are potential confounding factors
for response to L carnitine supplementation.
Perhaps the authors in their conclusion can add a note that this is a pilot study and results of
this study should be validated with a well designed prospective study to avoid all biases and
confounders.
|
BMC
|
12876_2025_3730_ReviewerReport_V2_R2.pdf
|
{
"criticism": 2,
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[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Effect of L-carnitine Supplementation on Muscle Cramps in Liver Cirrhosis: Results from\na Retrospective Cohort Study\nVersion: 2 Date: 11 Jan 2025\nReviewer's report:\nThank you for your response to the comments.\nAbsence of baseline data like 1.disease severity (CTP/ MELD scores) 2. Nutritional status 3.\nseverity of sarcopenia makes it difficult to conclude if these are potential confounding factors\nfor response to L carnitine supplementation.\nPerhaps the authors in their conclusion can add a note that this is a pilot study and results of\nthis study should be validated with a well designed prospective study to avoid all biases and\nconfounders.",
"role": "assistant"
}
] | 2,025
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0
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Review for 10.1186/s12876-025-03738-w
|
Reviewed - bmc_gastroenterology
|
Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and
MBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC
cohort
Version: 2 Date: 25 Dec 2024
Reviewer: Hawal Lateef Fateh
Reviewer's report:
|
Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and
MBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC
cohort
Version: 2 Date: 25 Dec 2024
Reviewer: Hawal Lateef Fateh
Reviewer's report:
|
BMC
|
12876_2025_3738_ReviewerReport_V2_R3.pdf
|
{
"criticism": 0,
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"results_and_discussion": 0,
"suggestion_and_solution": 0,
"total": 1
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|
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}
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[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and\nMBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC\ncohort\nVersion: 2 Date: 25 Dec 2024\nReviewer: Hawal Lateef Fateh\nReviewer's report:",
"role": "assistant"
}
] | 2,025
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0
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|
Review for 10.1186/s12876-025-03738-w
|
Reviewed - bmc_gastroenterology
|
Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and
MBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC
cohort
Version: 2 Date: 12 Jan 2025
Reviewer: Zhaohui Tang
Reviewer's report:
This paper explores the genetic predisposition of NASH-related HCC in Sri Lanka, focusing
on five known variants in PNPLA3, TM6SF2, and MBOAT7 genes. The study analyzes
tumor characteristics (tumor nodularity, size, AFP levels) and potential biomarkers (leukocyte
telomere length, miR-122 expression) in 48 NASH-HCC patients. Notably, particular PNPLA3
variants (rs2281135, rs2294918) are shown to correlate with tumor nodularity, higher miR-122
expression, and distinct demographic/anthropometric features (e.g., age, BMI). Overall, the
work highlights the importance of specific genetic variants in tumor aggressiveness, contributing
to ongoing discussions on precision screening for HCC in NASH patients.
However#there are still some issues to be addressed before it’s suitable for publication:
1.Could you provide additional details on the power calculation used to determine that 48
patients would be sufficient to detect significant genetic associations?
2.Could you elaborate on whether these strong associations (especially PNPLA3 rs2281135)
persist in other ethnic groups or in a larger, more diverse study cohort?
3.Although the work is significant for Sri Lankan populations, additional insight or discussion
on how these findings might translate to broader or multi-ethnic contexts could strengthen the
paper’s global relevance.
4.Besides age and BMI, are there plans to investigate the impact of other lifestyle and metabolic
risk factors on the identified SNPs and their association with NASH-HCC?
|
Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and
MBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC
cohort
Version: 2 Date: 12 Jan 2025
Reviewer: Zhaohui Tang
Reviewer's report:
This paper explores the genetic predisposition of NASH-related HCC in Sri Lanka, focusing
on five known variants in PNPLA3, TM6SF2, and MBOAT7 genes. The study analyzes
tumor characteristics (tumor nodularity, size, AFP levels) and potential biomarkers (leukocyte
telomere length, miR-122 expression) in 48 NASH-HCC patients. Notably, particular PNPLA3
variants (rs2281135, rs2294918) are shown to correlate with tumor nodularity, higher miR-122
expression, and distinct demographic/anthropometric features (e.g., age, BMI). Overall, the
work highlights the importance of specific genetic variants in tumor aggressiveness, contributing
to ongoing discussions on precision screening for HCC in NASH patients.
However#there are still some issues to be addressed before it’s suitable for publication:
1.Could you provide additional details on the power calculation used to determine that 48
patients would be sufficient to detect significant genetic associations?
2.Could you elaborate on whether these strong associations (especially PNPLA3 rs2281135)
persist in other ethnic groups or in a larger, more diverse study cohort?
3.Although the work is significant for Sri Lankan populations, additional insight or discussion
on how these findings might translate to broader or multi-ethnic contexts could strengthen the
paper’s global relevance.
4.Besides age and BMI, are there plans to investigate the impact of other lifestyle and metabolic
risk factors on the identified SNPs and their association with NASH-HCC?
|
BMC
|
12876_2025_3738_ReviewerReport_V2_R4.pdf
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"role": "user"
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"content": "Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and\nMBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC\ncohort\nVersion: 2 Date: 12 Jan 2025\nReviewer: Zhaohui Tang\nReviewer's report:\nThis paper explores the genetic predisposition of NASH-related HCC in Sri Lanka, focusing\non five known variants in PNPLA3, TM6SF2, and MBOAT7 genes. The study analyzes\ntumor characteristics (tumor nodularity, size, AFP levels) and potential biomarkers (leukocyte\ntelomere length, miR-122 expression) in 48 NASH-HCC patients. Notably, particular PNPLA3\nvariants (rs2281135, rs2294918) are shown to correlate with tumor nodularity, higher miR-122\nexpression, and distinct demographic/anthropometric features (e.g., age, BMI). Overall, the\nwork highlights the importance of specific genetic variants in tumor aggressiveness, contributing\nto ongoing discussions on precision screening for HCC in NASH patients.\nHowever#there are still some issues to be addressed before it’s suitable for publication:\n1.Could you provide additional details on the power calculation used to determine that 48\npatients would be sufficient to detect significant genetic associations?\n2.Could you elaborate on whether these strong associations (especially PNPLA3 rs2281135)\npersist in other ethnic groups or in a larger, more diverse study cohort?\n3.Although the work is significant for Sri Lankan populations, additional insight or discussion\non how these findings might translate to broader or multi-ethnic contexts could strengthen the\npaper’s global relevance.\n4.Besides age and BMI, are there plans to investigate the impact of other lifestyle and metabolic\nrisk factors on the identified SNPs and their association with NASH-HCC?",
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Review for 10.1186/s12876-025-03738-w
|
Reviewed - bmc_gastroenterology
|
Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and
MBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC
cohort
Version: 3 Date: 28 Jan 2025
Reviewer: Hawal Lateef Fateh
Reviewer's report:
- Ensure the title reflects the study scope clearly and concisely.
- Verify if the abstract provides a structured summary (background, methods, results,
conclusion) while maintaining brevity.
- Assess if the introduction effectively justifies the research, clearly presenting the gap in the
literature and the study's objectives.
- Suggest adding more specific references or updating citations if needed.
- Verify if all experimental procedures are clearly described and reproducible.
- Suggest clarifications or elaborations on sample size justification, statistical methods, or
experimental protocols.
- Evaluate if the data presentation is clear, consistent, and free from redundancy.
- Ensure tables and figures are self-explanatory and enhance comprehension.
- Point out if any statistical analyses lack adequate description or context.
- Assess if the discussion appropriately interprets findings, acknowledges limitations, and aligns
with the objectives.
- Recommend emphasizing key findings and minimizing overgeneralization.
- Suggest grammar, spelling, and structural improvements to improve readability.
- Check adherence to journal formatting guidelines.
- Verify citation accuracy and formatting consistency.
|
Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and
MBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC
cohort
Version: 3 Date: 28 Jan 2025
Reviewer: Hawal Lateef Fateh
Reviewer's report:
- Ensure the title reflects the study scope clearly and concisely.
- Verify if the abstract provides a structured summary (background, methods, results,
conclusion) while maintaining brevity.
- Assess if the introduction effectively justifies the research, clearly presenting the gap in the
literature and the study's objectives.
- Suggest adding more specific references or updating citations if needed.
- Verify if all experimental procedures are clearly described and reproducible.
- Suggest clarifications or elaborations on sample size justification, statistical methods, or
experimental protocols.
- Evaluate if the data presentation is clear, consistent, and free from redundancy.
- Ensure tables and figures are self-explanatory and enhance comprehension.
- Point out if any statistical analyses lack adequate description or context.
- Assess if the discussion appropriately interprets findings, acknowledges limitations, and aligns
with the objectives.
- Recommend emphasizing key findings and minimizing overgeneralization.
- Suggest grammar, spelling, and structural improvements to improve readability.
- Check adherence to journal formatting guidelines.
- Verify citation accuracy and formatting consistency.
|
BMC
|
12876_2025_3738_ReviewerReport_V3_R3.pdf
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"role": "user"
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"content": "Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and\nMBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC\ncohort\nVersion: 3 Date: 28 Jan 2025\nReviewer: Hawal Lateef Fateh\nReviewer's report:\n- Ensure the title reflects the study scope clearly and concisely.\n- Verify if the abstract provides a structured summary (background, methods, results,\nconclusion) while maintaining brevity.\n- Assess if the introduction effectively justifies the research, clearly presenting the gap in the\nliterature and the study's objectives.\n- Suggest adding more specific references or updating citations if needed.\n- Verify if all experimental procedures are clearly described and reproducible.\n- Suggest clarifications or elaborations on sample size justification, statistical methods, or\nexperimental protocols.\n- Evaluate if the data presentation is clear, consistent, and free from redundancy.\n- Ensure tables and figures are self-explanatory and enhance comprehension.\n- Point out if any statistical analyses lack adequate description or context.\n- Assess if the discussion appropriately interprets findings, acknowledges limitations, and aligns\nwith the objectives.\n- Recommend emphasizing key findings and minimizing overgeneralization.\n- Suggest grammar, spelling, and structural improvements to improve readability.\n- Check adherence to journal formatting guidelines.\n- Verify citation accuracy and formatting consistency.",
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Review for 10.1186/s12876-025-03738-w
|
Reviewed - bmc_gastroenterology
|
Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and
MBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC
cohort
Version: 3 Date: 04 Feb 2025
Reviewer: Zhaohui Tang
Reviewer's report:
Thank you for the author's patient and meticulous answers. However, I still have some doubts
that need to be clarified:
1. How was the study powered to detect associations for “TM6SF2” and “MBOAT7” SNPs,
given their lack of significance?
2. Were multiple testing corrections applied? If not, how might uncorrected p-values impact the
interpretation of “PNPLA3” associations?
3. Can the authors elaborate on the biological mechanisms linking “PNPLA3” rs2281135 to
miR-122 elevation and tumor nodularity?
4. Why were cirrhotic and non-cirrhotic HCC patients not stratified in analyses, given prior
evidence of SNP associations with cirrhosis?
5. Could the observed age/BMI associations with “PNPLA3” rs2281135 reflect survivorship
bias or confounding factors (e.g., comorbidities)?
6. Overrepresentation of Sinhalese individuals (47/48) limits generalizability to other ethnic
groups in Sri Lanka or globally.
|
Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and
MBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC
cohort
Version: 3 Date: 04 Feb 2025
Reviewer: Zhaohui Tang
Reviewer's report:
Thank you for the author's patient and meticulous answers. However, I still have some doubts
that need to be clarified:
1. How was the study powered to detect associations for “TM6SF2” and “MBOAT7” SNPs,
given their lack of significance?
2. Were multiple testing corrections applied? If not, how might uncorrected p-values impact the
interpretation of “PNPLA3” associations?
3. Can the authors elaborate on the biological mechanisms linking “PNPLA3” rs2281135 to
miR-122 elevation and tumor nodularity?
4. Why were cirrhotic and non-cirrhotic HCC patients not stratified in analyses, given prior
evidence of SNP associations with cirrhosis?
5. Could the observed age/BMI associations with “PNPLA3” rs2281135 reflect survivorship
bias or confounding factors (e.g., comorbidities)?
6. Overrepresentation of Sinhalese individuals (47/48) limits generalizability to other ethnic
groups in Sri Lanka or globally.
|
BMC
|
12876_2025_3738_ReviewerReport_V3_R4.pdf
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"content": "Title: Association between single nucleotide polymorphisms in PNPLA3, TM6SF2 and\nMBOAT7 genes and markers of cancer aggressiveness in a Sri Lankan NASH-related HCC\ncohort\nVersion: 3 Date: 04 Feb 2025\nReviewer: Zhaohui Tang\nReviewer's report:\nThank you for the author's patient and meticulous answers. However, I still have some doubts\nthat need to be clarified:\n1. How was the study powered to detect associations for “TM6SF2” and “MBOAT7” SNPs,\ngiven their lack of significance?\n2. Were multiple testing corrections applied? If not, how might uncorrected p-values impact the\ninterpretation of “PNPLA3” associations?\n3. Can the authors elaborate on the biological mechanisms linking “PNPLA3” rs2281135 to\nmiR-122 elevation and tumor nodularity?\n4. Why were cirrhotic and non-cirrhotic HCC patients not stratified in analyses, given prior\nevidence of SNP associations with cirrhosis?\n5. Could the observed age/BMI associations with “PNPLA3” rs2281135 reflect survivorship\nbias or confounding factors (e.g., comorbidities)?\n6. Overrepresentation of Sinhalese individuals (47/48) limits generalizability to other ethnic\ngroups in Sri Lanka or globally.",
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Review for 10.1186/s12876-025-03685-6
|
Reviewed - bmc_gastroenterology
|
Title: Quality of life, functional impairment and healthcare experiences of patients with irritable
bowel syndrome in Norway: An online survey
Version: 4 Date: 20 Aug 2024
Reviewer: Ewa Ma#ecka-Panas
Reviewer's report:
This is the very comprehensive report with the rarely large number of patients evaluated.The
study aim was to determine the impact of IBS on the quality of life, functional impairment and
healthcare experiences of patients in Norway.The problem is widely known, but surprisingly
not that widely addressed.Some parts of the data provided are widely known, as low HRDL,
delay in medical help seeking, however economic burden of IBS was more rarely studied.My
main problem here is the IBS diagnosic criteria and the medical data of the studied group. The
statement that the patients were diagned by medical doctor in not informative enough.It should
be specified, if this were general practicioners or gastroenterologists or other specialist.Did they
use Rome IV IBS diagnosis criteria or other diagnostics? Were there associated diseases, which
could alter the results? The Rome IV criteria are mentioned in the discussion, but this is not clear
that that was the main diagnostic criteria, which should be stated in the material section.The
statement that IBS patients are not satisfied with the medical treatment is very familiar to all
gastroenterologists, since it takes time to gain the indispensable patients confidence on one
hand , but on the other hand the MD's time is scarce everywhere.Therefore, the authors should
underline, which obtained data represent the true novelty
|
Title: Quality of life, functional impairment and healthcare experiences of patients with irritable
bowel syndrome in Norway: An online survey
Version: 4 Date: 20 Aug 2024
Reviewer: Ewa Ma#ecka-Panas
Reviewer's report:
This is the very comprehensive report with the rarely large number of patients evaluated.The
study aim was to determine the impact of IBS on the quality of life, functional impairment and
healthcare experiences of patients in Norway.The problem is widely known, but surprisingly
not that widely addressed.Some parts of the data provided are widely known, as low HRDL,
delay in medical help seeking, however economic burden of IBS was more rarely studied.My
main problem here is the IBS diagnosic criteria and the medical data of the studied group. The
statement that the patients were diagned by medical doctor in not informative enough.It should
be specified, if this were general practicioners or gastroenterologists or other specialist.Did they
use Rome IV IBS diagnosis criteria or other diagnostics? Were there associated diseases, which
could alter the results? The Rome IV criteria are mentioned in the discussion, but this is not clear
that that was the main diagnostic criteria, which should be stated in the material section.The
statement that IBS patients are not satisfied with the medical treatment is very familiar to all
gastroenterologists, since it takes time to gain the indispensable patients confidence on one
hand , but on the other hand the MD's time is scarce everywhere.Therefore, the authors should
underline, which obtained data represent the true novelty
|
BMC
|
12876_2025_3685_ReviewerReport_V4_R1.pdf
|
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"role": "user"
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"content": "Title: Quality of life, functional impairment and healthcare experiences of patients with irritable\nbowel syndrome in Norway: An online survey\nVersion: 4 Date: 20 Aug 2024\nReviewer: Ewa Ma#ecka-Panas\nReviewer's report:\nThis is the very comprehensive report with the rarely large number of patients evaluated.The\nstudy aim was to determine the impact of IBS on the quality of life, functional impairment and\nhealthcare experiences of patients in Norway.The problem is widely known, but surprisingly\nnot that widely addressed.Some parts of the data provided are widely known, as low HRDL,\ndelay in medical help seeking, however economic burden of IBS was more rarely studied.My\nmain problem here is the IBS diagnosic criteria and the medical data of the studied group. The\nstatement that the patients were diagned by medical doctor in not informative enough.It should\nbe specified, if this were general practicioners or gastroenterologists or other specialist.Did they\nuse Rome IV IBS diagnosis criteria or other diagnostics? Were there associated diseases, which\ncould alter the results? The Rome IV criteria are mentioned in the discussion, but this is not clear\nthat that was the main diagnostic criteria, which should be stated in the material section.The\nstatement that IBS patients are not satisfied with the medical treatment is very familiar to all\ngastroenterologists, since it takes time to gain the indispensable patients confidence on one\nhand , but on the other hand the MD's time is scarce everywhere.Therefore, the authors should\nunderline, which obtained data represent the true novelty",
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|
Review for 10.1186/s12876-025-03685-6
|
Reviewed - bmc_gastroenterology
|
Title: Quality of life, functional impairment and healthcare experiences of patients with irritable
bowel syndrome in Norway: An online survey
Version: 4 Date: 31 Jan 2025
Reviewer's report:
Thank you for this survey, which adds to our knowledge of IBS in Norway with real-life data.
I have just a few comments:
1- I'm not convinced by the relevance of the responses from people under the age of 18, i.e.
25 persons (according to question 2) and 38 persons according to the ‘school pupil’ category
(question 4). We are not sure that they are capable of understanding and answering the questions.
If it wasn't the parents who answered for them, I suggest that these questionnaires should not
be included in the analysis.
2- You rightly excluded 327 questionnaires from the analysis because the diagnosis had not been
made by a doctor. I am surprised to find results for n= 2727 (in figure 5 ). These questionnaires
should be excluded from the analysis.
I would go further and also exclude the 158 questionnaires where people answered question
7: "Yes, it was diagnosed by another doctor (not a GP or gastrointestinal specialist)". In my
opinion, only a GP or gastroenterologist can correctly diagnose IBS.
It would also have been better to cross this with the response ‘I haven't been diagnosed by a
doctor 249’ in question 10.
3- There seems to be a percentage error in figure 4a. In fact, there are 158 people who were not
seen either by a GP or by the gastroenterologist according to question 7.
4- In Table 1, you were able to classify people according to their type of IBS, i.e. IBS-C, IBS-
D or IBS-M. Did you get this information directly from the people or did you deduce it? In my
opinion, question 8 doesn't allow you to classify patients with any certainty because it doesn't
meet the definition. For example, an IBS patient with constipation predominance must have hard
stools > 25% of the time and soft stools < 25% of the time.
To be correct, these should be indicated in the same way as the other symptoms (as for headache
and fatigue) in the table.
5- We do not understand how the ‘unemployed’ category is calculated.
Table 1 shows 1035 (38%) “unemployed”. In the discussion section, it says: ‘The present survey
revealed that the unemployment rate among IBS patients was 29%, which is therefore more than
8-fold that of the general population.’
I think there may be some confusion about the term “unemployed”. At times in your article it
refers to all the categories in question 4 without the ‘employed’ category, and at other times it
refers to ‘people of working age who are looking for work’.
Please clarify these points.
6- It would have been interesting to have information on income brackets or socio-professional
categories.
|
Title: Quality of life, functional impairment and healthcare experiences of patients with irritable
bowel syndrome in Norway: An online survey
Version: 4 Date: 31 Jan 2025
Reviewer's report:
Thank you for this survey, which adds to our knowledge of IBS in Norway with real-life data.
I have just a few comments:
1- I'm not convinced by the relevance of the responses from people under the age of 18, i.e.
25 persons (according to question 2) and 38 persons according to the ‘school pupil’ category
(question 4). We are not sure that they are capable of understanding and answering the questions.
If it wasn't the parents who answered for them, I suggest that these questionnaires should not
be included in the analysis.
2- You rightly excluded 327 questionnaires from the analysis because the diagnosis had not been
made by a doctor. I am surprised to find results for n= 2727 (in figure 5 ). These questionnaires
should be excluded from the analysis.
I would go further and also exclude the 158 questionnaires where people answered question
7: "Yes, it was diagnosed by another doctor (not a GP or gastrointestinal specialist)". In my
opinion, only a GP or gastroenterologist can correctly diagnose IBS.
It would also have been better to cross this with the response ‘I haven't been diagnosed by a
doctor 249’ in question 10.
3- There seems to be a percentage error in figure 4a. In fact, there are 158 people who were not
seen either by a GP or by the gastroenterologist according to question 7.
4- In Table 1, you were able to classify people according to their type of IBS, i.e. IBS-C, IBS-
D or IBS-M. Did you get this information directly from the people or did you deduce it? In my
opinion, question 8 doesn't allow you to classify patients with any certainty because it doesn't
meet the definition. For example, an IBS patient with constipation predominance must have hard
stools > 25% of the time and soft stools < 25% of the time.
To be correct, these should be indicated in the same way as the other symptoms (as for headache
and fatigue) in the table.
5- We do not understand how the ‘unemployed’ category is calculated.
Table 1 shows 1035 (38%) “unemployed”. In the discussion section, it says: ‘The present survey
revealed that the unemployment rate among IBS patients was 29%, which is therefore more than
8-fold that of the general population.’
I think there may be some confusion about the term “unemployed”. At times in your article it
refers to all the categories in question 4 without the ‘employed’ category, and at other times it
refers to ‘people of working age who are looking for work’.
Please clarify these points.
6- It would have been interesting to have information on income brackets or socio-professional
categories.
|
BMC
|
12876_2025_3685_ReviewerReport_V4_R2.pdf
|
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"role": "user"
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"content": "Title: Quality of life, functional impairment and healthcare experiences of patients with irritable\nbowel syndrome in Norway: An online survey\nVersion: 4 Date: 31 Jan 2025\nReviewer's report:\nThank you for this survey, which adds to our knowledge of IBS in Norway with real-life data.\nI have just a few comments:\n1- I'm not convinced by the relevance of the responses from people under the age of 18, i.e.\n25 persons (according to question 2) and 38 persons according to the ‘school pupil’ category\n(question 4). We are not sure that they are capable of understanding and answering the questions.\nIf it wasn't the parents who answered for them, I suggest that these questionnaires should not\nbe included in the analysis.\n2- You rightly excluded 327 questionnaires from the analysis because the diagnosis had not been\nmade by a doctor. I am surprised to find results for n= 2727 (in figure 5 ). These questionnaires\nshould be excluded from the analysis.\nI would go further and also exclude the 158 questionnaires where people answered question\n7: \"Yes, it was diagnosed by another doctor (not a GP or gastrointestinal specialist)\". In my\nopinion, only a GP or gastroenterologist can correctly diagnose IBS.\nIt would also have been better to cross this with the response ‘I haven't been diagnosed by a\ndoctor 249’ in question 10.\n3- There seems to be a percentage error in figure 4a. In fact, there are 158 people who were not\nseen either by a GP or by the gastroenterologist according to question 7.\n4- In Table 1, you were able to classify people according to their type of IBS, i.e. IBS-C, IBS-\nD or IBS-M. Did you get this information directly from the people or did you deduce it? In my\nopinion, question 8 doesn't allow you to classify patients with any certainty because it doesn't\nmeet the definition. For example, an IBS patient with constipation predominance must have hard\nstools > 25% of the time and soft stools < 25% of the time.\nTo be correct, these should be indicated in the same way as the other symptoms (as for headache\nand fatigue) in the table.\n5- We do not understand how the ‘unemployed’ category is calculated.\nTable 1 shows 1035 (38%) “unemployed”. In the discussion section, it says: ‘The present survey\nrevealed that the unemployment rate among IBS patients was 29%, which is therefore more than\n8-fold that of the general population.’\nI think there may be some confusion about the term “unemployed”. At times in your article it\nrefers to all the categories in question 4 without the ‘employed’ category, and at other times it\nrefers to ‘people of working age who are looking for work’.\nPlease clarify these points.\n6- It would have been interesting to have information on income brackets or socio-professional\ncategories.",
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Review for 10.1186/s12876-025-03685-6
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Reviewed - bmc_gastroenterology
|
Title: Quality of life, functional impairment and healthcare experiences of patients with irritable
bowel syndrome in Norway: An online survey
Version: 5 Date: 03 Feb 2025
Reviewer's report:
Reviewer 2
Thank you for your comments, which we believe has improved the manuscript considerably.
1-I'm not convinced by the relevance of the responses from people under the age of 18, i.e.
25 persons (according to question 2) and 38 persons according to the ‘school pupil’ category
(question 4). We are not sure that they are capable of understanding and answering the questions.
If it wasn't the parents who answered for them, I suggest that these questionnaires should not
be included in the analysis.
Response: We agree completely with the reviewer. People under 18 years of age were among
the 327 persons answered the survey were excluded. This was clarified in page 4, line and table
1 (marked yellow).
Reviewer’s response : Ok
2-You rightly excluded 327 questionnaires from the analysis because the diagnosis had not
been made by a doctor. I am surprised to find results for n= 2727 (in figure 5 ). These
questionnaires should be excluded from the analysis. I would go further and also exclude the
158 questionnaires where people answered question 7: "Yes, it was diagnosed by another doctor
(not a GP or gastrointestinal specialist)". In my opinion, only a GP or gastroenterologist can
correctly diagnose IBS. It would also have been better to cross this with the response ‘I haven't
been diagnosed by a doctor 249’ in question 10.
Response: This was corrected in the figures.
Reviewer’s response : Ok
3-There seems to be a percentage error in figure 4a. In fact, there are 158 people who were not
seen either by a GP or by the gastroenterologist according to question 7.
Response: The was corrected in the figures.
Reviewer’s response : Figure 3a remains unchanged.
Either the 3rd category is taken into account, i.e. n=2400 (i.e. 805 +1473+158), in which case
the percentages must be modified and the 3rd category included in the graph.
Or you do not want to take into account the 3rd category n=158, then the total number of
employees is equal to 2242.
Please make one of the 2 choices.
4- In Table 1, you were able to classify people according to their type of IBS, i.e. IBS-C, IBS
D or IBS-M. Did you get this information directly from the people or did you deduce it? In my
opinion, question 8 doesn't allow you to classify patients with any certainty because it doesn't
meet the definition. For example, an IBS patient with constipation predominance must have
hard stools > 25% of the time and soft stools < 25% of the time. To be correct, these should be
indicated in the same way as the other symptoms (as for headache and fatigue) in the table.
Response: We agree with the reviewer. This was corrected in Table 1 (marked yellow)
Reviewer’s response : Forgive me, but it seems to me that the data on the table has not been
changed. You can still read:
Table 1. Demographic and clinical characteristics of the irritable bowel syndrome (IBS) patients
who participated in the survey.
.....
IBS-D 1024 (37%)
IBS-C 728 (27%)
IBS-M 975 (36%)
.......
Data are n, n (%), or median [range] values.
IBS-D, diarrhoea-predominant IBS; IBS-C, constipation-predominant IBS;
IBS-M, mixed-diarrhoea-and-constipation IBS
5-We do not understand how the ‘unemployed’ category is calculated. Table 1 shows 1035
(38%) “unemployed”. In the discussion section, it says: ‘The present survey revealed that the
unemployment rate among IBS patients was 29%, which is therefore more than 8-fold that of
the general population.’ I think there may be some confusion about the term “unemployed”. At
times in your article it refers to all the categories in question 4 without the ‘employed’ category,
and at other times it refers to ‘people of working age who are looking for work’. Please clarify
these points.
Response: You are quite right. We clarified this in page 7, lines 6-8 (marked yellow).
Reviewer’s response: Forgive me, but the only element in yellow on page 7 is the following
sentence: “It noteworthy that it takes time to gain the indispensable patients confidence where
MD's time for each patient is limited.” I don't see your clarification.
6- It would have been interesting to have information on income brackets or socio professional
categories.
Response: We agree with the reviewer, but we do not have this information
Reviewer’s response: Ok
|
Title: Quality of life, functional impairment and healthcare experiences of patients with irritable
bowel syndrome in Norway: An online survey
Version: 5 Date: 03 Feb 2025
Reviewer's report:
Reviewer 2
Thank you for your comments, which we believe has improved the manuscript considerably.
1-I'm not convinced by the relevance of the responses from people under the age of 18, i.e.
25 persons (according to question 2) and 38 persons according to the ‘school pupil’ category
(question 4). We are not sure that they are capable of understanding and answering the questions.
If it wasn't the parents who answered for them, I suggest that these questionnaires should not
be included in the analysis.
Response: We agree completely with the reviewer. People under 18 years of age were among
the 327 persons answered the survey were excluded. This was clarified in page 4, line and table
1 (marked yellow).
Reviewer’s response : Ok
2-You rightly excluded 327 questionnaires from the analysis because the diagnosis had not
been made by a doctor. I am surprised to find results for n= 2727 (in figure 5 ). These
questionnaires should be excluded from the analysis. I would go further and also exclude the
158 questionnaires where people answered question 7: "Yes, it was diagnosed by another doctor
(not a GP or gastrointestinal specialist)". In my opinion, only a GP or gastroenterologist can
correctly diagnose IBS. It would also have been better to cross this with the response ‘I haven't
been diagnosed by a doctor 249’ in question 10.
Response: This was corrected in the figures.
Reviewer’s response : Ok
3-There seems to be a percentage error in figure 4a. In fact, there are 158 people who were not
seen either by a GP or by the gastroenterologist according to question 7.
Response: The was corrected in the figures.
Reviewer’s response : Figure 3a remains unchanged.
Either the 3rd category is taken into account, i.e. n=2400 (i.e. 805 +1473+158), in which case
the percentages must be modified and the 3rd category included in the graph.
Or you do not want to take into account the 3rd category n=158, then the total number of
employees is equal to 2242.
Please make one of the 2 choices.
4- In Table 1, you were able to classify people according to their type of IBS, i.e. IBS-C, IBS
D or IBS-M. Did you get this information directly from the people or did you deduce it? In my
opinion, question 8 doesn't allow you to classify patients with any certainty because it doesn't
meet the definition. For example, an IBS patient with constipation predominance must have
hard stools > 25% of the time and soft stools < 25% of the time. To be correct, these should be
indicated in the same way as the other symptoms (as for headache and fatigue) in the table.
Response: We agree with the reviewer. This was corrected in Table 1 (marked yellow)
Reviewer’s response : Forgive me, but it seems to me that the data on the table has not been
changed. You can still read:
Table 1. Demographic and clinical characteristics of the irritable bowel syndrome (IBS) patients
who participated in the survey.
.....
IBS-D 1024 (37%)
IBS-C 728 (27%)
IBS-M 975 (36%)
.......
Data are n, n (%), or median [range] values.
IBS-D, diarrhoea-predominant IBS; IBS-C, constipation-predominant IBS;
IBS-M, mixed-diarrhoea-and-constipation IBS
5-We do not understand how the ‘unemployed’ category is calculated. Table 1 shows 1035
(38%) “unemployed”. In the discussion section, it says: ‘The present survey revealed that the
unemployment rate among IBS patients was 29%, which is therefore more than 8-fold that of
the general population.’ I think there may be some confusion about the term “unemployed”. At
times in your article it refers to all the categories in question 4 without the ‘employed’ category,
and at other times it refers to ‘people of working age who are looking for work’. Please clarify
these points.
Response: You are quite right. We clarified this in page 7, lines 6-8 (marked yellow).
Reviewer’s response: Forgive me, but the only element in yellow on page 7 is the following
sentence: “It noteworthy that it takes time to gain the indispensable patients confidence where
MD's time for each patient is limited.” I don't see your clarification.
6- It would have been interesting to have information on income brackets or socio professional
categories.
Response: We agree with the reviewer, but we do not have this information
Reviewer’s response: Ok
|
BMC
|
12876_2025_3685_ReviewerReport_V5_R2.pdf
|
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"role": "user"
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"content": "Title: Quality of life, functional impairment and healthcare experiences of patients with irritable\nbowel syndrome in Norway: An online survey\nVersion: 5 Date: 03 Feb 2025\nReviewer's report:\nReviewer 2\nThank you for your comments, which we believe has improved the manuscript considerably.\n1-I'm not convinced by the relevance of the responses from people under the age of 18, i.e.\n25 persons (according to question 2) and 38 persons according to the ‘school pupil’ category\n(question 4). We are not sure that they are capable of understanding and answering the questions.\nIf it wasn't the parents who answered for them, I suggest that these questionnaires should not\nbe included in the analysis.\nResponse: We agree completely with the reviewer. People under 18 years of age were among\nthe 327 persons answered the survey were excluded. This was clarified in page 4, line and table\n1 (marked yellow).\nReviewer’s response : Ok\n2-You rightly excluded 327 questionnaires from the analysis because the diagnosis had not\nbeen made by a doctor. I am surprised to find results for n= 2727 (in figure 5 ). These\nquestionnaires should be excluded from the analysis. I would go further and also exclude the\n158 questionnaires where people answered question 7: \"Yes, it was diagnosed by another doctor\n(not a GP or gastrointestinal specialist)\". In my opinion, only a GP or gastroenterologist can\ncorrectly diagnose IBS. It would also have been better to cross this with the response ‘I haven't\nbeen diagnosed by a doctor 249’ in question 10.\nResponse: This was corrected in the figures.\nReviewer’s response : Ok\n3-There seems to be a percentage error in figure 4a. In fact, there are 158 people who were not\nseen either by a GP or by the gastroenterologist according to question 7.\nResponse: The was corrected in the figures.\nReviewer’s response : Figure 3a remains unchanged.\nEither the 3rd category is taken into account, i.e. n=2400 (i.e. 805 +1473+158), in which case\nthe percentages must be modified and the 3rd category included in the graph.\nOr you do not want to take into account the 3rd category n=158, then the total number of\nemployees is equal to 2242.\nPlease make one of the 2 choices.\n4- In Table 1, you were able to classify people according to their type of IBS, i.e. IBS-C, IBS\nD or IBS-M. Did you get this information directly from the people or did you deduce it? In my\nopinion, question 8 doesn't allow you to classify patients with any certainty because it doesn't\nmeet the definition. For example, an IBS patient with constipation predominance must have\nhard stools > 25% of the time and soft stools < 25% of the time. To be correct, these should be\nindicated in the same way as the other symptoms (as for headache and fatigue) in the table.\nResponse: We agree with the reviewer. This was corrected in Table 1 (marked yellow)\nReviewer’s response : Forgive me, but it seems to me that the data on the table has not been\nchanged. You can still read:\nTable 1. Demographic and clinical characteristics of the irritable bowel syndrome (IBS) patients\nwho participated in the survey.\n.....\nIBS-D 1024 (37%)\nIBS-C 728 (27%)\nIBS-M 975 (36%)\n.......\nData are n, n (%), or median [range] values.\nIBS-D, diarrhoea-predominant IBS; IBS-C, constipation-predominant IBS;\nIBS-M, mixed-diarrhoea-and-constipation IBS\n5-We do not understand how the ‘unemployed’ category is calculated. Table 1 shows 1035\n(38%) “unemployed”. In the discussion section, it says: ‘The present survey revealed that the\nunemployment rate among IBS patients was 29%, which is therefore more than 8-fold that of\nthe general population.’ I think there may be some confusion about the term “unemployed”. At\ntimes in your article it refers to all the categories in question 4 without the ‘employed’ category,\nand at other times it refers to ‘people of working age who are looking for work’. Please clarify\nthese points.\nResponse: You are quite right. We clarified this in page 7, lines 6-8 (marked yellow).\nReviewer’s response: Forgive me, but the only element in yellow on page 7 is the following\nsentence: “It noteworthy that it takes time to gain the indispensable patients confidence where\nMD's time for each patient is limited.” I don't see your clarification.\n6- It would have been interesting to have information on income brackets or socio professional\ncategories.\nResponse: We agree with the reviewer, but we do not have this information\nReviewer’s response: Ok",
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Review for 10.1186/s12876-025-03685-6
|
Reviewed - bmc_gastroenterology
|
Title: Quality of life, functional impairment and healthcare experiences of patients with irritable
bowel syndrome in Norway: An online survey
Version: 7 Date: 12 Feb 2025
Reviewer's report:
I have no more new comments. The authors took into account all the previous comments. I
accept the article for publication.
|
Title: Quality of life, functional impairment and healthcare experiences of patients with irritable
bowel syndrome in Norway: An online survey
Version: 7 Date: 12 Feb 2025
Reviewer's report:
I have no more new comments. The authors took into account all the previous comments. I
accept the article for publication.
|
BMC
|
12876_2025_3685_ReviewerReport_V7_R2.pdf
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"role": "user"
},
{
"content": "Title: Quality of life, functional impairment and healthcare experiences of patients with irritable\nbowel syndrome in Norway: An online survey\nVersion: 7 Date: 12 Feb 2025\nReviewer's report:\nI have no more new comments. The authors took into account all the previous comments. I\naccept the article for publication.",
"role": "assistant"
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] | 2,025
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||
0
| 0
|
Review for 10.1186/s12876-025-03677-6
|
Reviewed - bmc_gastroenterology
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 1 Date: 25 Nov 2024
Reviewer's report:
It is a worthwhile job#however there are some issues that need to be addressed.
1. Some important variables were not included in the analysis, such as history of hepatic
encephalopathy.
2. Univariate analysis showed that ascites was also an independent risk factor. Why was it not
included in the multivariate analysis#
3. Unreasonable use of charts: Tables 1 and 3 can be merged into one table and repeatedly
expressed in Table 1 and Figure 1.
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 1 Date: 25 Nov 2024
Reviewer's report:
It is a worthwhile job#however there are some issues that need to be addressed.
1. Some important variables were not included in the analysis, such as history of hepatic
encephalopathy.
2. Univariate analysis showed that ascites was also an independent risk factor. Why was it not
included in the multivariate analysis#
3. Unreasonable use of charts: Tables 1 and 3 can be merged into one table and repeatedly
expressed in Table 1 and Figure 1.
|
BMC
|
12876_2025_3677_ReviewerReport_V1_R4.pdf
|
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"role": "user"
},
{
"content": "Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in\nliver cirrhosis\nVersion: 1 Date: 25 Nov 2024\nReviewer's report:\nIt is a worthwhile job#however there are some issues that need to be addressed.\n1. Some important variables were not included in the analysis, such as history of hepatic\nencephalopathy.\n2. Univariate analysis showed that ascites was also an independent risk factor. Why was it not\nincluded in the multivariate analysis#\n3. Unreasonable use of charts: Tables 1 and 3 can be merged into one table and repeatedly\nexpressed in Table 1 and Figure 1.",
"role": "assistant"
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||
0
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|
Review for 10.1186/s12876-025-03677-6
|
Reviewed - bmc_gastroenterology
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 1 Date: 26 Nov 2024
Reviewer's report:
The authors collected baseline information and clinical data for 291 patients with cirrhosis,
aimed to identify risk factors for upper gastrointestinal bleeding (UGIB), and developed a
predictive model. However, the study's description is unclear, making it difficult to understand
the entire research process. One key question is whether the patients had UGIB at baseline. If
UGIB was present, the study appears to compare baseline differences between UGIB and non-
UGIB patients to develop a nomogram (as inferred from the authors’ results). However, the
mention of follow-up is confusing. Were all patients free of UGIB at baseline, and did the authors
follow them for six months to observe UGIB occurrence before developing the nomogram? If
so, why was Cox regression not used?
The following suggestions may improve the completeness of the manuscript:
1.The variable selection method based on simple logistic regression, which could lead to
significant multicollinearity among included variables. The authors should conduct collinearity
analysis or generate a correlation heatmap.
2.“Studies have shown that certain laboratory markers, such as total bilirubin (TBIL), serum
creatinine (Scr), and total cholesterol (TC), along with clinical assessments like liver stiffness
(LS), spleen stiffness (SS), and the presence of abdominal fluid, are associated with the
occurrence of UGIB in cirrhotic patients. Although some clinical studies support these findings,
their sample sizes are small, and the critical values vary.” This section lacks references.
3.Please confirm whether this is a prospective or retrospective study. If prospective,why data
collection performed using electronic health records? But, the abstract describes the study as
“retrospectively enrolled.”
4..A detailed description of the patient enrollment process is needed. For retrospective studies,
the diagnostic codes(ICD-codes#used to identify patients should be included.
5.The sentence “Patients in the cirrhosis group must meet the diagnostic criteria for upper
gastrointestinal bleeding” appears to contain an error. Were all cirrhotic patients required to
meet UGIB diagnostic criteria? Please clarify.
6.The phrase “patients can cooperate with long-term follow-up” is unclear. Was a follow-up
period defined? Does whether patients completed follow-up affect the results?
7.How were patients with a history of UGIB managed? Such patients have a significantly higher
risk of UGIB recurrence, which may impact results.
8.The term “cirrhotic UGIB group” is uncommon. Did this refer to esophagogastric variceal
hemorrhage (EGVH)? If a cirrhotic patient has UGIB caused by peptic ulcer bleeding, does this
also qualify as “cirrhotic UGIB”? Please clarify.
9.Were patients receiving antiviral therapy or nonselective beta-blockers (NSBBs) included?
These treatments significantly influence UGIB risk.
10.How was missing data handled? Were patients with missing data excluded?
11.The variable selection process (univariate followed by multivariate analysis) is overly
simplistic. At least stepwise regression should be used.
12.Figure 1 duplicates the information already presented in Table 1. It would be more appropriate
to replace Figure 1 with a flowchart illustrating the patient inclusion process.
13.The reported UGIB rate of 48.1% (140/291) is unusually high and inconsistent with
epidemiological data. Please confirm whether all eligible cases from the study period were
included.
14.Age and sex were not included in univariate or multivariate analyses, but previous studies
suggest that age is a risk factor for UGIB and should be analyzed.
15.The discussion mentions several models (e.g., Child-Pugh score, MELD, ALBI, Yang LB
et al.). Why were ROC and DCA comparisons not performed between the proposed model and
these established models?
16.The predictive model was not validated. Cross-validation or bootstrap validation is essential,
especially given the limited sample size.
17.The manuscript states that the follow-up period was six months. Were only patients without
UGIB at baseline followed to observe UGIB occurrence? Clarification is required.
18.Reporting guidelines (e.g., TRIPOD) should be included.
19.The authors are advised to avoid using the term “early” in the title, as clinical guidelines
provide a specific definition for “early”EGVH in cirrhotic patients. This study is a case-control
design comparing UGIB and non-UGIB groups and does not define “early.”
20.Professional English editing is recommended, as the manuscript contains multiple
grammatical and stylistic errors.
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 1 Date: 26 Nov 2024
Reviewer's report:
The authors collected baseline information and clinical data for 291 patients with cirrhosis,
aimed to identify risk factors for upper gastrointestinal bleeding (UGIB), and developed a
predictive model. However, the study's description is unclear, making it difficult to understand
the entire research process. One key question is whether the patients had UGIB at baseline. If
UGIB was present, the study appears to compare baseline differences between UGIB and non-
UGIB patients to develop a nomogram (as inferred from the authors’ results). However, the
mention of follow-up is confusing. Were all patients free of UGIB at baseline, and did the authors
follow them for six months to observe UGIB occurrence before developing the nomogram? If
so, why was Cox regression not used?
The following suggestions may improve the completeness of the manuscript:
1.The variable selection method based on simple logistic regression, which could lead to
significant multicollinearity among included variables. The authors should conduct collinearity
analysis or generate a correlation heatmap.
2.“Studies have shown that certain laboratory markers, such as total bilirubin (TBIL), serum
creatinine (Scr), and total cholesterol (TC), along with clinical assessments like liver stiffness
(LS), spleen stiffness (SS), and the presence of abdominal fluid, are associated with the
occurrence of UGIB in cirrhotic patients. Although some clinical studies support these findings,
their sample sizes are small, and the critical values vary.” This section lacks references.
3.Please confirm whether this is a prospective or retrospective study. If prospective,why data
collection performed using electronic health records? But, the abstract describes the study as
“retrospectively enrolled.”
4..A detailed description of the patient enrollment process is needed. For retrospective studies,
the diagnostic codes(ICD-codes#used to identify patients should be included.
5.The sentence “Patients in the cirrhosis group must meet the diagnostic criteria for upper
gastrointestinal bleeding” appears to contain an error. Were all cirrhotic patients required to
meet UGIB diagnostic criteria? Please clarify.
6.The phrase “patients can cooperate with long-term follow-up” is unclear. Was a follow-up
period defined? Does whether patients completed follow-up affect the results?
7.How were patients with a history of UGIB managed? Such patients have a significantly higher
risk of UGIB recurrence, which may impact results.
8.The term “cirrhotic UGIB group” is uncommon. Did this refer to esophagogastric variceal
hemorrhage (EGVH)? If a cirrhotic patient has UGIB caused by peptic ulcer bleeding, does this
also qualify as “cirrhotic UGIB”? Please clarify.
9.Were patients receiving antiviral therapy or nonselective beta-blockers (NSBBs) included?
These treatments significantly influence UGIB risk.
10.How was missing data handled? Were patients with missing data excluded?
11.The variable selection process (univariate followed by multivariate analysis) is overly
simplistic. At least stepwise regression should be used.
12.Figure 1 duplicates the information already presented in Table 1. It would be more appropriate
to replace Figure 1 with a flowchart illustrating the patient inclusion process.
13.The reported UGIB rate of 48.1% (140/291) is unusually high and inconsistent with
epidemiological data. Please confirm whether all eligible cases from the study period were
included.
14.Age and sex were not included in univariate or multivariate analyses, but previous studies
suggest that age is a risk factor for UGIB and should be analyzed.
15.The discussion mentions several models (e.g., Child-Pugh score, MELD, ALBI, Yang LB
et al.). Why were ROC and DCA comparisons not performed between the proposed model and
these established models?
16.The predictive model was not validated. Cross-validation or bootstrap validation is essential,
especially given the limited sample size.
17.The manuscript states that the follow-up period was six months. Were only patients without
UGIB at baseline followed to observe UGIB occurrence? Clarification is required.
18.Reporting guidelines (e.g., TRIPOD) should be included.
19.The authors are advised to avoid using the term “early” in the title, as clinical guidelines
provide a specific definition for “early”EGVH in cirrhotic patients. This study is a case-control
design comparing UGIB and non-UGIB groups and does not define “early.”
20.Professional English editing is recommended, as the manuscript contains multiple
grammatical and stylistic errors.
|
BMC
|
12876_2025_3677_ReviewerReport_V1_R2.pdf
|
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"content": "Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in\nliver cirrhosis\nVersion: 1 Date: 26 Nov 2024\nReviewer's report:\nThe authors collected baseline information and clinical data for 291 patients with cirrhosis,\naimed to identify risk factors for upper gastrointestinal bleeding (UGIB), and developed a\npredictive model. However, the study's description is unclear, making it difficult to understand\nthe entire research process. One key question is whether the patients had UGIB at baseline. If\nUGIB was present, the study appears to compare baseline differences between UGIB and non-\nUGIB patients to develop a nomogram (as inferred from the authors’ results). However, the\nmention of follow-up is confusing. Were all patients free of UGIB at baseline, and did the authors\nfollow them for six months to observe UGIB occurrence before developing the nomogram? If\nso, why was Cox regression not used?\nThe following suggestions may improve the completeness of the manuscript:\n1.The variable selection method based on simple logistic regression, which could lead to\nsignificant multicollinearity among included variables. The authors should conduct collinearity\nanalysis or generate a correlation heatmap.\n2.“Studies have shown that certain laboratory markers, such as total bilirubin (TBIL), serum\ncreatinine (Scr), and total cholesterol (TC), along with clinical assessments like liver stiffness\n(LS), spleen stiffness (SS), and the presence of abdominal fluid, are associated with the\noccurrence of UGIB in cirrhotic patients. Although some clinical studies support these findings,\ntheir sample sizes are small, and the critical values vary.” This section lacks references.\n3.Please confirm whether this is a prospective or retrospective study. If prospective,why data\ncollection performed using electronic health records? But, the abstract describes the study as\n“retrospectively enrolled.”\n4..A detailed description of the patient enrollment process is needed. For retrospective studies,\nthe diagnostic codes(ICD-codes#used to identify patients should be included.\n5.The sentence “Patients in the cirrhosis group must meet the diagnostic criteria for upper\ngastrointestinal bleeding” appears to contain an error. Were all cirrhotic patients required to\nmeet UGIB diagnostic criteria? Please clarify.\n6.The phrase “patients can cooperate with long-term follow-up” is unclear. Was a follow-up\nperiod defined? Does whether patients completed follow-up affect the results?\n7.How were patients with a history of UGIB managed? Such patients have a significantly higher\nrisk of UGIB recurrence, which may impact results.\n8.The term “cirrhotic UGIB group” is uncommon. Did this refer to esophagogastric variceal\nhemorrhage (EGVH)? If a cirrhotic patient has UGIB caused by peptic ulcer bleeding, does this\nalso qualify as “cirrhotic UGIB”? Please clarify.\n9.Were patients receiving antiviral therapy or nonselective beta-blockers (NSBBs) included?\nThese treatments significantly influence UGIB risk.\n10.How was missing data handled? Were patients with missing data excluded?\n11.The variable selection process (univariate followed by multivariate analysis) is overly\nsimplistic. At least stepwise regression should be used.\n12.Figure 1 duplicates the information already presented in Table 1. It would be more appropriate\nto replace Figure 1 with a flowchart illustrating the patient inclusion process.\n13.The reported UGIB rate of 48.1% (140/291) is unusually high and inconsistent with\nepidemiological data. Please confirm whether all eligible cases from the study period were\nincluded.\n14.Age and sex were not included in univariate or multivariate analyses, but previous studies\nsuggest that age is a risk factor for UGIB and should be analyzed.\n15.The discussion mentions several models (e.g., Child-Pugh score, MELD, ALBI, Yang LB\net al.). Why were ROC and DCA comparisons not performed between the proposed model and\nthese established models?\n16.The predictive model was not validated. Cross-validation or bootstrap validation is essential,\nespecially given the limited sample size.\n17.The manuscript states that the follow-up period was six months. Were only patients without\nUGIB at baseline followed to observe UGIB occurrence? Clarification is required.\n18.Reporting guidelines (e.g., TRIPOD) should be included.\n19.The authors are advised to avoid using the term “early” in the title, as clinical guidelines\nprovide a specific definition for “early”EGVH in cirrhotic patients. This study is a case-control\ndesign comparing UGIB and non-UGIB groups and does not define “early.”\n20.Professional English editing is recommended, as the manuscript contains multiple\ngrammatical and stylistic errors.",
"role": "assistant"
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0
| 0
|
Review for 10.1186/s12876-025-03677-6
|
Reviewed - bmc_gastroenterology
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 2 Date: 22 Dec 2024
Reviewer: Billy Siahaan
Reviewer's report:
Comment from reviewer :
1.Congratulation for your work , but I still confused about the method of collecting data and
method you use in this study. Could you describe more detail about “who experienced UGIB
within six months of discharge, were included in the study” , is the laboratory , fibroscan and
endoscopy were conducted at the same time of hospitalisation ? or all the variable were
collecting before any important treatment that may altered the result ?
2.I recommend you get additional exclusion regarding portal vein thrombosis or any non
cirrhotic condition that may have a different value from the spleen stiffness measurement and
the prognostic
3.“Of these, 99 patients had hepatitis B “ , what about the other etiology ? could you describe
and include in your baseline characteristic ? Its also important to difference between the use of
antiviral treatment because it has difference result in my opinion
4.If you had etiologies from MAFLD , I am not sure if the cholesterol level maybe altered and
could be a big bias for this research.
5. Could you describe what fibroscan type do you used especially for measurement of spleen
stiffness? Because the accuracy is different between 50 hz and 100hz ( spleen dedicated
fibroscan)
6.In this research you compare the model with other models like child pugh score. Could you
describe more detail about the method you used for get AUC from child pugh score model in
correlation with the upper gastrointestinal bleeding event
7.Did you had any record regarding the use of albumin transfusion during treatment at the
hospital? Please describe more detail especially in the variable that related to the study
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 2 Date: 22 Dec 2024
Reviewer: Billy Siahaan
Reviewer's report:
Comment from reviewer :
1.Congratulation for your work , but I still confused about the method of collecting data and
method you use in this study. Could you describe more detail about “who experienced UGIB
within six months of discharge, were included in the study” , is the laboratory , fibroscan and
endoscopy were conducted at the same time of hospitalisation ? or all the variable were
collecting before any important treatment that may altered the result ?
2.I recommend you get additional exclusion regarding portal vein thrombosis or any non
cirrhotic condition that may have a different value from the spleen stiffness measurement and
the prognostic
3.“Of these, 99 patients had hepatitis B “ , what about the other etiology ? could you describe
and include in your baseline characteristic ? Its also important to difference between the use of
antiviral treatment because it has difference result in my opinion
4.If you had etiologies from MAFLD , I am not sure if the cholesterol level maybe altered and
could be a big bias for this research.
5. Could you describe what fibroscan type do you used especially for measurement of spleen
stiffness? Because the accuracy is different between 50 hz and 100hz ( spleen dedicated
fibroscan)
6.In this research you compare the model with other models like child pugh score. Could you
describe more detail about the method you used for get AUC from child pugh score model in
correlation with the upper gastrointestinal bleeding event
7.Did you had any record regarding the use of albumin transfusion during treatment at the
hospital? Please describe more detail especially in the variable that related to the study
|
BMC
|
12876_2025_3677_ReviewerReport_V2_R3.pdf
|
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"content": "Please review this paper.",
"role": "user"
},
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"content": "Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in\nliver cirrhosis\nVersion: 2 Date: 22 Dec 2024\nReviewer: Billy Siahaan\nReviewer's report:\nComment from reviewer :\n1.Congratulation for your work , but I still confused about the method of collecting data and\nmethod you use in this study. Could you describe more detail about “who experienced UGIB\nwithin six months of discharge, were included in the study” , is the laboratory , fibroscan and\nendoscopy were conducted at the same time of hospitalisation ? or all the variable were\ncollecting before any important treatment that may altered the result ?\n2.I recommend you get additional exclusion regarding portal vein thrombosis or any non\ncirrhotic condition that may have a different value from the spleen stiffness measurement and\nthe prognostic\n3.“Of these, 99 patients had hepatitis B “ , what about the other etiology ? could you describe\nand include in your baseline characteristic ? Its also important to difference between the use of\nantiviral treatment because it has difference result in my opinion\n4.If you had etiologies from MAFLD , I am not sure if the cholesterol level maybe altered and\ncould be a big bias for this research.\n5. Could you describe what fibroscan type do you used especially for measurement of spleen\nstiffness? Because the accuracy is different between 50 hz and 100hz ( spleen dedicated\nfibroscan)\n6.In this research you compare the model with other models like child pugh score. Could you\ndescribe more detail about the method you used for get AUC from child pugh score model in\ncorrelation with the upper gastrointestinal bleeding event\n7.Did you had any record regarding the use of albumin transfusion during treatment at the\nhospital? Please describe more detail especially in the variable that related to the study",
"role": "assistant"
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] | 2,025
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||
0
| 0
|
Review for 10.1186/s12876-025-03677-6
|
Reviewed - bmc_gastroenterology
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 2 Date: 24 Dec 2024
Reviewer's report:
The authors have provided a thorough explanation and revisions. It is now clear that this is a
retrospective case-control study, and all patients had no history of UGIB at baseline. This is a
critical point, as patients with a history of UGIB are at higher risk for rebleeding.
I suggest minor revision:
First, change "no previous history of gastrointestinal bleeding" to the exclusion criteria (i.e.,
"patients with a history of gastrointestinal bleeding were excluded").
Second, expand the limitations section to address the absence of data on patients’ use of non-
selective beta-blockers (NSBBs) and antiviral therapies, as these factors could influence the
outcomes.
Finally, avoid using the term “matched,” as it may raise concerns about the randomization
process and the lack of a clear 1:1 or 1:2 matching ratio. Instead, revise this description to:
"These patients were compared with 151 patients with cirrhosis hospitalized during the same
period at the same hospital, who were discharged within six months without developing UGIB."
This revised phrasing indicates that all non-UGIB patients during this period were included.
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 2 Date: 24 Dec 2024
Reviewer's report:
The authors have provided a thorough explanation and revisions. It is now clear that this is a
retrospective case-control study, and all patients had no history of UGIB at baseline. This is a
critical point, as patients with a history of UGIB are at higher risk for rebleeding.
I suggest minor revision:
First, change "no previous history of gastrointestinal bleeding" to the exclusion criteria (i.e.,
"patients with a history of gastrointestinal bleeding were excluded").
Second, expand the limitations section to address the absence of data on patients’ use of non-
selective beta-blockers (NSBBs) and antiviral therapies, as these factors could influence the
outcomes.
Finally, avoid using the term “matched,” as it may raise concerns about the randomization
process and the lack of a clear 1:1 or 1:2 matching ratio. Instead, revise this description to:
"These patients were compared with 151 patients with cirrhosis hospitalized during the same
period at the same hospital, who were discharged within six months without developing UGIB."
This revised phrasing indicates that all non-UGIB patients during this period were included.
|
BMC
|
12876_2025_3677_ReviewerReport_V2_R2.pdf
|
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"suggestion_and_solution": 4,
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"content": "Please review this paper.",
"role": "user"
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"content": "Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in\nliver cirrhosis\nVersion: 2 Date: 24 Dec 2024\nReviewer's report:\nThe authors have provided a thorough explanation and revisions. It is now clear that this is a\nretrospective case-control study, and all patients had no history of UGIB at baseline. This is a\ncritical point, as patients with a history of UGIB are at higher risk for rebleeding.\nI suggest minor revision:\nFirst, change \"no previous history of gastrointestinal bleeding\" to the exclusion criteria (i.e.,\n\"patients with a history of gastrointestinal bleeding were excluded\").\nSecond, expand the limitations section to address the absence of data on patients’ use of non-\nselective beta-blockers (NSBBs) and antiviral therapies, as these factors could influence the\noutcomes.\nFinally, avoid using the term “matched,” as it may raise concerns about the randomization\nprocess and the lack of a clear 1:1 or 1:2 matching ratio. Instead, revise this description to:\n\"These patients were compared with 151 patients with cirrhosis hospitalized during the same\nperiod at the same hospital, who were discharged within six months without developing UGIB.\"\nThis revised phrasing indicates that all non-UGIB patients during this period were included.",
"role": "assistant"
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Review for 10.1186/s12876-025-03677-6
|
Reviewed - bmc_gastroenterology
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 2 Date: 01 Jan 2025
Reviewer's report:
Univariate analysis showed significant differences in ascites, hepatic encephalogy, LS, SS, PLT,
AST, APRI, FIB-4, ALB, TBIL, Scr, FIB, TC, and PT, all above statistically significant factors
should be included in the multivariate analysis, and then the model should be constructed.
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 2 Date: 01 Jan 2025
Reviewer's report:
Univariate analysis showed significant differences in ascites, hepatic encephalogy, LS, SS, PLT,
AST, APRI, FIB-4, ALB, TBIL, Scr, FIB, TC, and PT, all above statistically significant factors
should be included in the multivariate analysis, and then the model should be constructed.
|
BMC
|
12876_2025_3677_ReviewerReport_V2_R4.pdf
|
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{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in\nliver cirrhosis\nVersion: 2 Date: 01 Jan 2025\nReviewer's report:\nUnivariate analysis showed significant differences in ascites, hepatic encephalogy, LS, SS, PLT,\nAST, APRI, FIB-4, ALB, TBIL, Scr, FIB, TC, and PT, all above statistically significant factors\nshould be included in the multivariate analysis, and then the model should be constructed.",
"role": "assistant"
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0
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|
Review for 10.1186/s12876-025-03677-6
|
Reviewed - bmc_gastroenterology
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 3 Date: 21 Jan 2025
Reviewer's report:
The author has addressed my comments well, and I believe this study is now ready for
acceptance.
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 3 Date: 21 Jan 2025
Reviewer's report:
The author has addressed my comments well, and I believe this study is now ready for
acceptance.
|
BMC
|
12876_2025_3677_ReviewerReport_V3_R2.pdf
|
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"content": "Please review this paper.",
"role": "user"
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{
"content": "Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in\nliver cirrhosis\nVersion: 3 Date: 21 Jan 2025\nReviewer's report:\nThe author has addressed my comments well, and I believe this study is now ready for\nacceptance.",
"role": "assistant"
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0
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|
Review for 10.1186/s12876-025-03677-6
|
Reviewed - bmc_gastroenterology
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 3 Date: 29 Jan 2025
Reviewer: Billy Siahaan
Reviewer's report:
thank you for your response and revised
|
Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in
liver cirrhosis
Version: 3 Date: 29 Jan 2025
Reviewer: Billy Siahaan
Reviewer's report:
thank you for your response and revised
|
BMC
|
12876_2025_3677_ReviewerReport_V3_R3.pdf
|
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"role": "user"
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"content": "Title: Development and evaluation of a predictive model of upper gastrointestinal bleeding in\nliver cirrhosis\nVersion: 3 Date: 29 Jan 2025\nReviewer: Billy Siahaan\nReviewer's report:\nthank you for your response and revised",
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Review for 10.1186/s12876-025-03739-9
|
Reviewed - bmc_gastroenterology
|
Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice
Version: 1 Date: 27 Jan 2025
Reviewer's report:
This is a well-executed study demonstrating that platelets, neutrophils, and endothelial cells
from patients with obstructive jaundice (OJ) exhibit increased phosphatidylserine (PS) exposure
and shed PS+ microparticles (MPs). The authors further show that these prothrombotic surfaces
contribute to increased thrombotic activity and that blocking these surfaces with lactadherin
reduces liver damage in a bile duct ligation (BDL) mouse model. The study provides valuable
insight into the prothrombotic tendencies of OJ patients and offers a potential therapeutic avenue
for mitigating liver damage.
While the experimental design and results are robust, some conclusions drawn from the data are
not fully substantiated and require additional evidence or clarification. Below, I outline major
and minor concerns that should be addressed to strengthen the manuscript.
Major Concerns:
The authors used unconjugated bilirubin to demonstrate PS induction in blood cells and
HUVECs. However, in OJ patients, the majority of circulating bilirubin is conjugated, raising
concerns about the relevance of the experimental model. Conjugated bilirubin may not induce PS
exposure in the same way as unconjugated bilirubin. Moreover, bilirubin may be a confounder,
as its elevation in plasma is accompanied by increases in other components that could induce
PS exposure.
For instance, rising bile acids in OJ have been shown to promote prothrombotic tendencies
(Baker et al., Arteriosclerosis, Thrombosis, and Vascular Biology, 2019) and can directly induce
PS+ platelets (Unsworth et al., Arteriosclerosis, Thrombosis, and Vascular Biology, 2017). To
definitively determine bilirubin’s role as the deleterious effector, the authors should consider
depleting bilirubin from patient plasma and repeating the incubation experiments with blood
cells and HUVECs.
While decreased fibrin deposition in the livers of BDL mice after lactadherin treatment supports
the protective role of blocking PS+, the data do not conclusively link this effect to PS+ platelets,
neutrophils, or MPs identified in vitro. As the authors acknowledge in the discussion, PS
+ exposure in the liver may arise from hepatocytes or liver-resident cells secondary to bile
accumulation.
This limitation does not undermine the therapeutic relevance of targeting liver-specific PS+, but
it does raise questions about whether the PS+ cells evaluated in vitro (blood cells and HUVECs)
directly contribute to the observed in vivo effects. Further clarification or additional experiments
would strengthen this link.
Minor Concerns:
The abstract should be revised to provide a clearer explanation of the experimental settings in
which the respective results were obtained. This would help readers understand the study design
and its implications more effectively.
The sentence, "We found that OJ patients exhibited elevated levels of PS+ BCs, sera-cultured
ECs and associated MPs compared to the controls, which partly due to elevated unconjugated
bilirubin," is difficult to understand and should be rephrased for clarity.
The authors state that OJ patients exhibited lower platelet counts, but Table 1 shows no
significant difference. This discrepancy should be addressed, either by revising the statement or
explaining why the reported difference is relevant despite the lack of statistical significance.
Figure 2C: The observed reduction in extrinsic Xa after incubation with anti-TF raises questions,
as platelets do not express tissue factor. The authors should provide a plausible explanation for
this result or consider revising their interpretation.
"Davide Povero et al. observed a rise in the number of extracellular vesicles derived from
hepatocytes and cholangiocytes in the sera of cholestatic liver disease patients, however, these
results unable to reflect alterations in circulation cells." This sentence is missing a verb.
"However, whether PS exposure on hepatocyte in OJ still unclear." This sentence is also missing
a verb.
|
Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice
Version: 1 Date: 27 Jan 2025
Reviewer's report:
This is a well-executed study demonstrating that platelets, neutrophils, and endothelial cells
from patients with obstructive jaundice (OJ) exhibit increased phosphatidylserine (PS) exposure
and shed PS+ microparticles (MPs). The authors further show that these prothrombotic surfaces
contribute to increased thrombotic activity and that blocking these surfaces with lactadherin
reduces liver damage in a bile duct ligation (BDL) mouse model. The study provides valuable
insight into the prothrombotic tendencies of OJ patients and offers a potential therapeutic avenue
for mitigating liver damage.
While the experimental design and results are robust, some conclusions drawn from the data are
not fully substantiated and require additional evidence or clarification. Below, I outline major
and minor concerns that should be addressed to strengthen the manuscript.
Major Concerns:
The authors used unconjugated bilirubin to demonstrate PS induction in blood cells and
HUVECs. However, in OJ patients, the majority of circulating bilirubin is conjugated, raising
concerns about the relevance of the experimental model. Conjugated bilirubin may not induce PS
exposure in the same way as unconjugated bilirubin. Moreover, bilirubin may be a confounder,
as its elevation in plasma is accompanied by increases in other components that could induce
PS exposure.
For instance, rising bile acids in OJ have been shown to promote prothrombotic tendencies
(Baker et al., Arteriosclerosis, Thrombosis, and Vascular Biology, 2019) and can directly induce
PS+ platelets (Unsworth et al., Arteriosclerosis, Thrombosis, and Vascular Biology, 2017). To
definitively determine bilirubin’s role as the deleterious effector, the authors should consider
depleting bilirubin from patient plasma and repeating the incubation experiments with blood
cells and HUVECs.
While decreased fibrin deposition in the livers of BDL mice after lactadherin treatment supports
the protective role of blocking PS+, the data do not conclusively link this effect to PS+ platelets,
neutrophils, or MPs identified in vitro. As the authors acknowledge in the discussion, PS
+ exposure in the liver may arise from hepatocytes or liver-resident cells secondary to bile
accumulation.
This limitation does not undermine the therapeutic relevance of targeting liver-specific PS+, but
it does raise questions about whether the PS+ cells evaluated in vitro (blood cells and HUVECs)
directly contribute to the observed in vivo effects. Further clarification or additional experiments
would strengthen this link.
Minor Concerns:
The abstract should be revised to provide a clearer explanation of the experimental settings in
which the respective results were obtained. This would help readers understand the study design
and its implications more effectively.
The sentence, "We found that OJ patients exhibited elevated levels of PS+ BCs, sera-cultured
ECs and associated MPs compared to the controls, which partly due to elevated unconjugated
bilirubin," is difficult to understand and should be rephrased for clarity.
The authors state that OJ patients exhibited lower platelet counts, but Table 1 shows no
significant difference. This discrepancy should be addressed, either by revising the statement or
explaining why the reported difference is relevant despite the lack of statistical significance.
Figure 2C: The observed reduction in extrinsic Xa after incubation with anti-TF raises questions,
as platelets do not express tissue factor. The authors should provide a plausible explanation for
this result or consider revising their interpretation.
"Davide Povero et al. observed a rise in the number of extracellular vesicles derived from
hepatocytes and cholangiocytes in the sera of cholestatic liver disease patients, however, these
results unable to reflect alterations in circulation cells." This sentence is missing a verb.
"However, whether PS exposure on hepatocyte in OJ still unclear." This sentence is also missing
a verb.
|
BMC
|
12876_2025_3739_ReviewerReport_V1_R1.pdf
|
{
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},
{
"content": "Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice\nVersion: 1 Date: 27 Jan 2025\nReviewer's report:\nThis is a well-executed study demonstrating that platelets, neutrophils, and endothelial cells\nfrom patients with obstructive jaundice (OJ) exhibit increased phosphatidylserine (PS) exposure\nand shed PS+ microparticles (MPs). The authors further show that these prothrombotic surfaces\ncontribute to increased thrombotic activity and that blocking these surfaces with lactadherin\nreduces liver damage in a bile duct ligation (BDL) mouse model. The study provides valuable\ninsight into the prothrombotic tendencies of OJ patients and offers a potential therapeutic avenue\nfor mitigating liver damage.\nWhile the experimental design and results are robust, some conclusions drawn from the data are\nnot fully substantiated and require additional evidence or clarification. Below, I outline major\nand minor concerns that should be addressed to strengthen the manuscript.\nMajor Concerns:\nThe authors used unconjugated bilirubin to demonstrate PS induction in blood cells and\nHUVECs. However, in OJ patients, the majority of circulating bilirubin is conjugated, raising\nconcerns about the relevance of the experimental model. Conjugated bilirubin may not induce PS\nexposure in the same way as unconjugated bilirubin. Moreover, bilirubin may be a confounder,\nas its elevation in plasma is accompanied by increases in other components that could induce\nPS exposure.\nFor instance, rising bile acids in OJ have been shown to promote prothrombotic tendencies\n(Baker et al., Arteriosclerosis, Thrombosis, and Vascular Biology, 2019) and can directly induce\nPS+ platelets (Unsworth et al., Arteriosclerosis, Thrombosis, and Vascular Biology, 2017). To\ndefinitively determine bilirubin’s role as the deleterious effector, the authors should consider\ndepleting bilirubin from patient plasma and repeating the incubation experiments with blood\ncells and HUVECs.\nWhile decreased fibrin deposition in the livers of BDL mice after lactadherin treatment supports\nthe protective role of blocking PS+, the data do not conclusively link this effect to PS+ platelets,\nneutrophils, or MPs identified in vitro. As the authors acknowledge in the discussion, PS\n+ exposure in the liver may arise from hepatocytes or liver-resident cells secondary to bile\naccumulation.\nThis limitation does not undermine the therapeutic relevance of targeting liver-specific PS+, but\nit does raise questions about whether the PS+ cells evaluated in vitro (blood cells and HUVECs)\ndirectly contribute to the observed in vivo effects. Further clarification or additional experiments\nwould strengthen this link.\nMinor Concerns:\nThe abstract should be revised to provide a clearer explanation of the experimental settings in\nwhich the respective results were obtained. This would help readers understand the study design\nand its implications more effectively.\nThe sentence, \"We found that OJ patients exhibited elevated levels of PS+ BCs, sera-cultured\nECs and associated MPs compared to the controls, which partly due to elevated unconjugated\nbilirubin,\" is difficult to understand and should be rephrased for clarity.\nThe authors state that OJ patients exhibited lower platelet counts, but Table 1 shows no\nsignificant difference. This discrepancy should be addressed, either by revising the statement or\nexplaining why the reported difference is relevant despite the lack of statistical significance.\nFigure 2C: The observed reduction in extrinsic Xa after incubation with anti-TF raises questions,\nas platelets do not express tissue factor. The authors should provide a plausible explanation for\nthis result or consider revising their interpretation.\n\"Davide Povero et al. observed a rise in the number of extracellular vesicles derived from\nhepatocytes and cholangiocytes in the sera of cholestatic liver disease patients, however, these\nresults unable to reflect alterations in circulation cells.\" This sentence is missing a verb.\n\"However, whether PS exposure on hepatocyte in OJ still unclear.\" This sentence is also missing\na verb.",
"role": "assistant"
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] | 2,025
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0
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|
Review for 10.1186/s12876-025-03739-9
|
Reviewed - bmc_gastroenterology
|
Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice
Version: 1 Date: 28 Jan 2025
Reviewer: Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While tissue factor (TF) is briefly mentioned as playing a role in cholestasis-related
coagulopathy, it could be clearer whether TF expression is being directly studied in this research
or if it is being used as background information. If TF's role is not a focus of the current study,
it might be worth clarifying this point to avoid confusion.
-The introduction discusses the association of PS exposure with coagulation activation but
does not go into much detail regarding the molecular mechanisms involved. A more in-depth
explanation of how PS exposure leads to activation of the coagulation pathways (e.g., the
intrinsic/extrinsic pathways, prothrombinase complex formation) would strengthen the rationale
for studying PS in this context.
-It might be helpful to mention other possible contributors to coagulopathy in OJ, such as
elevated bilirubin, liver dysfunction, or inflammatory markers. This would further emphasize
the novelty of focusing on PS and its potential to serve as a central mechanistic link.
-The preparation of unconjugated bilirubin (UCB) is described in detail, but it would be helpful
to clarify the rationale behind the chosen concentrations (25, 50, 100 µM) and the significance
of the molar ratios of bilirubin to albumin. What is the expected physiological relevance of these
concentrations in the context of OJ? Adding this rationale would strengthen the experimental
design.
-The procedure for isolating microparticles (MPs) is clear, but the subsequent flow cytometry
analysis could be expanded. Specifically, it would be helpful to include more details on how the
MPs are quantified, particularly since MPs are being compared across different groups. A brief
explanation of how the MPs are counted (e.g., flow cytometric thresholding for MPs vs. larger
cells) would enhance reproducibility.
-The methods mention the use of lactadherin to inhibit PS-mediated procoagulant activity. It
might be useful to explain the expected outcome of lactadherin inhibition more clearly. For
example, will lactadherin reduce thrombin generation, and by what mechanism? This detail
could help readers understand the therapeutic potential of lactadherin more fully.
-The mouse BDL model is well-described, but it would be helpful to provide more context on
the expected outcomes of lactadherin treatment in the animal model. Is there a hypothesis about
how lactadherin might impact liver injury or coagulopathy in the BDL mice, and what specific
markers will be used to evaluate the effects?
-While the authors present a compelling narrative connecting PS exposure to hypercoagulability,
some aspects of the mechanistic pathways could be further clarified. For instance, the exact
molecular processes by which PS exposure on MPs and BCs leads to enhanced thrombin
generation could be more explicitly described. A deeper exploration into how PS facilitates the
prothrombinase complex assembly would enhance the biological relevance of the study.
-The study highlights a key finding that platelets in OJ patients exhibit PS exposure despite a
lower overall platelet count. The discussion briefly touches on enhanced splenic sequestration
and platelet accumulation in the hepatic sinusoidal space but could delve deeper into the
functional implications of this platelet dysfunction. Do these platelets become hyperreactive? Is
their altered behavior linked to increased thrombotic risk, or does this dysfunction represent an
earlier stage of platelet activation? Further discussion of the functional consequences of platelet
dysfunction in OJ could help strengthen the argument for targeting platelets in therapeutic
interventions.
-The role of hepatocytes in PS exposure is mentioned briefly but left unaddressed in terms
of mechanistic details. Given that hepatocyte apoptosis is a proposed feature of procoagulant
responses in liver disease, this should be more thoroughly integrated into the discussion. Are
hepatocyte-derived MPs contributing to the observed procoagulant state in OJ, or are they simply
a downstream effect? A more focused discussion on hepatocytes and their interaction with MPs,
especially in the context of cholestasis and hyperbilirubinemia, would further strengthen the
study’s conclusions.
|
Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice
Version: 1 Date: 28 Jan 2025
Reviewer: Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While tissue factor (TF) is briefly mentioned as playing a role in cholestasis-related
coagulopathy, it could be clearer whether TF expression is being directly studied in this research
or if it is being used as background information. If TF's role is not a focus of the current study,
it might be worth clarifying this point to avoid confusion.
-The introduction discusses the association of PS exposure with coagulation activation but
does not go into much detail regarding the molecular mechanisms involved. A more in-depth
explanation of how PS exposure leads to activation of the coagulation pathways (e.g., the
intrinsic/extrinsic pathways, prothrombinase complex formation) would strengthen the rationale
for studying PS in this context.
-It might be helpful to mention other possible contributors to coagulopathy in OJ, such as
elevated bilirubin, liver dysfunction, or inflammatory markers. This would further emphasize
the novelty of focusing on PS and its potential to serve as a central mechanistic link.
-The preparation of unconjugated bilirubin (UCB) is described in detail, but it would be helpful
to clarify the rationale behind the chosen concentrations (25, 50, 100 µM) and the significance
of the molar ratios of bilirubin to albumin. What is the expected physiological relevance of these
concentrations in the context of OJ? Adding this rationale would strengthen the experimental
design.
-The procedure for isolating microparticles (MPs) is clear, but the subsequent flow cytometry
analysis could be expanded. Specifically, it would be helpful to include more details on how the
MPs are quantified, particularly since MPs are being compared across different groups. A brief
explanation of how the MPs are counted (e.g., flow cytometric thresholding for MPs vs. larger
cells) would enhance reproducibility.
-The methods mention the use of lactadherin to inhibit PS-mediated procoagulant activity. It
might be useful to explain the expected outcome of lactadherin inhibition more clearly. For
example, will lactadherin reduce thrombin generation, and by what mechanism? This detail
could help readers understand the therapeutic potential of lactadherin more fully.
-The mouse BDL model is well-described, but it would be helpful to provide more context on
the expected outcomes of lactadherin treatment in the animal model. Is there a hypothesis about
how lactadherin might impact liver injury or coagulopathy in the BDL mice, and what specific
markers will be used to evaluate the effects?
-While the authors present a compelling narrative connecting PS exposure to hypercoagulability,
some aspects of the mechanistic pathways could be further clarified. For instance, the exact
molecular processes by which PS exposure on MPs and BCs leads to enhanced thrombin
generation could be more explicitly described. A deeper exploration into how PS facilitates the
prothrombinase complex assembly would enhance the biological relevance of the study.
-The study highlights a key finding that platelets in OJ patients exhibit PS exposure despite a
lower overall platelet count. The discussion briefly touches on enhanced splenic sequestration
and platelet accumulation in the hepatic sinusoidal space but could delve deeper into the
functional implications of this platelet dysfunction. Do these platelets become hyperreactive? Is
their altered behavior linked to increased thrombotic risk, or does this dysfunction represent an
earlier stage of platelet activation? Further discussion of the functional consequences of platelet
dysfunction in OJ could help strengthen the argument for targeting platelets in therapeutic
interventions.
-The role of hepatocytes in PS exposure is mentioned briefly but left unaddressed in terms
of mechanistic details. Given that hepatocyte apoptosis is a proposed feature of procoagulant
responses in liver disease, this should be more thoroughly integrated into the discussion. Are
hepatocyte-derived MPs contributing to the observed procoagulant state in OJ, or are they simply
a downstream effect? A more focused discussion on hepatocytes and their interaction with MPs,
especially in the context of cholestasis and hyperbilirubinemia, would further strengthen the
study’s conclusions.
|
BMC
|
12876_2025_3739_ReviewerReport_V1_R2.pdf
|
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"role": "user"
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"content": "Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice\nVersion: 1 Date: 28 Jan 2025\nReviewer: Anwar Ashraf Abouelnasr\nReviewer's report:\nDear Authors, please address the following points below\n-While tissue factor (TF) is briefly mentioned as playing a role in cholestasis-related\ncoagulopathy, it could be clearer whether TF expression is being directly studied in this research\nor if it is being used as background information. If TF's role is not a focus of the current study,\nit might be worth clarifying this point to avoid confusion.\n-The introduction discusses the association of PS exposure with coagulation activation but\ndoes not go into much detail regarding the molecular mechanisms involved. A more in-depth\nexplanation of how PS exposure leads to activation of the coagulation pathways (e.g., the\nintrinsic/extrinsic pathways, prothrombinase complex formation) would strengthen the rationale\nfor studying PS in this context.\n-It might be helpful to mention other possible contributors to coagulopathy in OJ, such as\nelevated bilirubin, liver dysfunction, or inflammatory markers. This would further emphasize\nthe novelty of focusing on PS and its potential to serve as a central mechanistic link.\n-The preparation of unconjugated bilirubin (UCB) is described in detail, but it would be helpful\nto clarify the rationale behind the chosen concentrations (25, 50, 100 µM) and the significance\nof the molar ratios of bilirubin to albumin. What is the expected physiological relevance of these\nconcentrations in the context of OJ? Adding this rationale would strengthen the experimental\ndesign.\n-The procedure for isolating microparticles (MPs) is clear, but the subsequent flow cytometry\nanalysis could be expanded. Specifically, it would be helpful to include more details on how the\nMPs are quantified, particularly since MPs are being compared across different groups. A brief\nexplanation of how the MPs are counted (e.g., flow cytometric thresholding for MPs vs. larger\ncells) would enhance reproducibility.\n-The methods mention the use of lactadherin to inhibit PS-mediated procoagulant activity. It\nmight be useful to explain the expected outcome of lactadherin inhibition more clearly. For\nexample, will lactadherin reduce thrombin generation, and by what mechanism? This detail\ncould help readers understand the therapeutic potential of lactadherin more fully.\n-The mouse BDL model is well-described, but it would be helpful to provide more context on\nthe expected outcomes of lactadherin treatment in the animal model. Is there a hypothesis about\nhow lactadherin might impact liver injury or coagulopathy in the BDL mice, and what specific\nmarkers will be used to evaluate the effects?\n-While the authors present a compelling narrative connecting PS exposure to hypercoagulability,\nsome aspects of the mechanistic pathways could be further clarified. For instance, the exact\nmolecular processes by which PS exposure on MPs and BCs leads to enhanced thrombin\ngeneration could be more explicitly described. A deeper exploration into how PS facilitates the\nprothrombinase complex assembly would enhance the biological relevance of the study.\n-The study highlights a key finding that platelets in OJ patients exhibit PS exposure despite a\nlower overall platelet count. The discussion briefly touches on enhanced splenic sequestration\nand platelet accumulation in the hepatic sinusoidal space but could delve deeper into the\nfunctional implications of this platelet dysfunction. Do these platelets become hyperreactive? Is\ntheir altered behavior linked to increased thrombotic risk, or does this dysfunction represent an\nearlier stage of platelet activation? Further discussion of the functional consequences of platelet\ndysfunction in OJ could help strengthen the argument for targeting platelets in therapeutic\ninterventions.\n-The role of hepatocytes in PS exposure is mentioned briefly but left unaddressed in terms\nof mechanistic details. Given that hepatocyte apoptosis is a proposed feature of procoagulant\nresponses in liver disease, this should be more thoroughly integrated into the discussion. Are\nhepatocyte-derived MPs contributing to the observed procoagulant state in OJ, or are they simply\na downstream effect? A more focused discussion on hepatocytes and their interaction with MPs,\nespecially in the context of cholestasis and hyperbilirubinemia, would further strengthen the\nstudy’s conclusions.",
"role": "assistant"
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] | 2,025
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||
0
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|
Review for 10.1186/s12876-025-03739-9
|
Reviewed - bmc_gastroenterology
|
Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice
Version: 2 Date: 14 Feb 2025
Reviewer: Anwar Ashraf Abouelnasr
Reviewer's report:
The responses are satisfactory.
|
Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice
Version: 2 Date: 14 Feb 2025
Reviewer: Anwar Ashraf Abouelnasr
Reviewer's report:
The responses are satisfactory.
|
BMC
|
12876_2025_3739_ReviewerReport_V2_R2.pdf
|
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"total": 1
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"content": "Please review this paper.",
"role": "user"
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"content": "Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice\nVersion: 2 Date: 14 Feb 2025\nReviewer: Anwar Ashraf Abouelnasr\nReviewer's report:\nThe responses are satisfactory.",
"role": "assistant"
}
] | 2,025
|
||
0
| 0
|
Review for 10.1186/s12876-025-03739-9
|
Reviewed - bmc_gastroenterology
|
Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice
Version: 2 Date: 24 Feb 2025
Reviewer's report:
All my concerns have been thoroughly addressed. The readability has significantly improved,
making it easier to interpret the findings in this revision. I recommend acceptance.
|
Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice
Version: 2 Date: 24 Feb 2025
Reviewer's report:
All my concerns have been thoroughly addressed. The readability has significantly improved,
making it easier to interpret the findings in this revision. I recommend acceptance.
|
BMC
|
12876_2025_3739_ReviewerReport_V2_R1.pdf
|
{
"criticism": 0,
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"materials_and_methods": 0,
"praise": 3,
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"content": "Please review this paper.",
"role": "user"
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{
"content": "Title: Phosphatidylserine induce thrombotic tendency and liver damage in obstructive jaundice\nVersion: 2 Date: 24 Feb 2025\nReviewer's report:\nAll my concerns have been thoroughly addressed. The readability has significantly improved,\nmaking it easier to interpret the findings in this revision. I recommend acceptance.",
"role": "assistant"
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0
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Review for 10.1186/s12876-025-03732-2
|
Reviewed - bmc_gastroenterology
|
Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the
ClinicalTrials.gov Database
Version: 2 Date: 23 Jan 2025
Reviewer: Joost Boeckmans
Reviewer's report:
Hui Du and colleagues provide an overview of clinical trials in MASLD registered on
ClinicalTrials.gov. The manuscript is descriptive but gives a practical overview. Certain
concepts could add innovative aspects, in which I hope my input can be useful:
Major
- Introduction: in my opinion, the introduction would benefit from discussing the potential drug
targets in MASLD in the context of the pathophysiology, instead of a lengthy discussion on
prevalence. In that view, the part on the pathogenesis could use an update as well, with the ‘two-
hit’ hypothesis being outdated and perhaps less relevant to describe seen the scope of the paper.
- The authors describe hepatic fat content as a frequent endpoint. What about the technique to
quantify this? Was this always MRI-PDFF? + what is usually considered as a relevant lipid
reduction? Same for histology, are there already some using AI?
- Based on the search, what are the advantages of current ‘most popular’ drugs under
development over the failed compounds? Eg. Elafibranor.
- What about personalized treatment developments? Eg. Regarding PNPLA3? When did these
kinds of approaches emerge?
All in all, I think it would be good to describe such temporal changes (i.e. last 3 points) in more
detail, since this informs about new developments
Minor
- Introduction: The global prevalence is around 38%, please see Riazi K, Azhari H, Charette
JH, Underwood FE, King JA, Afshar EE, Swain MG, Congly SE, Kaplan GG, Shaheen AA.
The prevalence and incidence of NAFLD worldwide: a systematic review and meta-analysis.
Lancet Gastroenterol Hepatol. 2022 Sep;7(9):851-861. doi: 10.1016/S2468-1253(22)00165-0.
Epub 2022 Jul 5. PMID: 35798021.
- Would be good to use the MASLD terminology (or MAFLD if regionally preferred) to create
some uniformity.
- Fig 3: Might be good to also have a grey box with ‘no trials’ registered or similar
- Abstract: “140 drug interventional trials primarily aimed to improve NAFLD through
mechanisms such as metabolic and energy balance”; would be informative to add a percentage
to this number. How did the targets change throughout the time?
- Better not to use adjectives as ‘meticulous’, or ‘rigorous’ when describing relatively simple
concepts (cfr methods section).
- Was gender (vs sex) adequately used?
- This quite recent article reported on the same topic: PMID:38327733. What is the added value
of this paper?
|
Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the
ClinicalTrials.gov Database
Version: 2 Date: 23 Jan 2025
Reviewer: Joost Boeckmans
Reviewer's report:
Hui Du and colleagues provide an overview of clinical trials in MASLD registered on
ClinicalTrials.gov. The manuscript is descriptive but gives a practical overview. Certain
concepts could add innovative aspects, in which I hope my input can be useful:
Major
- Introduction: in my opinion, the introduction would benefit from discussing the potential drug
targets in MASLD in the context of the pathophysiology, instead of a lengthy discussion on
prevalence. In that view, the part on the pathogenesis could use an update as well, with the ‘two-
hit’ hypothesis being outdated and perhaps less relevant to describe seen the scope of the paper.
- The authors describe hepatic fat content as a frequent endpoint. What about the technique to
quantify this? Was this always MRI-PDFF? + what is usually considered as a relevant lipid
reduction? Same for histology, are there already some using AI?
- Based on the search, what are the advantages of current ‘most popular’ drugs under
development over the failed compounds? Eg. Elafibranor.
- What about personalized treatment developments? Eg. Regarding PNPLA3? When did these
kinds of approaches emerge?
All in all, I think it would be good to describe such temporal changes (i.e. last 3 points) in more
detail, since this informs about new developments
Minor
- Introduction: The global prevalence is around 38%, please see Riazi K, Azhari H, Charette
JH, Underwood FE, King JA, Afshar EE, Swain MG, Congly SE, Kaplan GG, Shaheen AA.
The prevalence and incidence of NAFLD worldwide: a systematic review and meta-analysis.
Lancet Gastroenterol Hepatol. 2022 Sep;7(9):851-861. doi: 10.1016/S2468-1253(22)00165-0.
Epub 2022 Jul 5. PMID: 35798021.
- Would be good to use the MASLD terminology (or MAFLD if regionally preferred) to create
some uniformity.
- Fig 3: Might be good to also have a grey box with ‘no trials’ registered or similar
- Abstract: “140 drug interventional trials primarily aimed to improve NAFLD through
mechanisms such as metabolic and energy balance”; would be informative to add a percentage
to this number. How did the targets change throughout the time?
- Better not to use adjectives as ‘meticulous’, or ‘rigorous’ when describing relatively simple
concepts (cfr methods section).
- Was gender (vs sex) adequately used?
- This quite recent article reported on the same topic: PMID:38327733. What is the added value
of this paper?
|
BMC
|
12876_2025_3732_ReviewerReport_V2_R2.pdf
|
{
"criticism": 1,
"example": 1,
"importance_and_relevance": 2,
"materials_and_methods": 10,
"praise": 2,
"presentation_and_reporting": 6,
"results_and_discussion": 1,
"suggestion_and_solution": 7,
"total": 30
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"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the\nClinicalTrials.gov Database\nVersion: 2 Date: 23 Jan 2025\nReviewer: Joost Boeckmans\nReviewer's report:\nHui Du and colleagues provide an overview of clinical trials in MASLD registered on\nClinicalTrials.gov. The manuscript is descriptive but gives a practical overview. Certain\nconcepts could add innovative aspects, in which I hope my input can be useful:\nMajor\n- Introduction: in my opinion, the introduction would benefit from discussing the potential drug\ntargets in MASLD in the context of the pathophysiology, instead of a lengthy discussion on\nprevalence. In that view, the part on the pathogenesis could use an update as well, with the ‘two-\nhit’ hypothesis being outdated and perhaps less relevant to describe seen the scope of the paper.\n- The authors describe hepatic fat content as a frequent endpoint. What about the technique to\nquantify this? Was this always MRI-PDFF? + what is usually considered as a relevant lipid\nreduction? Same for histology, are there already some using AI?\n- Based on the search, what are the advantages of current ‘most popular’ drugs under\ndevelopment over the failed compounds? Eg. Elafibranor.\n- What about personalized treatment developments? Eg. Regarding PNPLA3? When did these\nkinds of approaches emerge?\nAll in all, I think it would be good to describe such temporal changes (i.e. last 3 points) in more\ndetail, since this informs about new developments\nMinor\n- Introduction: The global prevalence is around 38%, please see Riazi K, Azhari H, Charette\nJH, Underwood FE, King JA, Afshar EE, Swain MG, Congly SE, Kaplan GG, Shaheen AA.\nThe prevalence and incidence of NAFLD worldwide: a systematic review and meta-analysis.\nLancet Gastroenterol Hepatol. 2022 Sep;7(9):851-861. doi: 10.1016/S2468-1253(22)00165-0.\nEpub 2022 Jul 5. PMID: 35798021.\n- Would be good to use the MASLD terminology (or MAFLD if regionally preferred) to create\nsome uniformity.\n- Fig 3: Might be good to also have a grey box with ‘no trials’ registered or similar\n- Abstract: “140 drug interventional trials primarily aimed to improve NAFLD through\nmechanisms such as metabolic and energy balance”; would be informative to add a percentage\nto this number. How did the targets change throughout the time?\n- Better not to use adjectives as ‘meticulous’, or ‘rigorous’ when describing relatively simple\nconcepts (cfr methods section).\n- Was gender (vs sex) adequately used?\n- This quite recent article reported on the same topic: PMID:38327733. What is the added value\nof this paper?",
"role": "assistant"
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] | 2,025
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0
| 0
|
Review for 10.1186/s12876-025-03732-2
|
Reviewed - bmc_gastroenterology
|
Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the
ClinicalTrials.gov Database
Version: 2 Date: 26 Jan 2025
Reviewer's report:
This study provides an overview of the MASLD/NAFLD interventional clinical trials. However,
I have concerns about the conduct and decisions that need further clarification:
Key points:
1. Please use current terminology (i.e., MASLD) consistently throughout the manuscript.
2. Provide more detailed information on the methodology, including the full search strategy,
data handling (how? who? what was done?), and statistical analysis.
3. The authors show the global distribution of MASLD clinical trials. However, it is unclear
whether this distribution includes multinational trials, leading to uncertainty as to whether
this information is accurate. For example, there are MASH trials with sites in Argentina
(NCT03053050, NCT03205150, NCT02855164, NCT03517540), which is shown as having
0 trials. Please investigate the multinational trials further or clearly state that the countries
considered are only those registered in the CT.gov database and acknowledge this as a limitation.
In addition, a table showing the number of trials for each country and their further stratification
by income level (according to the World Bank country classification) would be welcome.
4. Please clarify why phases of studies were classified as 'NA' (not applicable).
Minor points:
1. Introduction: Please provide information on the prevalence of MASLD with updated data
(PMID: 36626630).
|
Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the
ClinicalTrials.gov Database
Version: 2 Date: 26 Jan 2025
Reviewer's report:
This study provides an overview of the MASLD/NAFLD interventional clinical trials. However,
I have concerns about the conduct and decisions that need further clarification:
Key points:
1. Please use current terminology (i.e., MASLD) consistently throughout the manuscript.
2. Provide more detailed information on the methodology, including the full search strategy,
data handling (how? who? what was done?), and statistical analysis.
3. The authors show the global distribution of MASLD clinical trials. However, it is unclear
whether this distribution includes multinational trials, leading to uncertainty as to whether
this information is accurate. For example, there are MASH trials with sites in Argentina
(NCT03053050, NCT03205150, NCT02855164, NCT03517540), which is shown as having
0 trials. Please investigate the multinational trials further or clearly state that the countries
considered are only those registered in the CT.gov database and acknowledge this as a limitation.
In addition, a table showing the number of trials for each country and their further stratification
by income level (according to the World Bank country classification) would be welcome.
4. Please clarify why phases of studies were classified as 'NA' (not applicable).
Minor points:
1. Introduction: Please provide information on the prevalence of MASLD with updated data
(PMID: 36626630).
|
BMC
|
12876_2025_3732_ReviewerReport_V2_R1.pdf
|
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"criticism": 2,
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"praise": 0,
"presentation_and_reporting": 5,
"results_and_discussion": 1,
"suggestion_and_solution": 7,
"total": 18
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"suggestion_and_solution": 0.3888888888888889
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| 1.333333
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[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the\nClinicalTrials.gov Database\nVersion: 2 Date: 26 Jan 2025\nReviewer's report:\nThis study provides an overview of the MASLD/NAFLD interventional clinical trials. However,\nI have concerns about the conduct and decisions that need further clarification:\nKey points:\n1. Please use current terminology (i.e., MASLD) consistently throughout the manuscript.\n2. Provide more detailed information on the methodology, including the full search strategy,\ndata handling (how? who? what was done?), and statistical analysis.\n3. The authors show the global distribution of MASLD clinical trials. However, it is unclear\nwhether this distribution includes multinational trials, leading to uncertainty as to whether\nthis information is accurate. For example, there are MASH trials with sites in Argentina\n(NCT03053050, NCT03205150, NCT02855164, NCT03517540), which is shown as having\n0 trials. Please investigate the multinational trials further or clearly state that the countries\nconsidered are only those registered in the CT.gov database and acknowledge this as a limitation.\nIn addition, a table showing the number of trials for each country and their further stratification\nby income level (according to the World Bank country classification) would be welcome.\n4. Please clarify why phases of studies were classified as 'NA' (not applicable).\nMinor points:\n1. Introduction: Please provide information on the prevalence of MASLD with updated data\n(PMID: 36626630).",
"role": "assistant"
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|
||
0
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|
Review for 10.1186/s12876-025-03732-2
|
Reviewed - bmc_gastroenterology
|
Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the
ClinicalTrials.gov Database
Version: 2 Date: 26 Jan 2025
Reviewer: Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While the multiple-strike theory is introduced, a bit more explanation of how these factors
interrelate (e.g., liver-gut axis, intestinal microbiota) could enhance clarity. For instance, a
brief mention of how gut microbiota alterations may influence liver inflammation and fat
accumulation could be helpful for a more comprehensive understanding.
-The statistics from China are crucial, but it would be valuable to include more global context
to highlight how the prevalence and burden of NAFLD in other regions compare. For instance,
the prevalence of NAFLD in the U.S. or Europe could give a broader perspective on the global
burden.
-The study mentions using ClinicalTrials.gov but does not specify if there were any additional
databases or sources considered for a more robust search. While ClinicalTrials.gov is a primary
source, acknowledging if other databases were consulted (e.g., PubMed, WHO International
Clinical Trials Registry Platform) could improve the comprehensiveness of the data.
-The statistical analysis section mentions the use of SAS software for frequency and percentage
calculations, but it would be helpful to elaborate on why this method was chosen. Was any
advanced analysis, such as regression modeling or time series analysis, used to explore trends
over the years?
-While the list of drug targets is useful, it could be even more valuable to discuss the efficacy
or challenges associated with these drug classes. For example, how effective are PPAR agonists
or GLP-1 analogs in treating NAFLD, and what are the hurdles they face in clinical trials?
-The mention of herbal medicines (silymarin and Korean red ginseng) stands out. It would be
helpful to briefly explore why these specific herbs were chosen and what results (if any) have
been observed. Is there any data on their effectiveness, or are these trials still in the early stages?
-While the inclusion of percentages (e.g., 8.77% of trials focused on behavioral interventions,
13.73% on dietary supplements) adds useful context, some readers may benefit from additional
explanation regarding how these figures relate to the broader dataset. For instance, a brief
comparison of the prevalence of lifestyle-focused trials versus pharmacological ones might help
highlight trends more clearly.
-The discussion delves into some detailed mechanistic pathways, such as the roles of FXR,
PPARs, and FGF21. While these points are insightful, the explanations could be more concise
and more clearly tied to the clinical implications. The mechanisms of action for certain drugs
(e.g., FXR agonists) could be summarized in simpler terms to improve accessibility for a wider
audience. Providing more tangible examples of how these mechanisms translate into clinical
outcomes might also strengthen the argument.
-The section mentions that there is a higher prevalence of NAFLD in men, and suggests a
potential hormonal influence in postmenopausal women, yet the discussion on gender is brief.
Expanding on gender-based differences in NAFLD progression and response to treatment would
add depth, especially given that gender-specific therapies might become an important area for
future trials.
-While the discussion briefly mentions the increasing prevalence of NAFLD in children, this
could be expanded. Specific trends, challenges, or findings related to pediatric clinical trials
would be valuable. Since NAFLD in children is an emerging concern, a deeper focus on how
clinical trials are addressing pediatric populations would strengthen this section.
-The study touches on the growing trend toward using non-invasive methods for assessing liver
fibrosis and NASH improvement. Expanding on which specific technologies or biomarkers are
being explored in clinical trials would be helpful. This section feels somewhat underdeveloped,
given the increasing relevance of non-invasive diagnostics in clinical practice.
|
Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the
ClinicalTrials.gov Database
Version: 2 Date: 26 Jan 2025
Reviewer: Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While the multiple-strike theory is introduced, a bit more explanation of how these factors
interrelate (e.g., liver-gut axis, intestinal microbiota) could enhance clarity. For instance, a
brief mention of how gut microbiota alterations may influence liver inflammation and fat
accumulation could be helpful for a more comprehensive understanding.
-The statistics from China are crucial, but it would be valuable to include more global context
to highlight how the prevalence and burden of NAFLD in other regions compare. For instance,
the prevalence of NAFLD in the U.S. or Europe could give a broader perspective on the global
burden.
-The study mentions using ClinicalTrials.gov but does not specify if there were any additional
databases or sources considered for a more robust search. While ClinicalTrials.gov is a primary
source, acknowledging if other databases were consulted (e.g., PubMed, WHO International
Clinical Trials Registry Platform) could improve the comprehensiveness of the data.
-The statistical analysis section mentions the use of SAS software for frequency and percentage
calculations, but it would be helpful to elaborate on why this method was chosen. Was any
advanced analysis, such as regression modeling or time series analysis, used to explore trends
over the years?
-While the list of drug targets is useful, it could be even more valuable to discuss the efficacy
or challenges associated with these drug classes. For example, how effective are PPAR agonists
or GLP-1 analogs in treating NAFLD, and what are the hurdles they face in clinical trials?
-The mention of herbal medicines (silymarin and Korean red ginseng) stands out. It would be
helpful to briefly explore why these specific herbs were chosen and what results (if any) have
been observed. Is there any data on their effectiveness, or are these trials still in the early stages?
-While the inclusion of percentages (e.g., 8.77% of trials focused on behavioral interventions,
13.73% on dietary supplements) adds useful context, some readers may benefit from additional
explanation regarding how these figures relate to the broader dataset. For instance, a brief
comparison of the prevalence of lifestyle-focused trials versus pharmacological ones might help
highlight trends more clearly.
-The discussion delves into some detailed mechanistic pathways, such as the roles of FXR,
PPARs, and FGF21. While these points are insightful, the explanations could be more concise
and more clearly tied to the clinical implications. The mechanisms of action for certain drugs
(e.g., FXR agonists) could be summarized in simpler terms to improve accessibility for a wider
audience. Providing more tangible examples of how these mechanisms translate into clinical
outcomes might also strengthen the argument.
-The section mentions that there is a higher prevalence of NAFLD in men, and suggests a
potential hormonal influence in postmenopausal women, yet the discussion on gender is brief.
Expanding on gender-based differences in NAFLD progression and response to treatment would
add depth, especially given that gender-specific therapies might become an important area for
future trials.
-While the discussion briefly mentions the increasing prevalence of NAFLD in children, this
could be expanded. Specific trends, challenges, or findings related to pediatric clinical trials
would be valuable. Since NAFLD in children is an emerging concern, a deeper focus on how
clinical trials are addressing pediatric populations would strengthen this section.
-The study touches on the growing trend toward using non-invasive methods for assessing liver
fibrosis and NASH improvement. Expanding on which specific technologies or biomarkers are
being explored in clinical trials would be helpful. This section feels somewhat underdeveloped,
given the increasing relevance of non-invasive diagnostics in clinical practice.
|
BMC
|
12876_2025_3732_ReviewerReport_V2_R3.pdf
|
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"total": 27
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"suggestion_and_solution": 0.6666666666666666
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"content": "Please review this paper.",
"role": "user"
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"content": "Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the\nClinicalTrials.gov Database\nVersion: 2 Date: 26 Jan 2025\nReviewer: Anwar Ashraf Abouelnasr\nReviewer's report:\nDear Authors, please address the following points below\n-While the multiple-strike theory is introduced, a bit more explanation of how these factors\ninterrelate (e.g., liver-gut axis, intestinal microbiota) could enhance clarity. For instance, a\nbrief mention of how gut microbiota alterations may influence liver inflammation and fat\naccumulation could be helpful for a more comprehensive understanding.\n-The statistics from China are crucial, but it would be valuable to include more global context\nto highlight how the prevalence and burden of NAFLD in other regions compare. For instance,\nthe prevalence of NAFLD in the U.S. or Europe could give a broader perspective on the global\nburden.\n-The study mentions using ClinicalTrials.gov but does not specify if there were any additional\ndatabases or sources considered for a more robust search. While ClinicalTrials.gov is a primary\nsource, acknowledging if other databases were consulted (e.g., PubMed, WHO International\nClinical Trials Registry Platform) could improve the comprehensiveness of the data.\n-The statistical analysis section mentions the use of SAS software for frequency and percentage\ncalculations, but it would be helpful to elaborate on why this method was chosen. Was any\nadvanced analysis, such as regression modeling or time series analysis, used to explore trends\nover the years?\n-While the list of drug targets is useful, it could be even more valuable to discuss the efficacy\nor challenges associated with these drug classes. For example, how effective are PPAR agonists\nor GLP-1 analogs in treating NAFLD, and what are the hurdles they face in clinical trials?\n-The mention of herbal medicines (silymarin and Korean red ginseng) stands out. It would be\nhelpful to briefly explore why these specific herbs were chosen and what results (if any) have\nbeen observed. Is there any data on their effectiveness, or are these trials still in the early stages?\n-While the inclusion of percentages (e.g., 8.77% of trials focused on behavioral interventions,\n13.73% on dietary supplements) adds useful context, some readers may benefit from additional\nexplanation regarding how these figures relate to the broader dataset. For instance, a brief\ncomparison of the prevalence of lifestyle-focused trials versus pharmacological ones might help\nhighlight trends more clearly.\n-The discussion delves into some detailed mechanistic pathways, such as the roles of FXR,\nPPARs, and FGF21. While these points are insightful, the explanations could be more concise\nand more clearly tied to the clinical implications. The mechanisms of action for certain drugs\n(e.g., FXR agonists) could be summarized in simpler terms to improve accessibility for a wider\naudience. Providing more tangible examples of how these mechanisms translate into clinical\noutcomes might also strengthen the argument.\n-The section mentions that there is a higher prevalence of NAFLD in men, and suggests a\npotential hormonal influence in postmenopausal women, yet the discussion on gender is brief.\nExpanding on gender-based differences in NAFLD progression and response to treatment would\nadd depth, especially given that gender-specific therapies might become an important area for\nfuture trials.\n-While the discussion briefly mentions the increasing prevalence of NAFLD in children, this\ncould be expanded. Specific trends, challenges, or findings related to pediatric clinical trials\nwould be valuable. Since NAFLD in children is an emerging concern, a deeper focus on how\nclinical trials are addressing pediatric populations would strengthen this section.\n-The study touches on the growing trend toward using non-invasive methods for assessing liver\nfibrosis and NASH improvement. Expanding on which specific technologies or biomarkers are\nbeing explored in clinical trials would be helpful. This section feels somewhat underdeveloped,\ngiven the increasing relevance of non-invasive diagnostics in clinical practice.",
"role": "assistant"
}
] | 2,025
|
||
0
| 0
|
Review for 10.1186/s12876-025-03732-2
|
Reviewed - bmc_gastroenterology
|
Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the
ClinicalTrials.gov Database
Version: 4 Date: 13 Feb 2025
Reviewer's report:
|
Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the
ClinicalTrials.gov Database
Version: 4 Date: 13 Feb 2025
Reviewer's report:
|
BMC
|
12876_2025_3732_ReviewerReport_V4_R1.pdf
|
{
"criticism": 0,
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"materials_and_methods": 1,
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"suggestion_and_solution": 0,
"total": 1
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[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the\nClinicalTrials.gov Database\nVersion: 4 Date: 13 Feb 2025\nReviewer's report:",
"role": "assistant"
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|
||
0
| 0
|
Review for 10.1186/s12876-025-03732-2
|
Reviewed - bmc_gastroenterology
|
Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the
ClinicalTrials.gov Database
Version: 4 Date: 13 Feb 2025
Reviewer: Anwar Ashraf Abouelnasr
Reviewer's report:
The responses are satisfactory.
|
Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the
ClinicalTrials.gov Database
Version: 4 Date: 13 Feb 2025
Reviewer: Anwar Ashraf Abouelnasr
Reviewer's report:
The responses are satisfactory.
|
BMC
|
12876_2025_3732_ReviewerReport_V4_R3.pdf
|
{
"criticism": 0,
"example": 0,
"importance_and_relevance": 0,
"materials_and_methods": 1,
"praise": 1,
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"total": 1
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}
| 2
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[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Analyzing NAFLD Interventional Clinical Trial Registration Based on the\nClinicalTrials.gov Database\nVersion: 4 Date: 13 Feb 2025\nReviewer: Anwar Ashraf Abouelnasr\nReviewer's report:\nThe responses are satisfactory.",
"role": "assistant"
}
] | 2,025
|
||
0
| 0
|
Review for 10.1186/s12876-025-03706-4
|
Reviewed - bmc_gastroenterology
|
Title: Weight-adjusted waist circumference index with hepatic steatosis and fibrosis in adult
females: a cross-sectional, nationally representative study (NHANES 2017–2020)
Version: 2 Date: 31 Jul 2024
Reviewer's report:
|
Title: Weight-adjusted waist circumference index with hepatic steatosis and fibrosis in adult
females: a cross-sectional, nationally representative study (NHANES 2017–2020)
Version: 2 Date: 31 Jul 2024
Reviewer's report:
|
BMC
|
12876_2025_3706_ReviewerReport_V2_R1.pdf
|
{
"criticism": 0,
"example": 0,
"importance_and_relevance": 0,
"materials_and_methods": 1,
"praise": 0,
"presentation_and_reporting": 0,
"results_and_discussion": 0,
"suggestion_and_solution": 0,
"total": 1
}
|
{
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"suggestion_and_solution": 0
}
| 1
| 0
|
[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Weight-adjusted waist circumference index with hepatic steatosis and fibrosis in adult\nfemales: a cross-sectional, nationally representative study (NHANES 2017–2020)\nVersion: 2 Date: 31 Jul 2024\nReviewer's report:",
"role": "assistant"
}
] | 2,025
|
||
0
| 0
|
Review for 10.1186/s12876-025-03706-4
|
Reviewed - bmc_gastroenterology
|
Title: Weight-adjusted waist circumference index with hepatic steatosis and fibrosis in adult
females: a cross-sectional, nationally representative study (NHANES 2017–2020)
Version: 2 Date: 08 Oct 2024
Reviewer's report:
We had the honor to review the manuscript on weight-adjusted waist circumference index and its
associations with liver disease (steatosis and fibrosis based on FibroScan) amongst females from
the NHANES 2017-2020 database. Although the findings are interesting and the topic deserves
further investigation the enthusiasm is limited due to the complexity of the study and lack of a
single strong story aiding the reader through this information.
Major
1. Although some other markers were investigated, it remains unclear to me if the WWI is better
in assessing the risk of steatosis and fibrosis compared to the other tests mentioned in this study.
2. Although one should always consider impact of sex on body composition and the associated
risks, I miss the comparison to the male counterpart. Is the WWI also better in males? Are there
different associations? Or can we use WWI in both female and males?
3. I am intrigued by the U shaped correlation for WWI and LSM. This seems to be in
contradiction with Table 1, where the lowers LSM was reported for Q1 and highest for Q4.
Might this due to (over)adjusting? Among the Q1, were there also more patients with clinically
relevant increased LSM?
4. Although the data is interesting, I have difficulties extracting useful conclusions for further
research and/or clinical practice. I recommend the authors to assess carefully what the main
messages would be of this paper and how the tables and figures could contribute to this message.
Minor
1. Please check for style and grammar. Some sentences are duplicate or in contradiction. For
example, the first sentence is duplicated in the data analysis section and the table legends are
sometime duplicated, especially the models, however, they are not the same models which is
confusing.
|
Title: Weight-adjusted waist circumference index with hepatic steatosis and fibrosis in adult
females: a cross-sectional, nationally representative study (NHANES 2017–2020)
Version: 2 Date: 08 Oct 2024
Reviewer's report:
We had the honor to review the manuscript on weight-adjusted waist circumference index and its
associations with liver disease (steatosis and fibrosis based on FibroScan) amongst females from
the NHANES 2017-2020 database. Although the findings are interesting and the topic deserves
further investigation the enthusiasm is limited due to the complexity of the study and lack of a
single strong story aiding the reader through this information.
Major
1. Although some other markers were investigated, it remains unclear to me if the WWI is better
in assessing the risk of steatosis and fibrosis compared to the other tests mentioned in this study.
2. Although one should always consider impact of sex on body composition and the associated
risks, I miss the comparison to the male counterpart. Is the WWI also better in males? Are there
different associations? Or can we use WWI in both female and males?
3. I am intrigued by the U shaped correlation for WWI and LSM. This seems to be in
contradiction with Table 1, where the lowers LSM was reported for Q1 and highest for Q4.
Might this due to (over)adjusting? Among the Q1, were there also more patients with clinically
relevant increased LSM?
4. Although the data is interesting, I have difficulties extracting useful conclusions for further
research and/or clinical practice. I recommend the authors to assess carefully what the main
messages would be of this paper and how the tables and figures could contribute to this message.
Minor
1. Please check for style and grammar. Some sentences are duplicate or in contradiction. For
example, the first sentence is duplicated in the data analysis section and the table legends are
sometime duplicated, especially the models, however, they are not the same models which is
confusing.
|
BMC
|
12876_2025_3706_ReviewerReport_V2_R3.pdf
|
{
"criticism": 7,
"example": 2,
"importance_and_relevance": 2,
"materials_and_methods": 7,
"praise": 2,
"presentation_and_reporting": 3,
"results_and_discussion": 3,
"suggestion_and_solution": 3,
"total": 21
}
|
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}
| 1.380952
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[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Weight-adjusted waist circumference index with hepatic steatosis and fibrosis in adult\nfemales: a cross-sectional, nationally representative study (NHANES 2017–2020)\nVersion: 2 Date: 08 Oct 2024\nReviewer's report:\nWe had the honor to review the manuscript on weight-adjusted waist circumference index and its\nassociations with liver disease (steatosis and fibrosis based on FibroScan) amongst females from\nthe NHANES 2017-2020 database. Although the findings are interesting and the topic deserves\nfurther investigation the enthusiasm is limited due to the complexity of the study and lack of a\nsingle strong story aiding the reader through this information.\nMajor\n1. Although some other markers were investigated, it remains unclear to me if the WWI is better\nin assessing the risk of steatosis and fibrosis compared to the other tests mentioned in this study.\n2. Although one should always consider impact of sex on body composition and the associated\nrisks, I miss the comparison to the male counterpart. Is the WWI also better in males? Are there\ndifferent associations? Or can we use WWI in both female and males?\n3. I am intrigued by the U shaped correlation for WWI and LSM. This seems to be in\ncontradiction with Table 1, where the lowers LSM was reported for Q1 and highest for Q4.\nMight this due to (over)adjusting? Among the Q1, were there also more patients with clinically\nrelevant increased LSM?\n4. Although the data is interesting, I have difficulties extracting useful conclusions for further\nresearch and/or clinical practice. I recommend the authors to assess carefully what the main\nmessages would be of this paper and how the tables and figures could contribute to this message.\nMinor\n1. Please check for style and grammar. Some sentences are duplicate or in contradiction. For\nexample, the first sentence is duplicated in the data analysis section and the table legends are\nsometime duplicated, especially the models, however, they are not the same models which is\nconfusing.",
"role": "assistant"
}
] | 2,025
|
||
0
| 0
|
Review for 10.1186/s12876-025-03706-4
|
Reviewed - bmc_gastroenterology
|
Title: Weight-adjusted waist circumference index with hepatic steatosis and fibrosis in adult
females: a cross-sectional, nationally representative study (NHANES 2017–2020)
Version: 6 Date: 13 Jan 2025
Reviewer's report:
I endorse the changes made by the authors. They address the previously mentioned issues.
|
Title: Weight-adjusted waist circumference index with hepatic steatosis and fibrosis in adult
females: a cross-sectional, nationally representative study (NHANES 2017–2020)
Version: 6 Date: 13 Jan 2025
Reviewer's report:
I endorse the changes made by the authors. They address the previously mentioned issues.
|
BMC
|
12876_2025_3706_ReviewerReport_V6_R3.pdf
|
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"total": 2
}
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| 0
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{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Weight-adjusted waist circumference index with hepatic steatosis and fibrosis in adult\nfemales: a cross-sectional, nationally representative study (NHANES 2017–2020)\nVersion: 6 Date: 13 Jan 2025\nReviewer's report:\nI endorse the changes made by the authors. They address the previously mentioned issues.",
"role": "assistant"
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||
0
| 0
|
Review for 10.1186/s12876-025-03727-z
|
Reviewed - bmc_gastroenterology
|
Title: Association between avoidant/restrictive food intake disorder risk, dietary attitudes and
behaviors among Chinese patients with inflammatory bowel disease: A cross-sectional study
Version: 1 Date: 23 Jan 2025
Reviewer's report:
The authors confirmed the association between IBD and ARFID and examined the prevalence
of ARFID and its associated factors in a sample of around 500 individuals. They reported that
factors such as having Crohn's disease, having an active disease, having an attitude to managing
symptoms, and having a specific dietary history were associated with ARFID.
Many of the points are similar to those previously reported and there is considered to be little
new evidence. In addition, the low generalisability of the study needs to be discussed in several
respects, including the following.
First, the likelihood that participants in the study would be committed to the diet in the first place
needs to be discussed, and how patients who would not wish to participate in the study would
be treated needs to be fully discussed.
Secondly, the participants were, on average, 37.2 years old (28-46), and it should be mentioned
that most were this young. In other words, it is important to note that the elderly, who are more
prone to nutritional disorders, etc., were not considered.
It should also be mentioned that more than two-thirds of the participants have a university
education or higher. This is because interest in dietetics may be influenced by the presence of
education.
About the results:
Are the results in Table 4 univariate analyses? If they are multivariate analyses, a description
should be added to the Method statistics, and it should also be stated in Table 4 that it is a
multivariate analysis.
If a multivariate analysis has not been performed, this should be clearly stated and the Discussion
should state that the risk factors obtained in this study were univariate and independent.
A satisfactory explanation of the above points and a correction of the article is needed.
|
Title: Association between avoidant/restrictive food intake disorder risk, dietary attitudes and
behaviors among Chinese patients with inflammatory bowel disease: A cross-sectional study
Version: 1 Date: 23 Jan 2025
Reviewer's report:
The authors confirmed the association between IBD and ARFID and examined the prevalence
of ARFID and its associated factors in a sample of around 500 individuals. They reported that
factors such as having Crohn's disease, having an active disease, having an attitude to managing
symptoms, and having a specific dietary history were associated with ARFID.
Many of the points are similar to those previously reported and there is considered to be little
new evidence. In addition, the low generalisability of the study needs to be discussed in several
respects, including the following.
First, the likelihood that participants in the study would be committed to the diet in the first place
needs to be discussed, and how patients who would not wish to participate in the study would
be treated needs to be fully discussed.
Secondly, the participants were, on average, 37.2 years old (28-46), and it should be mentioned
that most were this young. In other words, it is important to note that the elderly, who are more
prone to nutritional disorders, etc., were not considered.
It should also be mentioned that more than two-thirds of the participants have a university
education or higher. This is because interest in dietetics may be influenced by the presence of
education.
About the results:
Are the results in Table 4 univariate analyses? If they are multivariate analyses, a description
should be added to the Method statistics, and it should also be stated in Table 4 that it is a
multivariate analysis.
If a multivariate analysis has not been performed, this should be clearly stated and the Discussion
should state that the risk factors obtained in this study were univariate and independent.
A satisfactory explanation of the above points and a correction of the article is needed.
|
BMC
|
12876_2025_3727_ReviewerReport_V1_R1.pdf
|
{
"criticism": 2,
"example": 0,
"importance_and_relevance": 2,
"materials_and_methods": 8,
"praise": 1,
"presentation_and_reporting": 6,
"results_and_discussion": 5,
"suggestion_and_solution": 8,
"total": 13
}
|
{
"criticism": 0.15384615384615385,
"example": 0,
"importance_and_relevance": 0.15384615384615385,
"materials_and_methods": 0.6153846153846154,
"praise": 0.07692307692307693,
"presentation_and_reporting": 0.46153846153846156,
"results_and_discussion": 0.38461538461538464,
"suggestion_and_solution": 0.6153846153846154
}
| 2.461538
| 0
|
[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Association between avoidant/restrictive food intake disorder risk, dietary attitudes and\nbehaviors among Chinese patients with inflammatory bowel disease: A cross-sectional study\nVersion: 1 Date: 23 Jan 2025\nReviewer's report:\nThe authors confirmed the association between IBD and ARFID and examined the prevalence\nof ARFID and its associated factors in a sample of around 500 individuals. They reported that\nfactors such as having Crohn's disease, having an active disease, having an attitude to managing\nsymptoms, and having a specific dietary history were associated with ARFID.\nMany of the points are similar to those previously reported and there is considered to be little\nnew evidence. In addition, the low generalisability of the study needs to be discussed in several\nrespects, including the following.\nFirst, the likelihood that participants in the study would be committed to the diet in the first place\nneeds to be discussed, and how patients who would not wish to participate in the study would\nbe treated needs to be fully discussed.\nSecondly, the participants were, on average, 37.2 years old (28-46), and it should be mentioned\nthat most were this young. In other words, it is important to note that the elderly, who are more\nprone to nutritional disorders, etc., were not considered.\nIt should also be mentioned that more than two-thirds of the participants have a university\neducation or higher. This is because interest in dietetics may be influenced by the presence of\neducation.\nAbout the results:\nAre the results in Table 4 univariate analyses? If they are multivariate analyses, a description\nshould be added to the Method statistics, and it should also be stated in Table 4 that it is a\nmultivariate analysis.\nIf a multivariate analysis has not been performed, this should be clearly stated and the Discussion\nshould state that the risk factors obtained in this study were univariate and independent.\nA satisfactory explanation of the above points and a correction of the article is needed.",
"role": "assistant"
}
] | 2,025
|
||
0
| 0
|
Review for 10.1186/s12876-025-03727-z
|
Reviewed - bmc_gastroenterology
|
Title: Association between avoidant/restrictive food intake disorder risk, dietary attitudes and
behaviors among Chinese patients with inflammatory bowel disease: A cross-sectional study
Version: 1 Date: 29 Jan 2025
Reviewer's report:
|
Title: Association between avoidant/restrictive food intake disorder risk, dietary attitudes and
behaviors among Chinese patients with inflammatory bowel disease: A cross-sectional study
Version: 1 Date: 29 Jan 2025
Reviewer's report:
|
BMC
|
12876_2025_3727_ReviewerReport_V1_R3.pdf
|
{
"criticism": 0,
"example": 0,
"importance_and_relevance": 0,
"materials_and_methods": 0,
"praise": 0,
"presentation_and_reporting": 0,
"results_and_discussion": 0,
"suggestion_and_solution": 0,
"total": 1
}
|
{
"criticism": 0,
"example": 0,
"importance_and_relevance": 0,
"materials_and_methods": 0,
"praise": 0,
"presentation_and_reporting": 0,
"results_and_discussion": 0,
"suggestion_and_solution": 0
}
| 0
| 0
|
[
{
"content": "Please review this paper.",
"role": "user"
},
{
"content": "Title: Association between avoidant/restrictive food intake disorder risk, dietary attitudes and\nbehaviors among Chinese patients with inflammatory bowel disease: A cross-sectional study\nVersion: 1 Date: 29 Jan 2025\nReviewer's report:",
"role": "assistant"
}
] | 2,025
|
End of preview. Expand
in Data Studio
BMC Gastroenterology Peer Reviews
This dataset contains peer reviews from BMC, standardized to match the format of the pawin205/PeerRT dataset.
Dataset Structure
Each record contains the following attributes:
relative_rank: Default value (0).win_prob: Default value (0.0).title: Title of the paper.abstract: Abstract of the paper.full_text: Full text of the paper (or review text if unavailable).review: The peer review text.source: Source of the data ('BMC').review_src: Original filename of the review.criteria_count: Dictionary containing counts of specific criteria in the review (e.g., criticism, praise).dimension_scores: Dictionary containing scores for various dimensions.overall_score: Computed overall score (reward value).thinking_trace: Placeholder (empty).prompt: Placeholder (empty).prompt_length: Placeholder (0).conversations: List of dictionaries representing the conversation (User/Assistant format).year: Year of publication (if available).
Usage
from datasets import load_dataset
dataset = load_dataset("JerMa88/BMC_Gastroenterology_Peer_Reviews")
print(dataset['train'][0])
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