Title: Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a
lipidomic study
Version: 0 Date: 02 Aug 2024
Reviewer's report:
Øystein Kittel Moe et al. evaluated mucosal lipid shifts in treatment refractory inflammatory
bowel disease. This is a very interesting area of research with the potential to identify predictors
of response/new targets for treatment. However, there are some limitations that should be
addressed:
1.      The authors mention various inflammatory and treatment pathways in the background and
discussion sections that do not seem to pertain directly to your data on lipids (eg JAK/STAT and
S1P pathways as well as PEMT, PDTSS2, and ELOVL3). Consider omitting this information
or clarify how it pertains to your findings.
2.      While it is useful to have information on patients treated with vedolizumab, it is difficult to
draw any conclusions from the data you have with only 2 patients in this study on vedolizumab.
3.      It would be clinically useful to know about other variables that can affect mucosal
lipid levels such as serum lipid levels, BMI, and nutritional status (perhaps evaluated through
prealbumin levels or other nutritional markers) and if these could affect the results.
4.      Please expand on the choice to use anti-TNF mucosal transcript as a marker for disease
remission as this is not a commonly used measure or standardized treatment goal.
5.      More information is needed regarding sampling location such as large or small bowel which
could affect baseline lipid levels as well as targeted biopsies for those patients in remission.
Were biopsies taken from areas where these patients were known to have the most severe disease
in the past (I.E. rectum in patient with UC proctitis in remission)?
6.      It is unclear why there was no significant difference between lipid profiles of refractory UC
patients and those in remission. Further discussion of possible reasons behind this is indicated.
Thank you again for your submission. This area of study holds promise, and I hope these
clarifications will serve to strengthen the message of your research
Title: Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a
lipidomic study
Version: 0 Date: 02 Aug 2024
Reviewer's report:
Øystein Kittel Moe et al. evaluated mucosal lipid shifts in treatment refractory inflammatory
bowel disease. This is a very interesting area of research with the potential to identify predictors
of response/new targets for treatment. However, there are some limitations that should be
addressed:
1.      The authors mention various inflammatory and treatment pathways in the background and
discussion sections that do not seem to pertain directly to your data on lipids (eg JAK/STAT and
S1P pathways as well as PEMT, PDTSS2, and ELOVL3). Consider omitting this information
or clarify how it pertains to your findings.
2.      While it is useful to have information on patients treated with vedolizumab, it is difficult to
draw any conclusions from the data you have with only 2 patients in this study on vedolizumab.
3.      It would be clinically useful to know about other variables that can affect mucosal
lipid levels such as serum lipid levels, BMI, and nutritional status (perhaps evaluated through
prealbumin levels or other nutritional markers) and if these could affect the results.
4.      Please expand on the choice to use anti-TNF mucosal transcript as a marker for disease
remission as this is not a commonly used measure or standardized treatment goal.
5.      More information is needed regarding sampling location such as large or small bowel which
could affect baseline lipid levels as well as targeted biopsies for those patients in remission.
Were biopsies taken from areas where these patients were known to have the most severe disease
in the past (I.E. rectum in patient with UC proctitis in remission)?
6.      It is unclear why there was no significant difference between lipid profiles of refractory UC
patients and those in remission. Further discussion of possible reasons behind this is indicated.
Thank you again for your submission. This area of study holds promise, and I hope these
clarifications will serve to strengthen the message of your research
Please review this paper.
user
Title: Marked mucosal lipid shifts in treatment refractory inflammatory bowel disease: a
lipidomic study
Version: 0 Date: 02 Aug 2024
Reviewer's report:
Øystein Kittel Moe et al. evaluated mucosal lipid shifts in treatment refractory inflammatory
bowel disease. This is a very interesting area of research with the potential to identify predictors
of response/new targets for treatment. However, there are some limitations that should be
addressed:
1.      The authors mention various inflammatory and treatment pathways in the background and
discussion sections that do not seem to pertain directly to your data on lipids (eg JAK/STAT and
S1P pathways as well as PEMT, PDTSS2, and ELOVL3). Consider omitting this information
or clarify how it pertains to your findings.
2.      While it is useful to have information on patients treated with vedolizumab, it is difficult to
draw any conclusions from the data you have with only 2 patients in this study on vedolizumab.
3.      It would be clinically useful to know about other variables that can affect mucosal
lipid levels such as serum lipid levels, BMI, and nutritional status (perhaps evaluated through
prealbumin levels or other nutritional markers) and if these could affect the results.
4.      Please expand on the choice to use anti-TNF mucosal transcript as a marker for disease
remission as this is not a commonly used measure or standardized treatment goal.
5.      More information is needed regarding sampling location such as large or small bowel which
could affect baseline lipid levels as well as targeted biopsies for those patients in remission.
Were biopsies taken from areas where these patients were known to have the most severe disease
in the past (I.E. rectum in patient with UC proctitis in remission)?
6.      It is unclear why there was no significant difference between lipid profiles of refractory UC
patients and those in remission. Further discussion of possible reasons behind this is indicated.
Thank you again for your submission. This area of study holds promise, and I hope these
clarifications will serve to strengthen the message of your research
assistant