Title: The effect of propranolol on gastrointestinal motility and permeability in patients with
cirrhosis and significant portal hypertension
Version: 2 Date: 14 Jul 2024
Reviewer's report:
Thank you for addressing most of the issues raised
1. Pertaining to footnote in Table 2, I now understand what the authors meant. The footnote is
still incorrect and it should read "Values for permeabilities are expressed as median and range
in parenthesis".
2. I raised the query on subgroup analysis of OCTT, IP, inflammatory markers and BT, on how
the increase or decrease was defined. Based on the authors' clarification, if one hypothetical
study participant's LPS level was 6.1pg/ml at baseline and 6.0pg/ml after NSBB, the authors
would consider this study participant's LPS to have decreased? My concern is, if this was the
case, then would the minimal 0.1pg/ml decrease clinically relevant or significant? Using an
unrelated example of response to NSBB, if a patient has HVPG 15mmHg at baseline off NSBB
and 14mmHg on NSBB, the patient would have been regarded as having a decrease in HVPG
but this is clinically not significant because response required at least 10% decline rather than
any decline. Please clarify.
3. I may have missed the authors' clarification under Discussion on the contradictory results of
this study with regards to change in LPS and other inflammatory markers compared to reference
27. Could the authors discuss the differences between the results of the 2 studies and suggest
the reasons for the findings (dose of propranolol as the authors had suggested).
4. Thank you for putting forward the hypothesis on how NSBB affects the paracellular pathway.
I was hoping for the authors to include their response into Discussion as it is very pertinent to
findings of the study.
Title: The effect of propranolol on gastrointestinal motility and permeability in patients with
cirrhosis and significant portal hypertension
Version: 2 Date: 14 Jul 2024
Reviewer's report:
Thank you for addressing most of the issues raised
1. Pertaining to footnote in Table 2, I now understand what the authors meant. The footnote is
still incorrect and it should read "Values for permeabilities are expressed as median and range
in parenthesis".
2. I raised the query on subgroup analysis of OCTT, IP, inflammatory markers and BT, on how
the increase or decrease was defined. Based on the authors' clarification, if one hypothetical
study participant's LPS level was 6.1pg/ml at baseline and 6.0pg/ml after NSBB, the authors
would consider this study participant's LPS to have decreased? My concern is, if this was the
case, then would the minimal 0.1pg/ml decrease clinically relevant or significant? Using an
unrelated example of response to NSBB, if a patient has HVPG 15mmHg at baseline off NSBB
and 14mmHg on NSBB, the patient would have been regarded as having a decrease in HVPG
but this is clinically not significant because response required at least 10% decline rather than
any decline. Please clarify.
3. I may have missed the authors' clarification under Discussion on the contradictory results of
this study with regards to change in LPS and other inflammatory markers compared to reference
27. Could the authors discuss the differences between the results of the 2 studies and suggest
the reasons for the findings (dose of propranolol as the authors had suggested).
4. Thank you for putting forward the hypothesis on how NSBB affects the paracellular pathway.
I was hoping for the authors to include their response into Discussion as it is very pertinent to
findings of the study.
Please review this paper.
user
Title: The effect of propranolol on gastrointestinal motility and permeability in patients with
cirrhosis and significant portal hypertension
Version: 2 Date: 14 Jul 2024
Reviewer's report:
Thank you for addressing most of the issues raised
1. Pertaining to footnote in Table 2, I now understand what the authors meant. The footnote is
still incorrect and it should read "Values for permeabilities are expressed as median and range
in parenthesis".
2. I raised the query on subgroup analysis of OCTT, IP, inflammatory markers and BT, on how
the increase or decrease was defined. Based on the authors' clarification, if one hypothetical
study participant's LPS level was 6.1pg/ml at baseline and 6.0pg/ml after NSBB, the authors
would consider this study participant's LPS to have decreased? My concern is, if this was the
case, then would the minimal 0.1pg/ml decrease clinically relevant or significant? Using an
unrelated example of response to NSBB, if a patient has HVPG 15mmHg at baseline off NSBB
and 14mmHg on NSBB, the patient would have been regarded as having a decrease in HVPG
but this is clinically not significant because response required at least 10% decline rather than
any decline. Please clarify.
3. I may have missed the authors' clarification under Discussion on the contradictory results of
this study with regards to change in LPS and other inflammatory markers compared to reference
27. Could the authors discuss the differences between the results of the 2 studies and suggest
the reasons for the findings (dose of propranolol as the authors had suggested).
4. Thank you for putting forward the hypothesis on how NSBB affects the paracellular pathway.
I was hoping for the authors to include their response into Discussion as it is very pertinent to
findings of the study.
assistant