Title: Variations in TM6SF2, PCSK9 and PCSK7 genes and risk of hepatic steatosis after liver
transplantation: a cross-sectional study
Version: 1 Date: 25 Mar 2021
Reviewer:  Nikoletta Maria Tagkou
Reviewer's report:
Overall, this is a very interesting and properly designed cross-sectional study that aimed to
investigate the association between three genetic variants and the presence of hepatic steatosis
in liver transplant recipients. Nevertheless, there are a few amendments that can be made before
this paper is proceeded for publication.
The abstract is clear and well-structured and the aim of the study is properly stated.
In the Introduction the authors mention that there are no clinical studies concerning PCSK9 and
PCSK7 and liver steatosis. Maybe the authors should consider studying the following recent
studies concerning PCSK9:
1. Paquette M et al. Circulating PCSK9 is associated with liver biomarkers and hepatic steatosis.
Clin Biochem. 2020 Mar;77:20-25. doi: 10.1016/j.clinbiochem.2020.01.003.
2. Grimaudo S et al. PCSK9 rs11591147 R46L loss-of-function variant protects against liver
damage in individuals with NAFLD. Liver Int. 2021 Feb;41(2):321-332. doi: 10.1111/liv.14711.
Concerning PCSK7, they should consider citing the study by Dongiovanni P et al. in the
Introduction, too.
In the Results section, the authors should elucidate why they chose to divide the patients in those
with “low-grade” (S1) and “high-grade” (S2-3) steatosis, since the official CAP steatosis staging
in mild-S1, moderate-S2, and severe-S3 steatosis.
In the Discussion, some general information on the genetic polymorphisms are already
mentioned in the Introduction and they should not be repeated. Furthermore, in this part the
authors should consider stating the limitations of their study.
Finally, Table 4 title should be corrected, as it presents patients with low or high grade hepatic
steatosis.
There are also some minor syntactical errors throughout the text, for example some articles that
are missing, that should be easy for the authors to locate and correct.
Title: Variations in TM6SF2, PCSK9 and PCSK7 genes and risk of hepatic steatosis after liver
transplantation: a cross-sectional study
Version: 1 Date: 25 Mar 2021
Reviewer:  Nikoletta Maria Tagkou
Reviewer's report:
Overall, this is a very interesting and properly designed cross-sectional study that aimed to
investigate the association between three genetic variants and the presence of hepatic steatosis
in liver transplant recipients. Nevertheless, there are a few amendments that can be made before
this paper is proceeded for publication.
The abstract is clear and well-structured and the aim of the study is properly stated.
In the Introduction the authors mention that there are no clinical studies concerning PCSK9 and
PCSK7 and liver steatosis. Maybe the authors should consider studying the following recent
studies concerning PCSK9:
1. Paquette M et al. Circulating PCSK9 is associated with liver biomarkers and hepatic steatosis.
Clin Biochem. 2020 Mar;77:20-25. doi: 10.1016/j.clinbiochem.2020.01.003.
2. Grimaudo S et al. PCSK9 rs11591147 R46L loss-of-function variant protects against liver
damage in individuals with NAFLD. Liver Int. 2021 Feb;41(2):321-332. doi: 10.1111/liv.14711.
Concerning PCSK7, they should consider citing the study by Dongiovanni P et al. in the
Introduction, too.
In the Results section, the authors should elucidate why they chose to divide the patients in those
with “low-grade” (S1) and “high-grade” (S2-3) steatosis, since the official CAP steatosis staging
in mild-S1, moderate-S2, and severe-S3 steatosis.
In the Discussion, some general information on the genetic polymorphisms are already
mentioned in the Introduction and they should not be repeated. Furthermore, in this part the
authors should consider stating the limitations of their study.
Finally, Table 4 title should be corrected, as it presents patients with low or high grade hepatic
steatosis.
There are also some minor syntactical errors throughout the text, for example some articles that
are missing, that should be easy for the authors to locate and correct.
Please review this paper.
user
Title: Variations in TM6SF2, PCSK9 and PCSK7 genes and risk of hepatic steatosis after liver
transplantation: a cross-sectional study
Version: 1 Date: 25 Mar 2021
Reviewer:  Nikoletta Maria Tagkou
Reviewer's report:
Overall, this is a very interesting and properly designed cross-sectional study that aimed to
investigate the association between three genetic variants and the presence of hepatic steatosis
in liver transplant recipients. Nevertheless, there are a few amendments that can be made before
this paper is proceeded for publication.
The abstract is clear and well-structured and the aim of the study is properly stated.
In the Introduction the authors mention that there are no clinical studies concerning PCSK9 and
PCSK7 and liver steatosis. Maybe the authors should consider studying the following recent
studies concerning PCSK9:
1. Paquette M et al. Circulating PCSK9 is associated with liver biomarkers and hepatic steatosis.
Clin Biochem. 2020 Mar;77:20-25. doi: 10.1016/j.clinbiochem.2020.01.003.
2. Grimaudo S et al. PCSK9 rs11591147 R46L loss-of-function variant protects against liver
damage in individuals with NAFLD. Liver Int. 2021 Feb;41(2):321-332. doi: 10.1111/liv.14711.
Concerning PCSK7, they should consider citing the study by Dongiovanni P et al. in the
Introduction, too.
In the Results section, the authors should elucidate why they chose to divide the patients in those
with “low-grade” (S1) and “high-grade” (S2-3) steatosis, since the official CAP steatosis staging
in mild-S1, moderate-S2, and severe-S3 steatosis.
In the Discussion, some general information on the genetic polymorphisms are already
mentioned in the Introduction and they should not be repeated. Furthermore, in this part the
authors should consider stating the limitations of their study.
Finally, Table 4 title should be corrected, as it presents patients with low or high grade hepatic
steatosis.
There are also some minor syntactical errors throughout the text, for example some articles that
are missing, that should be easy for the authors to locate and correct.
assistant