Reviewer's report
Title:The effect of H. pylori eradication on meal-associated changes in plasma
ghrelin and leptin
Version: 1Date:25 November 2010
Reviewer: Lucia Pacifico
Reviewer's report:
The aim of the present paper by Francois et al. was to evaluate the effect of H.
pylori eradication on meal-associated changes in serum ghrelin and leptin levels,
and body weight.
Comments
1. H. pylori-negative has BMI significantly different in comparison with H.
pylori-positive group. Since all studied parameters (ghrelin, leptin) are greatly
influenced by weight, height, or BMI, direct comparisons of groups with different
BMI using statistics applied in the present study, give biased results.
1A. BMI is a fat accumulation index. Waist circumference could have been used
as well.
2. Did the Authors measure body fat composition? An MRI could have been used
to estimate fat distribution precisely, especially the subcutaneous fat, which has
the strongest correlation with leptin (95% of circulating leptin is produced from
this tissue).
3. There is no control group of healthy subjects.
4. The fact that 81.5% of the H. pylori-negative patients failed to complete the
follow-up is a disadvantage for the survey.
5. When referring to leptin, it would be best to state if it is the free (active) or
bound type of the hormone.
6. Published findings suggest ghrelin positive cells are found primarily in oxyntic
mucosa. Because of this, the association with antral inflammation seems likely to
be a marker of overall gastric inflammation. Repeat analysis of the association
between antral inflammation and ghrelin levels after correcting for corpus
inflammation would clarify the true association.
7. The Authors should discuss whether ghrelin levels reflect H. pylori infection or
whether they reflect the severity of gastritis from any cause.
8. The Authors have not addressed the question of changes in the ratio of the
circulating active and inactive form of ghrelin before and after eradication. Under
the assumption that the changes in BMI are not responsible for the changes in
circulating acyl ghrelin levels it would be interesting to know whether the ratio of
acyl- to desacyl-ghrelin is changed in favour to desacyl-ghrelin and whether this
ratio changed after eradication. In case the samples are still stored and have
been adequately collected it should be possible to answer this question.
Level of interest: An article of insufficient interest to warrant publication in a
scientific/medical journal
Quality of written English: Acceptable
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
Reviewer's report
Title:The effect of H. pylori eradication on meal-associated changes in plasma
ghrelin and leptin
Version: 1Date:25 November 2010
Reviewer: Lucia Pacifico
Reviewer's report:
The aim of the present paper by Francois et al. was to evaluate the effect of H.
pylori eradication on meal-associated changes in serum ghrelin and leptin levels,
and body weight.
Comments
1. H. pylori-negative has BMI significantly different in comparison with H.
pylori-positive group. Since all studied parameters (ghrelin, leptin) are greatly
influenced by weight, height, or BMI, direct comparisons of groups with different
BMI using statistics applied in the present study, give biased results.
1A. BMI is a fat accumulation index. Waist circumference could have been used
as well.
2. Did the Authors measure body fat composition? An MRI could have been used
to estimate fat distribution precisely, especially the subcutaneous fat, which has
the strongest correlation with leptin (95% of circulating leptin is produced from
this tissue).
3. There is no control group of healthy subjects.
4. The fact that 81.5% of the H. pylori-negative patients failed to complete the
follow-up is a disadvantage for the survey.
5. When referring to leptin, it would be best to state if it is the free (active) or
bound type of the hormone.
6. Published findings suggest ghrelin positive cells are found primarily in oxyntic
mucosa. Because of this, the association with antral inflammation seems likely to
be a marker of overall gastric inflammation. Repeat analysis of the association
between antral inflammation and ghrelin levels after correcting for corpus
inflammation would clarify the true association.
7. The Authors should discuss whether ghrelin levels reflect H. pylori infection or
whether they reflect the severity of gastritis from any cause.
8. The Authors have not addressed the question of changes in the ratio of the
circulating active and inactive form of ghrelin before and after eradication. Under
the assumption that the changes in BMI are not responsible for the changes in
circulating acyl ghrelin levels it would be interesting to know whether the ratio of
acyl- to desacyl-ghrelin is changed in favour to desacyl-ghrelin and whether this
ratio changed after eradication. In case the samples are still stored and have
been adequately collected it should be possible to answer this question.
Level of interest: An article of insufficient interest to warrant publication in a
scientific/medical journal
Quality of written English: Acceptable
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
Please review this paper.
user
Reviewer's report
Title:The effect of H. pylori eradication on meal-associated changes in plasma
ghrelin and leptin
Version: 1Date:25 November 2010
Reviewer: Lucia Pacifico
Reviewer's report:
The aim of the present paper by Francois et al. was to evaluate the effect of H.
pylori eradication on meal-associated changes in serum ghrelin and leptin levels,
and body weight.
Comments
1. H. pylori-negative has BMI significantly different in comparison with H.
pylori-positive group. Since all studied parameters (ghrelin, leptin) are greatly
influenced by weight, height, or BMI, direct comparisons of groups with different
BMI using statistics applied in the present study, give biased results.
1A. BMI is a fat accumulation index. Waist circumference could have been used
as well.
2. Did the Authors measure body fat composition? An MRI could have been used
to estimate fat distribution precisely, especially the subcutaneous fat, which has
the strongest correlation with leptin (95% of circulating leptin is produced from
this tissue).
3. There is no control group of healthy subjects.
4. The fact that 81.5% of the H. pylori-negative patients failed to complete the
follow-up is a disadvantage for the survey.
5. When referring to leptin, it would be best to state if it is the free (active) or
bound type of the hormone.
6. Published findings suggest ghrelin positive cells are found primarily in oxyntic
mucosa. Because of this, the association with antral inflammation seems likely to
be a marker of overall gastric inflammation. Repeat analysis of the association
between antral inflammation and ghrelin levels after correcting for corpus
inflammation would clarify the true association.
7. The Authors should discuss whether ghrelin levels reflect H. pylori infection or
whether they reflect the severity of gastritis from any cause.
8. The Authors have not addressed the question of changes in the ratio of the
circulating active and inactive form of ghrelin before and after eradication. Under
the assumption that the changes in BMI are not responsible for the changes in
circulating acyl ghrelin levels it would be interesting to know whether the ratio of
acyl- to desacyl-ghrelin is changed in favour to desacyl-ghrelin and whether this
ratio changed after eradication. In case the samples are still stored and have
been adequately collected it should be possible to answer this question.
Level of interest: An article of insufficient interest to warrant publication in a
scientific/medical journal
Quality of written English: Acceptable
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
assistant