Reviewer's report
Title:Quantitative Modeling of the Physiology of Ascites in Portal Hypertension
Version: 3Date:9 February 2012
Reviewer: Beate Appenrodt
Reviewer's report:
Levitt et al. describes a new, quantitative model for the pathomechanism of
ascites in portal hypertension. The authors explain in detail the two common
theories of evolving ascites, the underfill and the overflow theory.
They conclude that the mechanism of developuing ascites is only poorly
understood beside both theories.
Furthemore, they remark that the pathophysiology of the known plasma-ascitic
gradient of albumin is also poorly understood.
The manuscript is structured in three sections. In section III, a new quantitative
physical model describing ascites accumulation is discussed.
It is a very interesting and new attempt to explain the pathomechanism of
ascites.
However, there are some comments:
1) One main pathomechansim is the activation of the RAAS in portal
hypertension. Please discuss this mechanism more detailed.
1) On page 14 (E), SAAG as differential diagnostic marker between different
causes of ascites is discussed. “A SAAG of > 1.1 gm% is ... indicative of portal
hypertension (either cirrhotic or cardiac ascites).” The authors should explain the
pathophysiology of cardiac ascites in comparison to cirrhotic ascites. Portal
hypertension is not the common cause for cardiac ascites.
2) Please give references for a) “…administration of spironolactone or furosemid
decreases P(HVPG) by about 20%” and b) decrease in cardiac output with
corresponding fall in hepatic blood flow and P(HVPG) in the main text..
3) On page 17, the authors explain that clonidine produces a significant decrease
in P (HVPG).
Please explain the effect in more detail and add references.
It is not common that clonidine is used for treatment of varices. The authors
should comment on this and add references in the main text (not only in the
attachement).
5) The authors should also discuss the effect of terlipressin and vasopressin-2
antagonists in the treatment of ascites in the main text.
Minor comments:
1) Page 8, line 22 (section II, A.): please change ascetic in ascitic (or
contrariwise)
2) typing error: Page 20, 2 mmHg instead of 2 mm
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I do not have anything to declare.
Reviewer's report
Title:Quantitative Modeling of the Physiology of Ascites in Portal Hypertension
Version: 3Date:9 February 2012
Reviewer: Beate Appenrodt
Reviewer's report:
Levitt et al. describes a new, quantitative model for the pathomechanism of
ascites in portal hypertension. The authors explain in detail the two common
theories of evolving ascites, the underfill and the overflow theory.
They conclude that the mechanism of developuing ascites is only poorly
understood beside both theories.
Furthemore, they remark that the pathophysiology of the known plasma-ascitic
gradient of albumin is also poorly understood.
The manuscript is structured in three sections. In section III, a new quantitative
physical model describing ascites accumulation is discussed.
It is a very interesting and new attempt to explain the pathomechanism of
ascites.
However, there are some comments:
1) One main pathomechansim is the activation of the RAAS in portal
hypertension. Please discuss this mechanism more detailed.
1) On page 14 (E), SAAG as differential diagnostic marker between different
causes of ascites is discussed. “A SAAG of > 1.1 gm% is ... indicative of portal
hypertension (either cirrhotic or cardiac ascites).” The authors should explain the
pathophysiology of cardiac ascites in comparison to cirrhotic ascites. Portal
hypertension is not the common cause for cardiac ascites.
2) Please give references for a) “…administration of spironolactone or furosemid
decreases P(HVPG) by about 20%” and b) decrease in cardiac output with
corresponding fall in hepatic blood flow and P(HVPG) in the main text..
3) On page 17, the authors explain that clonidine produces a significant decrease
in P (HVPG).
Please explain the effect in more detail and add references.
It is not common that clonidine is used for treatment of varices. The authors
should comment on this and add references in the main text (not only in the
attachement).
5) The authors should also discuss the effect of terlipressin and vasopressin-2
antagonists in the treatment of ascites in the main text.
Minor comments:
1) Page 8, line 22 (section II, A.): please change ascetic in ascitic (or
contrariwise)
2) typing error: Page 20, 2 mmHg instead of 2 mm
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I do not have anything to declare.
Please review this paper.
user
Reviewer's report
Title:Quantitative Modeling of the Physiology of Ascites in Portal Hypertension
Version: 3Date:9 February 2012
Reviewer: Beate Appenrodt
Reviewer's report:
Levitt et al. describes a new, quantitative model for the pathomechanism of
ascites in portal hypertension. The authors explain in detail the two common
theories of evolving ascites, the underfill and the overflow theory.
They conclude that the mechanism of developuing ascites is only poorly
understood beside both theories.
Furthemore, they remark that the pathophysiology of the known plasma-ascitic
gradient of albumin is also poorly understood.
The manuscript is structured in three sections. In section III, a new quantitative
physical model describing ascites accumulation is discussed.
It is a very interesting and new attempt to explain the pathomechanism of
ascites.
However, there are some comments:
1) One main pathomechansim is the activation of the RAAS in portal
hypertension. Please discuss this mechanism more detailed.
1) On page 14 (E), SAAG as differential diagnostic marker between different
causes of ascites is discussed. “A SAAG of > 1.1 gm% is ... indicative of portal
hypertension (either cirrhotic or cardiac ascites).” The authors should explain the
pathophysiology of cardiac ascites in comparison to cirrhotic ascites. Portal
hypertension is not the common cause for cardiac ascites.
2) Please give references for a) “…administration of spironolactone or furosemid
decreases P(HVPG) by about 20%” and b) decrease in cardiac output with
corresponding fall in hepatic blood flow and P(HVPG) in the main text..
3) On page 17, the authors explain that clonidine produces a significant decrease
in P (HVPG).
Please explain the effect in more detail and add references.
It is not common that clonidine is used for treatment of varices. The authors
should comment on this and add references in the main text (not only in the
attachement).
5) The authors should also discuss the effect of terlipressin and vasopressin-2
antagonists in the treatment of ascites in the main text.
Minor comments:
1) Page 8, line 22 (section II, A.): please change ascetic in ascitic (or
contrariwise)
2) typing error: Page 20, 2 mmHg instead of 2 mm
Level of interest: An article of importance in its field
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I do not have anything to declare.
assistant