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Reply to Chang and Garcia-Pagan


Kovari, H; Ledergerber, B; Weber, R (2010). Reply to Chang and Garcia-Pagan. Clinical Infectious Diseases, 50(1):128-129.

Abstract

To the Editor—We thank Chang and Garcia-Pagan [1] for their interest in our study [2], and we offer the following reply. First, in our case-control study of human immunodeficiency virus (HIV)-infected patients with noncirrhotic portal hypertension (NCPH), inclusion criteria were the presence of endoscopically documented esophageal varices or hepatic venous pressure gradient (HVPG) ⩾10 mmHg, absence of hepatic cirrhosis on liver biopsy, and no common cause of liver disease. All of our case patients had endoscopically documented esophageal varices, and no patient was excluded because of a HVPG <10 mmHg. Eight of 15 case patients underwent hepatic hemodynamic evaluation; the median HVPG was 24.5 mmHg (range, 7–54 mmHg). Except in 1 case patient, all HVPG values were ⩾10 mmHg. Second, because most case patients received a diagnosis of NCPH at a time before liver elastography was regularly conducted, we did not evaluate liver stiffness values systematically. Third, we were not able to search for prothrombotic disorders, because cases were included retrospectively. However, in contrast to Chang et al [3], who did not find coagulopathies in their 8 patients, other reports have noted thrombophilic abnormality in affected patients [4–6]. This supports a multifactorial pathogenesis of NCPH in HIV infection, with antiretroviral therapy and a prothrombotic state leading to microthrombosis and vascular obstruction.

To the Editor—We thank Chang and Garcia-Pagan [1] for their interest in our study [2], and we offer the following reply. First, in our case-control study of human immunodeficiency virus (HIV)-infected patients with noncirrhotic portal hypertension (NCPH), inclusion criteria were the presence of endoscopically documented esophageal varices or hepatic venous pressure gradient (HVPG) ⩾10 mmHg, absence of hepatic cirrhosis on liver biopsy, and no common cause of liver disease. All of our case patients had endoscopically documented esophageal varices, and no patient was excluded because of a HVPG <10 mmHg. Eight of 15 case patients underwent hepatic hemodynamic evaluation; the median HVPG was 24.5 mmHg (range, 7–54 mmHg). Except in 1 case patient, all HVPG values were ⩾10 mmHg. Second, because most case patients received a diagnosis of NCPH at a time before liver elastography was regularly conducted, we did not evaluate liver stiffness values systematically. Third, we were not able to search for prothrombotic disorders, because cases were included retrospectively. However, in contrast to Chang et al [3], who did not find coagulopathies in their 8 patients, other reports have noted thrombophilic abnormality in affected patients [4–6]. This supports a multifactorial pathogenesis of NCPH in HIV infection, with antiretroviral therapy and a prothrombotic state leading to microthrombosis and vascular obstruction.

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Additional indexing

Other titles:Idiopathic portal hypertension in HIV-infected patients. Letter Reply.
Item Type:Journal Article, not refereed, further contribution
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Infectious Diseases
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2010
Deposited On:10 Jan 2011 08:26
Last Modified:05 Apr 2016 14:33
Publisher:University of Chicago Press
ISSN:1058-4838
Additional Information:© 2009 by the Infectious Diseases Society of America. All rights reserved.
Publisher DOI:https://doi.org/10.1086/649010
Permanent URL: https://doi.org/10.5167/uzh-41600

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