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.