Noncirrhotic portal hypertension in patients with human immunodeficiency virus-1 infection.

BACKGROUND & AIMS: Noncirrhotic portal hypertension (NCPH) is unusual in North American patients. This study characterized patients with NCPH and human immunodeficiency virus-1 (HIV-1) infection to identify potential risk factors for this association. METHODS: Eleven consecutive patients from our urban hepatology clinic with HIV-1 infection and NCPH were the subject of this series. Case histories, including medication lists and laboratory data, were analyzed. RESULTS: Age at diagnosis was 51 +/- 7 years. CD4 count was 303 +/- 185 cells/mL, and HIV viral load was <75 copies/mL in 9 patients. Didanosine was the only medication taken by all patients; 10 each had taken lamivudine and zidovudine. In the 10 patients tested, 8 had at least 1 thrombophilic abnormality; 6 were deficient in protein S, and 2 had multiple abnormalities. Nodular regenerative hyperplasia was observed in all 11 and portal venulopathy in 5 patients. All patients had esophageal varices; 3 developed variceal bleeding. Six patients had ascites; 2 required transjugular intrahepatic portal systemic shunt. CONCLUSIONS: Exposure to didanosine and/or a hypercoagulable tendency might predispose patients infected with HIV-1 to vascular changes resulting in NCPH.

Treatment extension to 72 weeks of peginterferon and ribavirin in hepatitis c genotype 1-infected slow responders.

UNLABELLED: In hepatitis C virus (HCV) genotype 1 infection, the duration of interferon-based therapy is a critical determinant in achieving sustained virologic response (SVR). Slow or late responders to peginterferon and ribavirin may benefit from an extended treatment course. We sought to determine if therapy extension could improve response rates in a United States population of slow responders. Slow response was defined by achieving at least a 2-log decrement in HCV RNA from baseline, yet having detectable HCV RNA at 12 weeks and undetectable HCV RNA at 24 weeks (polymerase chain reaction, TaqMan, Roche; detection limit 10 IU/mL). Patients were treatment-naïve, chronically infected genotype 1-infected slow responders to 1.5 mug/kg/week of peginterferon-alpha2b and 800-1400 mg/day of ribavirin and were randomly assigned 1:1 to complete a total of 48 or 72 weeks of therapy. Dose reductions and treatment discontinuations for adverse events or laboratory abnormalities were similar between the 2 treatment arms. End-of-treatment response rates were similar in the 72-week group compared with those in the 48-week group (48% versus 45%; P value not significant). Overall, the rate of SVR was superior in patients treated for 72 weeks versus 48 weeks (38% versus 18%, respectively; P = 0.026). CONCLUSION: Extending the treatment duration from 48 weeks to 72 weeks in genotype 1-infected patients with slow virologic response to peginterferon-alpha2b and weight-based ribavirin significantly improves SVR rates. Treatment extension does not seem to increase the rate of dose reduction or therapy discontinuation.