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Liver decompensation risk rose in severe portal HT.


Patients with chronic hepatitis C who develop cirrhosis with severe portal hypertension are at greater risk of progressing to liver decompensation within the first 5 years of treatment, even if they show a sustained virologic response to therapy, a cohort study has found.

The study of 100 patients with hepatitis C and compensated cirrhosis showed that the probability of developing a first episode of liver decompensation at 1, 5, and 7 years was 4%, 25%, and 28%, respectively, among patients with an hepatic venous pressure gradient (HVPG) value of 10 mm Hg or above, compared with 0, 0, and 16% in patients without cirrhosis with severe portal hypertension (CSPH).

Nearly three-quarters of the patients in the study had CSPH at baseline and 35% achieved a sustained virologic response, while 19% developed liver decompensation, according to Dr. Sabela Lens of the Institut d'lnvestigacions Biomediques August-PiSunyer, Barcelona, and coauthors.


"Although viral clearance was associated with a significant reduction in HVPG, this effect, at least 24 weeks after the end of treatment, was mild and only one-third of patients with a high-risk baseline situation with CSPH shifted to a condition of low risk for developing fiver decompensation," they wrote (Clin Gastro Hepatol. 2015. doi: 10.1016/j.cgh.2015.04.013).

"The results of our study show that baseline HVPG value before antiviral treatment is a strong predictor of liver decompensation on follow-up evaluation," Dr. Lens and associates noted.


Key clinical point: Sustained virologic response is no protection against liver decompensation in patients who develop cirrhosis with severe portal hypertension.

Major finding: Patients with severe portal hypertension at baseline are nearly twice as likely to develop liver compensation at 7 years as those without severe portal hypertension. Data source: Cohort study in 100 patients with hepatitis C and compensated cirrhosis.

Disclosures: The study was funded by the Institute de Salud Carlos III, and one author was funded by an unrestricted grant from Roche. There were no other conflicts of interest declared.

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Author:Nogrady, Bianca
Publication:Internal Medicine News
Date:Oct 1, 2015
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