Decompensated Cirrhosis Due to HCV:SVR Signals Good Prognosis

SVR Signals Good Prognosis in Decompensated Cirrhosis Due to HCV

By: MARY ANN MOON, Internal Medicine News Digital Network
02/24/11

A sustained virologic response to antiviral therapy signals a favorable prognosis in patients with decompensated cirrhosis due to chronic hepatitis C, reported Dr. Angelo Iacobellis and his colleagues in the March issue of Clinical Gastroenterology and Hepatology.

Mean survival was 20 months longer in patients who achieved a sustained virologic response (SVR) with antiviral therapy than in patients who did not achieve SVR (73 vs. 53 months; P = .004). Thus, antiviral therapy "might represent a life-sparing intervention" for patients who have progressed to the stage of liver decompensation and who aren’t eligible for liver transplant, said Dr. Iacobellis and his associates at Casa Sollievo della Sofferenza in San Giovanni Rotondo, Italy.

The authors previously reported on the short-term benefits of pegylated interferon alfa-2b plus ribavirin in patients whose cirrhosis had caused at least one episode of decompensation, as evidenced by esophageal bleeding, ascites, or hepatic encephalopathy. However, "for cirrhotic patients with advanced disease, achieving a sustained virologic response might be only a cosmetic goal of low clinical relevance if it does not guarantee a positive impact on their poor prognosis."

Therefore, Dr. Iacobellis and his colleagues studied the survival rates after 5-year follow-up in 75 patients (mean follow-up, 51 months; range, 3-78 months). A total of 24 patients achieved an SVR with either standard dosing (13 patients) or a low-dose regimen (11 patients).

"The main finding of our study was the improved survival of patients who attained a sustained virologic response." Mean survival was 73 months in patients who achieved an SVR, compared with 53 months in those who did not (Clin. Gastroenterol. Hepatol. 2011 March [doi:10.1016/j.cgh.2010.10.036]).

In all, 25 patients died during follow-up. Only two patients (8%) who had achieved SVR died, both of them from liver disease. In contrast, 23 of the 51 patients (43%) who had not achieved a sustained virologic response died – all but one of them from liver disease.

During follow-up, only 8 of the 24 treatment responders (33%) experienced further decompensation events such as bleeding, ascites, sepsis, or development of hepatocellular carcinoma. In contrast, 49 of the 51 treatment nonresponders (96%) experienced further decompensation events; this was a highly significant difference (P less than .0001).

There were 20 adverse events requiring hospitalization among the treatment responders, compared with 137 in treatment nonresponders. Readmission rates were eight times higher among nonresponders: 56 per 1,000 person-months, compared with 7 per 1,000 person-months for responders.

However, the achievement of SVR did not appear to affect the development of hepatocellular carcinoma. The malignancy developed in 21% of patients who had achieved an SVR and 22% of those who had not. The incidence rates were 3.7 per 1,000 person-months and 4.5 per 1,000 person-months, respectively, which was not a significant difference.

"This finding reinforces the concept that decompensated cirrhosis is a unique step of liver disease, in which derangement of liver architecture assumes a negative prognostic role on the probability of developing hepatocellular carcinoma," the investigators said.

"It is also worth noting that only 1 patient who attained a sustained virologic response was transplanted for hepatocellular cancer development, without a reinfection of the liver graft. In contrast, of the 7 patients without a sustained virologic response [who were approved for a liver transplant], 6 died while on the waiting list and 1 grafted patient had immediate [HCV] reinfection of the graft," they added.

This study received no industry support. Dr. Iacobellis and his associates reported no financial conflicts of interest.