The long-term outcomes of patients with compensated hepatitis C virus-related cirrhosis and history of parenteral exposure in the United States

Authors
Citation
Kq. Hu et Mj. Tong, The long-term outcomes of patients with compensated hepatitis C virus-related cirrhosis and history of parenteral exposure in the United States, HEPATOLOGY, 29(4), 1999, pp. 1311-1316
Citations number
29
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
HEPATOLOGY
ISSN journal
02709139 → ACNP
Volume
29
Issue
4
Year of publication
1999
Pages
1311 - 1316
Database
ISI
SICI code
0270-9139(199904)29:4<1311:TLOOPW>2.0.ZU;2-U
Abstract
It is well known that hepatitis C virus (HCV) infection may progress to cir rhosis and is linked to the development of hepatocellular carcinoma (HCC), Previous studies have shown that compensated HCV-cirrhosis is related to a certain morbidity and mortality in European patients, but little is known i n regard to the clinical outcomes of a similar group of patients in the Uni ted States. This study investigated this category of patients in terms of t he incidence of decompensation, development of HCC, mortality, and the pred ictive risk factors for morbidity and mortality. The potential effects of i nterferon (IFN) therapy on outcomes of the disease also were assessed. A to tal of 112 patients with compensated HCV-cirrhosis and a documented history of either intravenous drug abuse (IVDA) or transfusion were consecutively enrolled. The mean follow-up interval was 4.5; (2-7.7) years. The cumulativ e probabilities for decompensation and development of HCC were 22.2% and 10 .1% in 5 years, with an estimated yearly incidence of 4.4% and 2.0%, respec tively. The cumulative survival probability was 82.8% from entry and 51.1% from decompensation in 5 years, with estimated yearly events of mortality a nd liver transplantation of 3.4% and 9.8%, respectively. It was found that age at entry and initial exposure, initial levels of albumin, platelet coun t, and prothrombin time (PT) were predictive risk factors for developing de compensation, whereas age at entry and initial exposure, history of transfu sion, lower initial levels of albumin, platelet count, and viral load were predictive risk factors for events of mortality and liver transplantation. The incidence of decompensation was significantly lower in patients treated with IFN, but age may have played a contributory role. In contrast, neithe r HCC development nor mortality was significantly altered by IFN therapy. I n conclusion, our study indicated that patients with compensated HCV-cirrho sis in the United States progressed slowly and experienced eventual morbidi ty and mortality. Once decompensation develops, the disease will be more pr ogressive and result in even higher mortality. Further studies will be requ ired to determine the efficacy of IFN on clinical outcomes in this group of patients.