Modeling hepatic fibrosis in African American and Caucasian American patients with chronic hepatitis C virus infection
Fontana, Robert John; Kleiner, David E.; Bilonick, Richard; Terrault, Norah A.; Afdhal, Nezam H.; Belle, Steven H.; Jeffers, Lennox J.; Ramcharran, Darmendra; Ghany, Marc G.; Hoofnagle, Jay H.
2006-10
Citation
Fontana, Robert J.; Kleiner, David E.; Bilonick, Richard; Terrault, Norah; Afdhal, Nezam; Belle, Steven H.; Jeffers, Lennox J.; Ramcharran, Darmendra; Ghany, Marc G.; Hoofnagle, Jay H. (2006). "Modeling hepatic fibrosis in African American and Caucasian American patients with chronic hepatitis C virus infection Members of Virahep-C contributing to the study are listed in the Acknowledgment section. Potential conflict of interest: Dr. Fontana is a consultant and is on the Speakers' Bureau for Roche. Dr. Jeffers is a consultant, advises, received grants, and is on the Speakers' Bureau for Roche. He received grants from Bristol Myers Squibb. He is on the Speakers' Bureau for Schering. Dr. Afdhal received grants from EchoSens and Quest. He is a consultant and received grants from Prometheus. Dr. Afdhal is a consultant for and received grants from Schering Plough. ." Hepatology 44(4): 925-935. <http://hdl.handle.net/2027.42/55833>
Abstract
Assessment of histological stage is an integral part of disease management in patients infected with the hepatitis C virus (HCV). The aim of this study was to develop a model incorporating objective clinical and laboratory parameters to estimate the probability of severe fibrosis ( i.e. , Ishak fibrosis ≥ 3) in previously untreated African American (AA) and Caucasian American (CA) patients with HCV genotype 1. The Ishak fibrosis scores of 205 CA and 194 AA patients enrolled in the Viral Resistance to Antiviral Therapy of Chronic Hepatitis C study (Virahep-C) were modeled using simple and multiple logistic regression. The model was then validated in an independent cohort of 461 previously untreated patients with HCV. The distribution of fibrosis scores was similar in the AA and CA patients as was the proportion of patients with severe fibrosis (35% vs. 39%, P = .47). After accounting for the number of portal areas in the biopsy, patient age, serum aspartate aminotransferase, alkaline phosphatase, and platelet count were independently associated with severe fibrosis in the overall cohort, and the relationship with fibrosis was similar in both the AA and CA subgroups. The area under the receiver operating characteristic curve (AUROC) of the Virahep-C model (0.837) was significantly better than in other published models ( P = .0003). The AUROC of the Virahep-C model was 0.851 in the validation population. In conclusion , a model consisting of widely available clinical and laboratory features predicted severe hepatic fibrosis equally well in AA and CA patients with HCV genotype 1 and was superior to other published models. The excellent performance of the Virahep-C model in an external validation cohort suggests the findings are replicable and potentially generalizable. (H EPATOLOGY 2006;44:925–935.)Publisher
Wiley Subscription Services, Inc., A Wiley Company
ISSN
0270-9139 1527-3350
Other DOIs
PMID
17006909
Types
Article
URI
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=17006909&dopt=citationMetadata
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