Abstract |
Our aim was to analyze the influence of HLA-B haplotypes on liver fibrosis progression in HIV/hepatitis C virus (HCV) co-infected patients. Retrospective longitudinal study including HIV/HCV, non-cirrhotic and HCV treatment-naïve patients. The main outcome variable was liver fibrosis progression of at least one stage. One hundred and four patients constituted the study population (F0-F1: 62 (59.6%); F2: 22 (21.2%); F3: 20 (19.2%)). During a median follow-up of 54.5 months (IQR: 26.2-77), 45 patients (43.3%) showed an increase in the stage of liver fibrosis (time to event: 29 (IQR: 14-49.5) months). HLA-B18pos patients more frequently had a higher and faster fibrosis progression rate (73.3%; 24 (IQR: 8-29) months) than HLA-B18neg patients (38.2%; 34.5 (IQR: 14.7-51.2) months). This association was also observed in the development of F3-F4 fibrosis among F0-F2 patients (HLA-B18pos: 69.2%; 18 (6.5-37) months vs HLA-B18neg: 28.2%; 37 (IQR: 19-52) months). These results could impact the timing of HCV therapy in F0-F2 patients.
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Authors | M Frías, D Rodríguez-Cano, F Cuenca-López, J Macías, A Gordon, B Manzanares-Martín, J A Pineda, Á Camacho, J Torre-Cisneros, J Peña, A Rivero-Juárez, A Rivero |
Journal | The pharmacogenomics journal
(Pharmacogenomics J)
Vol. 17
Issue 6
Pg. 551-555
(12 2017)
ISSN: 1473-1150 [Electronic] United States |
PMID | 27241060
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
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Topics |
- Adult
- Coinfection
- Disease Progression
- Female
- Genotype
- HIV Infections
(complications, drug therapy, genetics, virology)
- HLA-B18 Antigen
(genetics)
- Hepatitis C
(complications, drug therapy, genetics, virology)
- Humans
- Liver Cirrhosis
(etiology, genetics, immunology)
- Male
- Middle Aged
- Retrospective Studies
- Risk Factors
- Severity of Illness Index
- Survival Analysis
- Time Factors
- Treatment Failure
- Viral Load
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