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Factors affecting liver fibrosis in human immunodeficiency virus-and hepatitis C virus-coinfected patients: impact of protease inhibitor therapy.
Hepatology. 2001 Aug; 34(2):283-7.Hep

Abstract

Hepatitis C virus (HCV)-related liver fibrosis progression is accelerated in human immunodeficiency virus (HIV)-infected patients. The effect of protease inhibitor (PI) therapy on liver fibrosis is unknown. The aim of this work was to analyze the impact of PI therapy on HCV-related liver fibrosis in HIV/HCV coinfected patients. We evaluated in a long-term follow-up retrospective cohort study the influence of antiretroviral therapy containing PI on liver fibrosis in 182 consecutive HIV/HCV coinfected patients. At liver biopsy, 63 patients had received PI and 119 patients had never been treated with PI. Relationships between liver histologic features, age, alcohol consumption, CD4 cell count, HIV-RNA load, and antiretroviral regimens were analyzed. Liver fibrosis stage was lower in patients receiving PIs by comparison with patients who had never received PIs (P =.03). The 5-, 15-, and 25-year cirrhosis rates were 2% versus 5%, 5% versus 18%, and 9% versus 27%, respectively, in patients who had received PIs compared with PI-untreated patients (P =.0006). Multivariate analysis identified 4 independent predictors of progression to cirrhosis: absence of protease inhibitor therapy (relative risk [RR] = 4.74, 95% confidence interval [CI], 1.34-16.67), heavy alcohol consumption (> or = 50 g daily) (RR = 4.71, 95% CI, 1.92-11.57), low CD4 cell count (<200/microL) (RR = 2.74, 95% CI, 1.17-6.41), and age at HCV contamination (> or = 20 years) (RR = 2.37, 95% CI, 1.04-5.38). In conclusion, protease inhibitor therapy might not accelerate progression to HCV-related cirrhosis. Furthermore, chronic use of antiretroviral therapy containing PI together with reduction of alcohol consumption and maintenance of high CD4 count could have a beneficial impact on liver fibrosis progression in HIV/HCV coinfected patients.

Authors+Show Affiliations

Service d'Hépato-Gastroentérologie, Service de Pharmacie, Service de Virologie, Service de Maladies Infectieuses, Groupe Hospitalier Pitié-Salpêtrière, Paris, France. ybenhamou@teaser.frNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11481613

Citation

Benhamou, Y, et al. "Factors Affecting Liver Fibrosis in Human Immunodeficiency Virus-and Hepatitis C Virus-coinfected Patients: Impact of Protease Inhibitor Therapy." Hepatology (Baltimore, Md.), vol. 34, no. 2, 2001, pp. 283-7.
Benhamou Y, Di Martino V, Bochet M, et al. Factors affecting liver fibrosis in human immunodeficiency virus-and hepatitis C virus-coinfected patients: impact of protease inhibitor therapy. Hepatology. 2001;34(2):283-7.
Benhamou, Y., Di Martino, V., Bochet, M., Colombet, G., Thibault, V., Liou, A., Katlama, C., & Poynard, T. (2001). Factors affecting liver fibrosis in human immunodeficiency virus-and hepatitis C virus-coinfected patients: impact of protease inhibitor therapy. Hepatology (Baltimore, Md.), 34(2), 283-7.
Benhamou Y, et al. Factors Affecting Liver Fibrosis in Human Immunodeficiency Virus-and Hepatitis C Virus-coinfected Patients: Impact of Protease Inhibitor Therapy. Hepatology. 2001;34(2):283-7. PubMed PMID: 11481613.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Factors affecting liver fibrosis in human immunodeficiency virus-and hepatitis C virus-coinfected patients: impact of protease inhibitor therapy. AU - Benhamou,Y, AU - Di Martino,V, AU - Bochet,M, AU - Colombet,G, AU - Thibault,V, AU - Liou,A, AU - Katlama,C, AU - Poynard,T, AU - ,, PY - 2001/8/2/pubmed PY - 2001/8/24/medline PY - 2001/8/2/entrez SP - 283 EP - 7 JF - Hepatology (Baltimore, Md.) JO - Hepatology VL - 34 IS - 2 N2 - Hepatitis C virus (HCV)-related liver fibrosis progression is accelerated in human immunodeficiency virus (HIV)-infected patients. The effect of protease inhibitor (PI) therapy on liver fibrosis is unknown. The aim of this work was to analyze the impact of PI therapy on HCV-related liver fibrosis in HIV/HCV coinfected patients. We evaluated in a long-term follow-up retrospective cohort study the influence of antiretroviral therapy containing PI on liver fibrosis in 182 consecutive HIV/HCV coinfected patients. At liver biopsy, 63 patients had received PI and 119 patients had never been treated with PI. Relationships between liver histologic features, age, alcohol consumption, CD4 cell count, HIV-RNA load, and antiretroviral regimens were analyzed. Liver fibrosis stage was lower in patients receiving PIs by comparison with patients who had never received PIs (P =.03). The 5-, 15-, and 25-year cirrhosis rates were 2% versus 5%, 5% versus 18%, and 9% versus 27%, respectively, in patients who had received PIs compared with PI-untreated patients (P =.0006). Multivariate analysis identified 4 independent predictors of progression to cirrhosis: absence of protease inhibitor therapy (relative risk [RR] = 4.74, 95% confidence interval [CI], 1.34-16.67), heavy alcohol consumption (> or = 50 g daily) (RR = 4.71, 95% CI, 1.92-11.57), low CD4 cell count (<200/microL) (RR = 2.74, 95% CI, 1.17-6.41), and age at HCV contamination (> or = 20 years) (RR = 2.37, 95% CI, 1.04-5.38). In conclusion, protease inhibitor therapy might not accelerate progression to HCV-related cirrhosis. Furthermore, chronic use of antiretroviral therapy containing PI together with reduction of alcohol consumption and maintenance of high CD4 count could have a beneficial impact on liver fibrosis progression in HIV/HCV coinfected patients. SN - 0270-9139 UR - https://www.unboundmedicine.com/medline/citation/11481613/Factors_affecting_liver_fibrosis_in_human_immunodeficiency_virus_and_hepatitis_C_virus_coinfected_patients:_impact_of_protease_inhibitor_therapy_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0270913901627940 DB - PRIME DP - Unbound Medicine ER -