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Progression of fibrosis in HIV and hepatitis C virus-coinfected patients treated with interferon plus ribavirin-based therapy: analysis of risk factors.
Clin Infect Dis. 2008 Mar 01; 46(5):768-74.CI

Abstract

BACKGROUND

We determined the prevalence and determinants of worsening fibrosis in patients coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) who were receiving anti-HCV therapy.

METHODS

Among 383 HIV-HCV-coinfected patients who received at least 1 dose of anti-HCV treatment (weekly subcutaneous injections of 1.5 mug/kg pegylated interferon-alpha-2b plus daily ribavirin or thrice-weekly subcutaneous injections of 3 MU of interferon-alpha-2b plus daily ribavirin for 48 weeks), paired pretreatment and posttreatment liver biopsy specimens were available and interpretable for 198 cases. Hepatic necroinflammation and fibrosis were graded with Ishak's classification. Histological worsening of fibrosis was defined as a score increase of > or =2 points in patients with fibrosis stage of <4 and as a score increase of 1 point in patients with stage-5 fibrosis.

RESULTS

The mean interval +/- standard deviation between the 2 biopsies was 109 +/- 34 weeks. Fibrosis worsened in 34 patients (17.1%). In univariate analysis, ongoing antiretroviral therapy, failure to achieve a sustained viral response, nucleoside reverse-transcriptase inhibitor therapy, didanosine therapy, and stavudine therapy were significantly associated with worsening of fibrosis. Didanosine (odds ratio, 3.34; 95% confidence interval, 1.39-7.96; P = .007) and failure to have a sustained viral response (odds ratio, 9.05; 95% confidence interval, 2.06-39.66; P = .003) remained significantly associated with worsening of fibrosis.

CONCLUSION

The mitochondrial toxicity of antiretrovirals, such as didanosine, seems to play a major role in worsening of fibrosis during HCV therapy. Therefore, anti-HCV therapy should ideally be administered before antiretroviral treatment initiation. If anti-HCV and anti-HIV treatments have to be administered concomitantly, then nucleoside reverse-transcriptase inhibitors with the lowest mitochondrial toxicity should be preferred.

Authors+Show Affiliations

Groupe Hospitalier Universitaire Est, Université Paris 6, INSERM U707, France. firouze.bani-sadr@tnn.ap-hop-paris.frNo affiliation info availableNo affiliation info availableNo 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
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18248298

Citation

Bani-Sadr, Firouzé, et al. "Progression of Fibrosis in HIV and Hepatitis C Virus-coinfected Patients Treated With Interferon Plus Ribavirin-based Therapy: Analysis of Risk Factors." Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America, vol. 46, no. 5, 2008, pp. 768-74.
Bani-Sadr F, Lapidus N, Bedossa P, et al. Progression of fibrosis in HIV and hepatitis C virus-coinfected patients treated with interferon plus ribavirin-based therapy: analysis of risk factors. Clin Infect Dis. 2008;46(5):768-74.
Bani-Sadr, F., Lapidus, N., Bedossa, P., De Boever, C. M., Perronne, C., Halfon, P., Pol, S., Carrat, F., & Cacoub, P. (2008). Progression of fibrosis in HIV and hepatitis C virus-coinfected patients treated with interferon plus ribavirin-based therapy: analysis of risk factors. Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America, 46(5), 768-74. https://doi.org/10.1086/527565
Bani-Sadr F, et al. Progression of Fibrosis in HIV and Hepatitis C Virus-coinfected Patients Treated With Interferon Plus Ribavirin-based Therapy: Analysis of Risk Factors. Clin Infect Dis. 2008 Mar 1;46(5):768-74. PubMed PMID: 18248298.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Progression of fibrosis in HIV and hepatitis C virus-coinfected patients treated with interferon plus ribavirin-based therapy: analysis of risk factors. AU - Bani-Sadr,Firouzé, AU - Lapidus,Nathanael, AU - Bedossa,Pierre, AU - De Boever,Corinne Merle, AU - Perronne,Christian, AU - Halfon,Philippe, AU - Pol,Stanislas, AU - Carrat,Fabrice, AU - Cacoub,Patrice, AU - ,, AU - ,, PY - 2008/2/6/pubmed PY - 2008/3/1/medline PY - 2008/2/6/entrez SP - 768 EP - 74 JF - Clinical infectious diseases : an official publication of the Infectious Diseases Society of America JO - Clin Infect Dis VL - 46 IS - 5 N2 - BACKGROUND: We determined the prevalence and determinants of worsening fibrosis in patients coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) who were receiving anti-HCV therapy. METHODS: Among 383 HIV-HCV-coinfected patients who received at least 1 dose of anti-HCV treatment (weekly subcutaneous injections of 1.5 mug/kg pegylated interferon-alpha-2b plus daily ribavirin or thrice-weekly subcutaneous injections of 3 MU of interferon-alpha-2b plus daily ribavirin for 48 weeks), paired pretreatment and posttreatment liver biopsy specimens were available and interpretable for 198 cases. Hepatic necroinflammation and fibrosis were graded with Ishak's classification. Histological worsening of fibrosis was defined as a score increase of > or =2 points in patients with fibrosis stage of <4 and as a score increase of 1 point in patients with stage-5 fibrosis. RESULTS: The mean interval +/- standard deviation between the 2 biopsies was 109 +/- 34 weeks. Fibrosis worsened in 34 patients (17.1%). In univariate analysis, ongoing antiretroviral therapy, failure to achieve a sustained viral response, nucleoside reverse-transcriptase inhibitor therapy, didanosine therapy, and stavudine therapy were significantly associated with worsening of fibrosis. Didanosine (odds ratio, 3.34; 95% confidence interval, 1.39-7.96; P = .007) and failure to have a sustained viral response (odds ratio, 9.05; 95% confidence interval, 2.06-39.66; P = .003) remained significantly associated with worsening of fibrosis. CONCLUSION: The mitochondrial toxicity of antiretrovirals, such as didanosine, seems to play a major role in worsening of fibrosis during HCV therapy. Therefore, anti-HCV therapy should ideally be administered before antiretroviral treatment initiation. If anti-HCV and anti-HIV treatments have to be administered concomitantly, then nucleoside reverse-transcriptase inhibitors with the lowest mitochondrial toxicity should be preferred. SN - 1537-6591 UR - https://www.unboundmedicine.com/medline/citation/18248298/Progression_of_fibrosis_in_HIV_and_hepatitis_C_virus_coinfected_patients_treated_with_interferon_plus_ribavirin_based_therapy:_analysis_of_risk_factors_ L2 - https://academic.oup.com/cid/article-lookup/doi/10.1086/527565 DB - PRIME DP - Unbound Medicine ER -