Influence of interferon-based therapy on liver fibrosis progression in HIV/HCV coinfected patients: a retrospective repeated liver biopsy analysis.
ABSTRACT Hepatitis C virus (HCV) coinfection is one of the leading causes of mortality in human immunodeficiency virus-infected patients. The current standard of care leads to cure only in a part of these patients. The course of the disease is determined by the rapidity of liver fibrosis progression (LFP). The influence of interferon on LFP in coinfected patients has yet not been evaluated by comparative liver biopsies.
We extracted data of patients who had serial liver biopsies from a hospital database. Histopathological findings were compared to factors possibly linked to fibrosis progression. Furthermore, we studied the impact of response to interferon treatment on fibrosis progression.
Hundred and twenty-six patients were included, 68 had received anti-HCV treatment, and 58 had not. The median time between the first and the last biopsy was 4 years. Worsened fibrosis was observed in 35 of 58 (60%) untreated patients, and 22 of 50 (44%) patients in the nonresponder/relapser group, and in 5 out of 18 (28%) in the SVR group. Liver fibrosis evolution was significantly better in patients achieving a SVR than in untreated and NR/R patients (p<0.02, odds-ratio [95% CI] for improvement vs. stability vs. worsening=3.16 [1.24-8.07]). This result persisted after adjustment for known predictors of liver fibrosis progression, HBsAg, CD4, and alcohol consumption: adjusted odds ratio=2.89 [1.09-7.68], p=0.03.
HCV treatment can stop fibrosis progression and induce its regression. Nonresponders to treatment may even have a fast fibrosis progression. It remains to be clarified if the same factors that induce nonresponse to treatment may also induce faster fibrosis progression.
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ABSTRACT: Introduction: Idiosyncratic drug induced liver injury (DILI) is rare, with an incidence of approximately 19 per 100,000 treated individuals. Areas covered: An update on the epidemiology, pathogenic mechanisms, diagnosis, outcome, risk factors for idiosyncratic drug-induced hepatotoxicity, specific classes of drug hepatotoxicity and biomarkers to predict DILI are covered. Cumulative drug exposure and HLA phenotypes play an important role in the pathogenesis of DILI. Patients who present with suspected DILI and jaundice should have biliary obstruction and acute viral hepatitis, including hepatitis E excluded. Immune-mediated DILI will respond to steroid therapy. Patients with an elevated bilirubin and a hepatocellular pattern of liver function tests have severe liver injury with a mortality of greater than 10% and a risk of acute liver failure. Women have an increased risk of hepatocellular DILI. Antibiotics, anticonvulsants, and antidepressant therapy remain the commonest causes of DILI in the Western Hemisphere. Statin therapy rarely causes severe liver injury. Expert opinion: The establishment of prospective registries for DILI has provided valuable data on the pathogenesis and outcome of DILI. Drug-specific computerised causality assessment tools should improve the diagnosis of DILI. The clinical utility of genetic polymorphisms associated with drug-specific DILI is limited.Expert Opinion on Drug Safety 09/2013; DOI:10.1517/14740338.2013.828032 · 2.74 Impact Factor
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ABSTRACT: Liver disease related to hepatitis B (HBV) or hepatitis C (HCV) infections among HIV infected patient population are currently a major cause of morbidity and mortality. They are extremely frequent, intravenous drug use being the most commonly documented route of transmission despite this practice is not a major concern in South America. Sexual transmission route is more prevalent in HBV coinfected patients. In South America, the most frequent HCV genotype identified in HIV patients is genotype 1a; genotypes A and F being the most prevalent among the HBV population. Even though effective therapy based on tenofovir regimens for HBV/HIV coinfected patients have been available for some years now, treatment recommendations still vary from country to country. Although novel, oral, more efficient drugs are being developed for HCV/HIV treatment, these options are very expensive and not yet available worldwide. This is especially so in regions such as South America. This review will discuss epidemiology, diagnosis and management of HBV and HCV coinfection in HIV infected patients with special focus in South America.Current Hepatitis Reports 12/2013; DOI:10.1007/s11901-013-0193-3
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ABSTRACT: Where active antiretroviral therapy (ART) is accessible, human immunodeficiency virus (HIV) is a survivable illness and effective ART can reduce HIV transmission. Chronic hepatitis C virus (HCV) has emerged as a threat to the survival of individuals harboring both HCV and HIV, due to high prevalence and aggressive disease course. The HCV/HIV coinfection epidemic has been driven by people who inject drugs (PWID), although incident HCV is rising among HIV-infected men who have sex with men in the absence of drug injection. Coinfected individuals warrant aggressive treatment of both viruses; although early ART initiation is recommended to reduce the rate of liver disease progression, the most effective way to decrease HCV-related morbidity and mortality in coinfection is to achieve HCV viral eradication. Direct-acting antiviral (DAA) agents will soon revolutionize HCV treatment. Clinical data are needed regarding the efficacy of DAAs in coinfected PWID. Drug-drug interaction studies between ART, DAAs, and opiate substitution therapy must be expedited. Coinfected PWID should have equitable and universal access to HIV/AIDS, HCV, and addiction prevention, care, and treatment. Essential basic steps include improving screening for both infections and engaging coinfected PWID in HIV and HCV care early after diagnoses. Developing strategies to expand access to HCV therapy for coinfected PWID is imperative to stem the HCV epidemic and limit the morbidity and mortality of those at greatest risk for HCV disease progression. The ultimate goal must be the elimination of HCV from all coinfected PWID.Clinical Infectious Diseases 07/2013; 57(suppl 2):S118-S124. DOI:10.1093/cid/cit326 · 9.42 Impact Factor