Nonalcoholic fatty liver disease and HIV infection
ABSTRACT As persons with HIV live longer, chronic liver disease is increasingly important. Nonalcoholic fatty liver disease (NAFLD) is characterized by excess fat in hepatocytes in patients without significant alcohol use. It can progress from steatosis to nonalcoholic steatohepatitis (NASH) to cirrhosis. Visceral obesity and insulin resistance are integral to the pathogenesis of NAFLD. Patients with HIV are at greater risk of NAFLD due to antiretroviral therapy and viral hepatitis coinfection. Antiretroviral therapy can lead to patterns of injury that include steatosis and NASH. Coinfection with hepatitis C virus increases the risk of insulin resistance and hepatic steatosis, and co-existent features of NASH have also been reported. Histological-based, longitudinal studies are needed that address the interactions of NAFLD and HIV infection, the effects of antiretroviral therapy and hepatotropic virus coinfection, and inform better management strategies.
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ABSTRACT: Since the advent of effective antiretroviral therapy (ART) for human immunodeficiency virus-1 (HIV), there has been a substantial decrease in deaths related to acquired immunodeficiency syndrome (AIDS). However, in the ART era, liver disease is now the most common non-AIDS-related cause of death among HIV-infected patients, accounting for 14%-18% of all deaths in this population and almost half of deaths among hospitalized HIV-infected patients. Just as the burden of non-AIDS morbidity and mortality has changed in the ART era, the types of liver disease the clinician is likely to encounter among these patients have changed as well. This review will discuss the causes of liver disease in the HIV-infected population in the ART era, including chronic hepatitis C virus, chronic hepatitis B virus, medication-related hepatotoxicity, alcohol abuse, nonalcoholic fatty liver disease, and AIDS-related liver diseases.Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 12/2010; 8(12):1002-12. DOI:10.1016/j.cgh.2010.08.024 · 5.64 Impact Factor
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ABSTRACT: Osteoporosis is increasingly reported in the aging HIV-positive population, and co-infection with hepatitis C virus (HCV) may further increase the risk of osteoporosis. However, it remains unclear whether HCV-related increased fracture risk is a function of the severity of liver disease. We calculated the time-updated APRI score (an indirect marker of hepatic fibrosis) in all HIV infected patients enrolled in the Veterans Affairs' Clinical Case Registry between 1984 and 2009. The association between HCV co-infection and incident osteoporotic fracture (defined as closed wrist, vertebral or hip fracture) was assessed in univariate and multivariate Cox survival models adjusting for traditional risk factors for osteoporosis and APRI score or the presence of cirrhosis. 772 osteoporotic fractures were identified among 56,660 HIV-infected patients (98.1% male; 31.3% HCV co-infected; median age: 44.0 years) contributing 305,237 patient-years of follow-up. Fracture rates were significantly higher among HIV/HCV patients than HIV-only patients (2.57 vs. 2.07/1000 patient-years, relative risk: 1.24, p < 0.0001). In a Cox multi-variable model including age, race, smoking, drug use, BMI and antiretroviral therapy, HCV co-infection remained an independent predictor of osteoporotic fractures after controlling for presence of cirrhosis (hazard ratio [HR]: 1.32; p < 0.001) or APRI score (HR: 1.30; p = 0.003). Among HIV/HCV co-infected patients, cirrhosis strongly predicted osteoporotic fractures (HR: 1.65; 95% CI: 1.11-2.44; p = 0.012), but APRI score was a weaker predictor (HR: 1.008; 95% CI: 1.002-1.014; p = 0.015). In conclusion, among HIV-infected patients, severity of liver disease partly explains the HCV-associated increased risk of osteoporotic fractures. Other determinants of this increased risk remain to be defined.Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research 12/2013; 28(12). DOI:10.1002/jbmr.1988 · 6.04 Impact Factor
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ABSTRACT: Non-cirrhotic portal hypertension (NCPH) has been associated with didanosine (ddI) exposure. We aimed to determine the number of individuals with NCPH within our cohort and define their characteristics. We identified individuals within our cohort with NCPH and performed a retrospective case note review. Cumulative antiretroviral therapy (ART) use was calculated and a statistical analysis performed to compare exposure to the rest of the clinic cohort for the same time period. Where available, data was collated on FibroScan®, echocardiography and coagulation profile. Seventeen patients were identified. Upper gastrointestinal bleeding was the most common presenting feature. Liver biopsy showed mild portal or periportal fibrosis in 13 (81%) and four with features of nodular regenerative hyperplasia. There was significantly greater exposure to ddl in this group (59.5 months) compared to the rest of the HIV cohort (21.1 months) P = <0.001. Eleven subjects has a liver elastography performed, six (55%) had a result greater than 9.6 kPa (consistent with greater than F2 disease by Metavir scoring). Echocardiography was performed in seven patients: four met criteria for pulmonary hypertension. This is consistent with other cohorts demonstrating an association between the didanosine exposure and NCPH. Our data also suggest an increased risk of pulmonary hypertension.International Journal of STD & AIDS 06/2011; 22(6):324-8. DOI:10.1258/ijsa.2010.010396 · 1.04 Impact Factor