The effects of alcohol abuse on HIV disease progression have not been definitively established. A prospective, 30-month, longitudinal study of 231 HIV(+) adults included history of alcohol and illicit drug use, adherence to antiretroviral therapy (ART), CD4(+) cell count, and HIV viral load every 6 months. Frequent alcohol users (two or more drinks daily) were 2.91 times (95% CI: 1.23-6.85, p = 0.015) more likely to present a decline of CD4 to

Crack-cocaine use facilitates HIV disease progression by reducing adherence in those on HAART and by accelerating disease progression independently of HAART.

Background Adequate zinc is critical for immune function; however, zinc deficiency occurs in >50% of HIV-infected adults. We examined the safety and efficacy of long-term zinc supplementation on HIV disease progression. Methods A prospective randomized controlled clinical trial was conducted with 231 HIV+ adults with low plasma zinc levels (<0.75 μg/ml), randomly assigned into zinc (12 mg of elemental zinc for women and 15 mg for men) or placebo, for 18 months. The primary endpoint was immunological failure. HIV-viral load and CD4+ cell count were determined every 6 months. Questionnaires, pill-counts, plasma zinc and C-reactive protein (hsCRP) were used to monitor adherence with study supplements and ART. Intent-to-treat analysis utilized multiple-event analysis, treating CD4+ cell count <200 cells/mm3 as recurrent immunological failure event. Cox proportional-hazard models and the general-linear model were used to analyze morbidity and mortality data. Results Zinc supplementation for 18 months reduced four-fold the likelihood of immunological failure, controlling for age, gender, lack of food, baseline CD4+ cell count, viral load, and antiretroviral therapy (RR=0.24[95%CI:0.10,0.56],p<0.002). Viral load indicated poor control with ART but was not affected by zinc supplementation. Zinc supplementation also reduced the rate of diarrhea by more than half (OR=0.4[95%CI:0.183-0.981],p=0.019) compared to placebo. There was no significant difference in mortality between the two groups. Conclusion This study demonstrated that long-term (18-month) zinc supplementation at nutritional levels delayed immunological failure and decreased diarrhea over time. This evidence supports the use of zinc supplementation as an adjunct therapy in HIV+ adult cohorts with poor viral control. Summary This study demonstrated that long-term (18-month) zinc supplementation at nutritional levels delayed immunological failure and decreased diarrhea over time. This evidence supports the use of zinc supplementation as an adjunct therapy in HIV+ adult cohorts with poor viral control.

HIV-related wasting continues to be common among HIV-infected drug users, even among HAART recipients. Food insecurity and viral load were the only independent predictors of wasting. The social and economic conditions affecting the lifestyle of HIV-infected drug users constitute a challenge for prevention and treatment of wasting.

The pathogenesis of HIV/hepatitis C virus (HCV) coinfection is poorly understood. We examined markers of oxidative stress, plasma antioxidants and liver disease in HIV/HCV-coinfected and HIV-monoinfected adults. MethodsDemographics, medical history, and proof of infection with HIV, hepatitis A virus (HAV), hepatitis B virus (HBV) and HCV were obtained. HIV viral load, CD4 cell count, complete blood count (CBC), complete metabolic panel, lipid profile, and plasma concentrations of zinc, selenium, and vitamins A and E were determined. Malondialdehyde (MDA) and glutathione peroxidase concentrations were obtained as measures of oxidative stress. Aminotransferase to platelet ratio index (APRI) and fibrosis index (FIB-4) markers were calculated. ResultsSignificant differences were found between HIV/HCV-coinfected and HIV-monoinfected participants in levels of alanine aminotransferase (ALT) (mean AE standard deviation: 51.4 AE 50.6 vs. 31.9 AE 43.1 U/L, respectively; P 5 0.014), aspartate aminotransferase (AST) (56.2 AE 40.9 vs. 34.4 AE 30.2 U/L; Po0.001), APRI (0.52 AE 0.37 vs. 0.255 AE 0.145; P 5 0.0001), FIB-4 (1.64 AE .0.91 vs. 1.03 AE 0.11; P 5 0.0015) and plasma albumin (3.74 AE 0.65 vs. 3.94 AE 0.52 g/dL; P 5 0.038). There were no significant differences in CD4 cell count, HIV viral load or antiretroviral therapy (ART) between groups. Mean MDA was significantly higher (1.897 AE 0.835 vs. 1.344 AE 0.223 nmol/mL, respectively; P 5 0.006) and plasma antioxidant concentrations were significantly lower [vitamin A, 39.5 AE 14.1 vs. 52.4 AE 16.2 mg/dL, respectively (P 5 0.0004); vitamin E, 8.29 AE 2.1 vs. 9.89 AE 4.5 mg/mL (P 5 0.043); zinc, 0.61 AE 0.14 vs. 0.67 AE 0.15 mg/L (P 5 0.016)] in the HIV/HCV-coinfected participants than in the HIV-monoinfected participants, and these differences remained significant after adjusting for age, gender, CD4 cell count, HIV viral load, injecting drug use and race. There were no significant differences in glutathione peroxidase concentration, selenium concentration, body mass index (BMI), alcohol use or tobacco use between groups. Glutathione peroxidase concentration significantly increased as liver disease advanced, as measured by APRI (b 5 0.00118; P 5 0.0082) and FIB-4 (b 5 0.0029; P 5 0.0177). Vitamin A concentration significantly decreased (b 5 À 0.00581; P 5 0.0417) as APRI increased. ConclusionHIV/HCV coinfection is associated with increased oxidative stress and decreased plasma antioxidant concentrations compared with HIV monoinfection. Research is needed to determine whether antioxidant supplementation delays liver disease in HIV/HCV coinfection. IntroductionAbout one-quarter to half of the persons infected with HIV in the USA are also infected with hepatitis C virus (HCV) [1]. As antiretroviral therapy (ART) has dramatically reduced HIV-1-related mortality from other causes, HIV/HCV The pathogenesis of HCV and the subsequent liver injury is poorly understood. The damage results from a combination of the immune response and direct effects of HCV on hepatocytes, including...