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...

HIV/HCV co-infection is becoming one of the main causes of death in HIV+ persons. We determined quality of life, clinical symptoms and health care utilization in HIV mono-infected and HIV/HCV co-infected chronic drug users. After consenting 218 HIV+ drug users, a physical examination and questionnaires on demographics, quality of life, drugs of abuse, and healthcare utilization were completed. Blood was drawn for HCV status, CD4 cell count, HIV viral load, CBC and chemistry. HIV/HCV co-infected participants had significantly higher risk of having poorer perceived outlook and health, presented significantly more frequent depression and physical symptoms, and used significantly more healthcare services than those infected with HIV only, after adjusting for age, gender, ethnicity, CD4 cell count, and viral load. Diminished quality of life in the HIV/HCV co-infected group was explained by increased frequency of depression, physical symptoms, healthcare utilization, and poor access to HCV treatment in this population.

Abstract:The frequency of coronary heart disease (CHD) is increasing among HIV seropositive persons. This phenomenon may be related to HIV disease itself, the use of antiretroviral medications and increased length of survival, or the synergism of these factors. In this study we have calculated the 10-year CHD risk estimate and the prevalence of metabolic syndrome in a cohort of 118 HIV seropositive chronic drug users, including those who are on HAART with or without protease inhibitors (PI). The results showed that the 10-year coronary heart disease risk among the HIV seropositive drug users was 4.8 ± 5.7, which is within the range of results published for other HIV infected cohorts. The 10-year CHD risk was significantly higher in men (5.9±6.1, p<0.001) than in women (1.7±2.4), due to their gender and the pre-menopausal mean age of the women (39.4±7.3 years of age), despite a significantly higher rate of abdominal obesity (54.8% in women vs. 8.1% in men, p<0.001) and lower HDL (61.3% in women vs. 40% in men, p=0.042). The rate of metabolic syndrome among our female HIV seropositive drug users was significantly higher (29% vs 10.3%, p=0.013) compared to men (10.3%). Participants with metabolic syndrome had a significantly higher 10-year CHD risk (27.8% vs. 10.2%, p=0.041) and higher mean BMI (28.6 ± 4.1 vs. 24.2±4, p<0.001) than those without the syndrome. The predominant proportion of the cohort had a high viral load, suggesting that their use of illicit drugs has an influence on either adherence or effectiveness of antiretroviral medication. Increased viral load was significantly associated with metabolic syndrome (OR=2.23, 95% CI:1.12, 4.47; p=0.023), high fasting glucose (OR=1.61, 95% CI: 1.02, 2.55; p=0.042) and low HDL levels (OR=1.41, 95%CI: 1.01, 1.98; p=0.046), after controlling for age gender, smoking, PI exposure, BMI and CD4. HAART with or without PI did not significantly impact the 10-year CHD risk estimate or metabolic syndrome in this cohort. The estimated effect of PI, however, was positively and significantly related to triglyceride levels (effect estimate=95.81; 95% CI:39.40, 152.21; p<0.01) after controlling for age, gender, smoking, viral load, CD4 cell count and BMI. Heavy use of cigarettes and crack/cocaine was inversely associated with obesity (OR=0. 84, 95% CI:0.67, 0.99; p=0.049; OR=0.43, 95% CI:0.19, 0.98; p=0.044, respectively), while use of marijuana tended to be associated with increased central obesity (p=0.08). Heavy cigarette smoking was significantly associated with low HDL (OR=3.06, 95% CI:1.18; 7.95, p=0.02). The significant association of higher viral load with CHD risk indicates that controlling viral load may be important in reducing CHD risk in HIV infected drug users.

Renal platinum distributions were determined in rabbits after administration of 0.4 mL of 1 mg/mL cisplatin by intravenous infusion, by injections into the left renal artery with aqueous contrast material and with lipid contrast material (Ethiodol), and by chemoembolization of the left renal artery with concurrent administration of various concentrations of two collagen carriers, Angiostat collagen for embolization and Gelfoam gelatin. Renal platinum concentration was measured in tissue homogenates at 2 1/2 hours with atomic absorption spectrometry. Target-kidney platinum levels were 5.4 and 6.9 times the contralateral-kidney levels after intraarterial infusion of aqueous and lipid contrast media, respectively. With Angiostat and Gelfoam chemoembolization, renal platinum retention and collagen concentration were linearly related (r = .87 and .81, P less than .001). Target-kidney-contralateral-kidney platinum ratios were 57:1 for 30 mg/mL Gelfoam and 220:1 for 10 mg/mL Angiostat. The difference in regional drug retention for Angiostat versus Gelfoam reflects the stable fiber integrity of Angiostat.