Zinc and selenium indicators and their relation to immunologic and metabolic parameters in male patients with human immunodeficiency virus.

OBJECTIVES: Micronutrient deficiencies are common among people living with HIV (PLWHIV). The clinical and immunologic consequences of micronutrient deficiencies have been poorly explored in the context of human immunodeficiency virus (HIV) infection. The aim of this study was to determine the prevalence of zinc and selenium deficiency (dietary intake and serum concentrations) and analyze their associations with absolute CD4+ T-cell counts, inflammation markers, and metabolic disorders in a cohort of antiretroviral-experienced HIV-infected individuals. METHODS: The zinc and selenium intakes of 124 HIV-infected men were estimated using 3-d food records. In a subcohort of 45 individuals, serum zinc and selenium concentrations and proinflammatory cytokines were determined. Body composition, bone mineral density (BMD), CD4+ T-cell counts, lipid profile, glucose, and blood pressure were determined and were associated with zinc and selenium dietary intake and serum concentrations. RESULTS: Of the PLWHIV studied, 58% had suboptimal intake of zinc and 8% demonstrated suboptimal intake of selenium. Serum deficiencies for zinc and selenium were 23.9% and 65.9%, respectively. Zinc and selenium intake were correlated with increased muscle mass. Selenium intake was associated with increased BMD of the lumbar region. An inverse correlation between serum selenium concentration and several proinflammatory cytokines (interleukin-1ß, interleukin-6, and tumor necrosis factor-α) was found. CONCLUSION: Suboptimal zinc and selenium intake and serum concentration deficiencies are highly prevalent in treated HIV-positive individuals and are associated with body composition, BMD, and inflammation. Clinical trials should be designed to explore the effect of zinc and selenium supplementation on metabolic, inflammatory, and immunologic parameters on the HIV-positive population.

Accuracy of Predictive Equations for Energy Expenditure in Mexicans Living With HIV/AIDS With and Without Antiretroviral Therapy.

INTRODUCTION: Determination of the resting energy expenditure (REE) is essential for planning nutrition therapy in patients with human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) to help to improve their nutrition status. We aim to evaluate the agreement and accuracy of prediction equations that estimate the REE in a Mexican population with a diagnosis of HIV/AIDS with and without antiretroviral therapy (ART). METHODS: A cross-sectional study in Mexican patients with HIV/AIDS with and without ART. Weight, height, and body composition measured with dual-energy x-ray absorptiometry were evaluated. The REE was determined with indirect calorimetry and estimated using the Mifflin-St Jeor (MSJ), Harris-Benedict (HB), Schofield 1 and 2, Cunningham, Melchior 91, Melchior 93, and Batterham equations. The Bland-Altman method assessed agreement between the real and estimated values, and the percent difference between these values was used to assess the prediction accuracy. RESULTS: Sixty-five adults without ART and 102 adults with ART were included. The mean REE (kcal/kg) was 24.8 ± 2.4 and 23.8 ± 3.6 in patients without and with ART, respectively. Good agreement and reliability were observed in the HB (intraclass correlation coefficient [ICC], 0.75; P < .05), Batterham (ICC, 0.79; P < .05), Schofield 1 (ICC, 0.74; P < .05), and Schofield 2 (ICC, 0.78; P < .05) results in individuals without ART. In individuals with ART, good agreement and reliability were observed with the HB equation (ICC, 0.76; P < .05). The MSJ equation showed good agreement with poor reliability (ICC, 0.05; P < .05). CONCLUSION: The equations with the best agreement and accuracy were Schofield 2, Batterham, and HB in individuals without ART and HB and MSJ in the population with ART.

Improving outcome of human immunodeficiency virus-infected patients in a Mexican intensive care unit.

BACKGROUND: In Latin America, insufficient data are available to improve local admission policies for human immunodeficiency virus (HIV) patients in the intensive care units (ICU). We undertook this study to evaluate the outcome and survival determinants of HIV patients in a Mexican ICU during three time periods. METHODS: From December 1985 through January 2006, a clinical chart-based, retrospective study of all HIV patients admitted to the ICU was conducted. Demographic, clinical and laboratory data; disease severity score (APACHE II) and mortality were evaluated. A comprehensive database was created and data were analyzed using survival and regression models. RESULTS: Ninety HIV patients were admitted to the ICU during the study: 16 (18%) in 1985-1992 (non-antiretroviral [ARV]-period), 21 (23%) in 1993-1996 (ARV-period), and 53 (58%) in 1996-2006 (highly active antiretroviral treatment [HAART] period). Leading reasons for admission were the need for mechanical ventilatory support (MVS, 85.5%), septic shock (23%), and non-HIV/AIDS complications (15.5%). Survival in the ICU increased from 12.5% (non-ARV period) to 57% (HAART period). Mortality during ICU stay was associated with MVS (HR: 3.2; 95% CI 1.0-10.2) and APACHE II > or =13 points (HR: 2.2; 95% CI 1.3-4.0). Use of steroids (HR: 0.4; 95% CI 0.2-0.8) and HAART (HR: 0.25; 95% CI 0.1-0.5) were associated with a lower risk of death. In multivariate analysis, septic shock was the main predictor of death in the ICU (HR: 2.4; 95% CI 1.1-5.2) and after discharge. HAART remained as a significant protective factor. CONCLUSIONS: Overall survival in Mexican HIV patients admitted to an ICU has substantially increased in recent years. These data should encourage policies that consider HIV patients as good candidates for receiving intensive care.

Uridine supplementation antagonizes zalcitabine-induced microvesicular steatohepatitis in mice.

UNLABELLED: Zalcitabine is an antiretroviral nucleoside analogue that exhibits long-term toxicity to hepatocytes by interfering with the replication of mitochondrial DNA (mtDNA). Uridine antagonizes this effect in vitro. In the present study we investigate the mechanisms of zalcitabine-induced hepatotoxicity in mice and explore therapeutic outcomes with oral uridine supplementation. BalbC mice (7 weeks of age, 9 mice in each group) were fed 0.36 mg/kg/d of zalcitabine (corresponding to human dosing adapted for body surface), or 13 mg/kg/d of zalcitabine. Both zalcitabine groups were treated with or without Mitocnol (0.34 g/kg/d), a dietary supplement with high bioavailability of uridine. Liver histology and mitochondrial functions were assessed after 15 weeks. One mouse exposed to high dose zalcitabine died at 19 weeks of age. Zalcitabine induced a dose dependent microvesicular steatohepatitis with abundant mitochondria. The organelles were enlarged and contained disrupted cristae. Terminal transferase dUTP nick end labeling (TUNEL) assays showed frequent hepatocyte apoptosis. mtDNA was depleted in liver tissue, cytochrome c-oxidase but not succinate dehydrogenase activities were decreased, superoxide and malondialdehyde were elevated. The expression of COX I, an mtDNA-encoded respiratory chain subunit was reduced, whereas COX IV, a nucleus-encoded subunit was preserved. Uridine supplementation normalized or attenuated all toxic abnormalities in both zalcitabine groups, but had no effects when given without zalcitabine. Uridine supplementation was without apparent side effects. CONCLUSION: Zalcitabine induces mtDNA-depletion in murine liver with consequent respiratory chain dysfunction, up-regulated synthesis of reactive oxygen species and microvesicular steatohepatitis. Uridine supplementation attenuates this mitochondrial hepatotoxicity without apparent intrinsic effects.