Abnormalities in liver function tests could be produced exclusively by direct inflammation in hepatocytes, caused by the human immunodeficiency virus (HIV). Mechanisms by which HIV causes hepatic damage are still unknown. Our aim was to determine the correlation between HIV viral load, and serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) as markers of hepatic damage in HIV naive infected patients. We performed a concordance cross-sectional study. Patients with antiviral treatment experience, hepatotoxic drugs use or co-infection were excluded. We used a Pearson's correlation coefficient to calculate the correlation between aminotransferases serum levels with HIV viral load. We enrolled 59 patients, 50 men and 9 women seen from 2006 to 2008. The mean (+/- SD) age of our subjects was 34.24 +/- 9.5, AST 37.73 +/- 29.94 IU/mL, ALT 43.34 +/- 42.41 IU/mL, HIV viral load 199,243 +/- 292,905 copies/mL, and CD4+ cells count 361 +/- 289 cells/mm(3). There was a moderately strong, positive correlation between AST serum levels and HIV viral load (r = 0.439, P < 0.001); and a weak correlation between ALT serum levels and HIV viral load (r = 0.276, P = 0.034); after adjusting the confounders in lineal regression model the correlation remained significant. Our results suggest that there is an association between HIV viral load and aminotransferases as markers of hepatic damage; we should improved recognition, diagnosis and potential therapy of hepatic damage in HIV infected patients.

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BackgroundHematologic manifestations of the human immunodeficiency virus (HIV) infection are a well-recognized complication of the disease and may be clinically important. Our objective was to determine the risk factors for anemia and its correlation with HIV treatment-naïve infected patients without co-infection or opportunistic diseases.FindingsWe performed a cross-sectional comparative study in which HIV treatment-naïve infected patients with anemia were compared with a control group of HIV patients without anemia. The interrelationship between risk factors and anemia was determined. Odds ratio and 95% confidence intervals were calculated, to adjust for the effects of potential confounders and we used a logistic regression model. Pearson's correlation coefficient was obtained to calculate the correlation between risk factors and hemoglobin.We enrolled 54 men and 9 women. Anemia was found in 13 patients; prevalence .20 (CI 95% 0.12-0.32). Severe anemia was found in only one patient (1.5%). Only CD4+ Cells Count <200 cells/mm3 was associated with increased risk of anemia in the multivariate analysis. There was a moderately strong, positive correlation between WBC and hemoglobin (r = 0.49, P < 0.001) and between CD4+ cell count and hemoglobin (r = 0.595, P < 0.001) and a moderately strong, negative correlation between HIV RNA viral load and hemoglobin (r = - 0.433, P < 0.001).ConclusionsAnemia is a common manifestation in the Mexican population without antiretroviral therapy. In HIV naïve patients a CD4+ Cell Count < 200 cells/mm3 was associated with an increased risk of anemia. There is a positive correlation between hemoglobin and CD4+ cell count.

BackgroundInfluenza virus pandemics vary dramatically in their severity and mortality. Thus, it is very important to identify populations with high risks of developing severe illness to reduce mortality in future pandemics. The purpose was to determine the mortality-associated risk factors in hospitalized Mexican patients infected with influenza A/H1N1.ResultsThe risk factors associated with mortality were: male sex [odds ratio (OR) = 5.25, confidence interval (CI) = 1.22–28.95], medical attention delayed >3 days (OR = 9.9, CI = 1.51–64.52), anti-flu therapy delayed >3 days (OR = 10.0, CI = 1.07–93.43), admission to intensive care unit (ICU) (OR = 9.9, CI = 1.51–64.52) and creatinine levels >1.0 mg/dL when admitted to hospital (OR = 11.2, CI = 1.05–120.32). After adjusting for the effects of potentially confounding variables in a logistic regression model, delayed medical attention (OR = 13.91, CI = 1.09–41.42, p = 0.044) and ICU hospitalization (OR = 11.02, CI = 1.59–76.25, p = 0.015) were the only predictors of mortality.ConclusionEarly medical attention is essential for reducing the mortality risk in patients with influenza A/H1N1, while a requirement for ICU management increases the risk.

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BackgroundThe Histoplasma urine antigen (HUAg) is the preferred method to diagnose progressive disseminated histoplasmosis (PDH) in HIV patients. In 2007, IMMY ALPHA Histoplasma EIA was approved for clinical for on-site use, and therefore useful for regions outside the United States. However, ALPHA-HUAg is considered inferior to the MVista-HUAg which is only available on referral. We aim to evaluate the diagnostic accuracy of ALPHA-HUAg.Methodology/Principal findingsWe conducted a multicenter, prospective, diagnostic test study in two secondary and eight tertiary-care facilities in Mexico. We included HIV patient with PDH suspicion and evaluated ALPHA-HUAg diagnostic accuracy using as reference standard the Histoplasma capsulatum growth on blood, bone marrow, and tissue cultures or compatible histopathologic exam (PDH–proven). We evaluated the results of 288 patients, 29.5% (85/288; 95% confidence interval [CI], 24.3–35.1) had PDH. The sensitivity of ALPHA-HUAg was 67.1% (95% CI, 56–76.8%) and the specificity was 97.5% (95% CI, 94.3%-99.1%). The positive likelihood ratio was 27.2 (95% CI; 11.6–74.4). In 10.5% of the PDH–proven patients, a co-existing opportunistic infection was diagnosed, mostly disseminated Mycobacterium avium complex infection.Conclusions/SignificanceWe observed a high specificity but low sensitivity of IMMY-HUAg. The test may be useful to start early antifungals, but a culture-based approach is necessary since co-infections are frequent and a negative IMMY-HUAg result does not rule out PDH.

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ObjectiveWe evaluated the effectiveness of darunavir (DRV) treatment plus an optimized background regimen in 120 HIV-1 treatment-experienced patients.DesignRetrospective cohort, multicenter study.MethodsAdults >16 years with virological treatment failure starting therapy with a DRV-containing regimen were included. Effectiveness was evaluated as the percentage of patients with an undetectable HIV-1 RNA viral load (<50 and <200 copies/mL) after 48 weeks, and changes in CD4+ cell counts. We evaluated the risk factors associated with treatment failure.ResultsOf the cohort, 83 % were men with a median age of 45 years (interquartile range, IQR 40–51). They had experienced treatment for a median of 13 years (IQR 9–17) with a median of six previous regimens (IQR 4–7), all using protease inhibitors. After treatment, 82 % (95 % confidence interval, CI 74–88 %) of patients had an HIV-1 RNA viral load <200 copies/mL and 69 % (95 % CI 60–76 %) had <50 copies/mL. The CD4+ cell count increased by 378 cells/μL (IQR 252–559; P < 0.001 vs. baseline). Risk factors associated with poor outcome were age >40 years [odds ratio, OR 0.15 (95 % CI 0.10–0.78); P = 0.015], use of raltegravir in the regimen [OR 0.37 (95 % CI 0.10–0.97); P = 0.046], and baseline CD4+ cell count <200 cells/μL [OR 2.79 (95 % CI 1.11–6.97); P = 0.028].ConclusionIn this Mexican cohort Darunavir was metabolically safe, well tolerated and achieved high rates of virological suppression in highly treatment-experienced patients infected with HIV-1.