Genotype-guided antiretroviral regimens in children with multidrug-resistant HIV-1 infection.

BACKGROUND: Genotyping tests were developed to attenuate the impact of viral resistance. Information about the efficacy in genotype base antiretroviral therapy in children is rare and even more in low- and middle-income countries. METHODS: Sixteen children with antiretroviral therapy (ART) failure and triple-class drug-resistant viruses were included in this study. Protease and retrotranscriptase genotypes were available for all patients. Switch of ART regimen was guided by genotyping data. The primary end point was virological suppression (<50 copies/ml) and immunological improvement after 48 wk of treatment with the new ART regimen. RESULTS: The median age of the patients was 14.5 y (interquartile range (IQR) 11-16.5). Median HIV-1 RNA viral load was 4.2 log10 (IQR: 3.4-4.8). The primary end point was found in 11 children (69%), and 13 children (81%) had an HIV-1 RNA viral load <200 copies/ml. Median (IQR) for the baseline CD4(+) cell count was 382 cells/µl (281-686 cells/µl), whereas after 48 wk of treatment with the new ART regimen, it was 640 cells/µl (361-936 cells/µl) (P < 0.001). CONCLUSION: Darunavir/ritonavir, raltegravir, and etravirine were well tolerated in the present pediatric population. These drugs provide good options for children exposed to extensive ART. Regimens guided by genotyping data were effective for children who had ART failure and multidrug-resistant HIV-1 infection.

Anal intraepithelial neoplasia among HIV-positive men who have sex with men.

Neoplasia is the second most common cause of mortality in HIV patients. The prevalence of anal cancer among men who have sex with men (MSM) has continued to increase since the introduction of antiretroviral therapy. We screened 94 HIV-infected MSM patients. We found high-grade squamous intraepithelial lesions (HSIL) in six of the patients. The calculated prevalence of HSIL was 6.4% (95% confidence interval: 2.9-13.2). The study and implementation of screening programs for high-risk groups is a priority.

Proximal renal tubular dysfunction related to antiretroviral therapy among HIV-infected patients in an HIV clinic in Mexico.

Proximal renal tubular dysfunction (PRTD) of varying severity has been associated with antiretroviral toxicity, especially related to the use of tenofovir (TDF). The aim of this study was to investigate whether HIV-infected patients who use a tenofovir-based regimen are at increased risk of tubular dysfunction. We conducted an observational, comparative, longitudinal, prospective study. Estimated glomerular filtration rate (eGFR) and markers of tubular damage to assess tubular dysfunction (fractional excretion of phosphate and uric acid, glycosuria, and proteinuria) were measured at baseline and at weeks 12 and 24. Of 111 participants, PRTD was found in 6.3% at week 12 and 9% at week 24, with no statistically significant difference between those on an abacavir (ABC)-containing regimen or a TDF-containing regimen. We also found an increase in triglycerides associated with the ABC-containing regimen compared with the TDF group. The use of an ABC- or TDF-containing regimen was independently associated with tubular dysfunction, but we found no significant differences between these groups, except when TDF was combined with a protease inhibitor. A better and more complete assessment of renal function is needed, because the presence of tubular dysfunction and proteinuria without impairment of eGFR may affect the renal safety of HIV-infected patients.

Effect of antiretroviral therapy on inflammatory markers of endothelial dysfunction in HIV treatment-naïve infected patients.

The aim of this study was to evaluate the effect of antiretroviral therapy on inflammatory markers of endothelial dysfunction in HIV treatment-naïve infected patients. This was a prospective cohort study in HIV treatment-naïve infected patients. The patients were assigned to a untreated group or a treatment group according to the therapeutic strategy received. Patients in the treatment group received efavirenz or lopinavir/ritonavir, each given with zidovudine and lamivudine. HIV RNA, CD4(+) cell count, and the levels of hsCRP, sCD40L, sICAM-1, sVCAM-1, and sE-selectin were measured before and 12 weeks after treatment. Fifty patients were enrolled: 13 in the untreated group and 37 in the treatment group; 48 (96%) completed the follow-up. The mean (± SD) age was 33 ± 9 years, and 38 (79%) were men. The median pretreatment CD4(+) cell counts were 263 cells/ml (IQR 118-341) in the treatment group and 658 cells/ml (IQR 475-887) in the untreated group. In the treatment group, the median serum sVCAM-1 and sICAM-1 levels decreased by a small but significant amount (1,400 and 228 ng/ml, respectively, P<0.05) from before to after the 12 weeks. These levels did not change in the untreated group. Antiretroviral therapy is associated with a decrease in sVCAM-1 and sICAM-1 levels after 12 weeks of treatment.

Risk factors and correlates for anemia in HIV treatment-naïve infected patients: a cross-sectional analytical study.

BACKGROUND: Hematologic 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. FINDINGS: We 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). CONCLUSIONS: Anemia 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.

APRI as a predictor of early viral response in chronic hepatitis C patients.

AIM: To evaluate the aspartate aminotransferase (AST) to platelet ratio index (APRI) as a predictive factor of early viral response in chronic hepatitis C naive patients. METHODS: We performed an ambispective case-control study. We enrolled chronic hepatitis C naive patients who were evaluated to start therapy with PEGylated interferon alpha-2b (1.5 mug/kg per week) and ribavirin (> 75 kg: 1200 mg and < 75 kg: 1000 mg). Patients were allocated into two groups, group 1: Hepatitis C patients with early viral response (EVR), group 2: Patients without EVR. Odds ratio (OR) and 95% confidence interval (CI) were calculated to assess the relationship between each risk factor and the EVR in both groups. RESULTS: During the study, 80 patients were analyzed, 45 retrospectively and 35 prospectively. The mean +/- SD age of our subjects was 42.9 +/- 12 years; weight 70 kg (+/- 11.19), AST 64.6 IU/mL (+/- 48.74), alanine aminotransferase (ALT) 76.3 IU/mL (+/- 63.08) and platelets 209 000 mill/mm(3) (+/- 84 429). Fifty-five (68.8%) were genotype 1 and 25 (31.3%) were genotype 2 or 3; the mean hepatitis C virus RNA viral load was 2 269 061 IU/mL (+/- 7 220 266). In the univariate analysis, APRI was not associated with EVR [OR 0.61 (95% CI 0.229-1.655, P = 0.33)], and the absence of EVR was only associated with genotype 1 [OR 0.28 (95% CI 0.08-0.94, P = 0.034)]. After adjustment in a logistic regression model, genotype 1 remains significant. CONCLUSION: APRI was not a predictor of EVR in chronic hepatitis C; Genotype 1 was the only predictive factor associated with the absence of EVR in our patients.