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Data regarding the association between HIV and diabetes mellitus (DM) are conflicting, with little known regarding the impact of including hemoglobin A1C (A1C) as a criterion for DM.Pooled logistic regression was used to quantify the association between HIV and DM in 1501 HIV-infected and 550 HIV-uninfected participants from the Women's Interagency HIV Study. Incident DM was defined using the following 3 criteria, definition I: fasting glucose (FG) ≥126 mg/dL, anti-DM medication or reporting DM diagnosis (with confirmation by FG ≥126 mg/dL or anti-DM medication); definition II: confirmation with a second FG ≥126 mg/dL, and definition III: addition of A1C ≥6.5% confirmed by FG ≥126 mg/dL or anti-DM medication.DM incidence per 100 person-years was 2.44, 1.55, and 1.70 for HIV-infected women; 1.89, 0.85, and 1.13 for HIV-uninfected women, using definition I, II, and III, respectively. After adjustment for traditional DM risk factors, HIV infection was associated with 1.23-, 1.90-, and 1.38-fold higher risk of incident DM, respectively; the association reached statistical significance only when confirmation with a second FG ≥126 mg/dL was required. Older age, obesity, and a family history of DM were each consistently and strongly associated with increased DM risk.HIV infection is consistently associated with greater risk of DM. Inclusion of an elevated A1C to define DM increases the accuracy of the diagnosis and only slightly attenuates the magnitude of the association otherwise observed between HIV and DM. By contrast, a DM diagnosis made without any confirmatory criteria for FG ≥126 mg/dL overestimates the incidence, while also underestimating the effects of HIV on DM risk, and should be avoided. [ABSTRACT FROM AUTHOR]

Plasma HIV-1 RNA was measured in 306 samples, collected from 273 highly active antiretroviral therapy-experienced men, using both the Roche COBAS TaqMan (limit of detection = 20 copies per milliliter) and Roche Amplicor (limit of detection = 50 copies per milliliter) assays. Mixtures of Gaussian distributions incorporating left-censored data were used in analyses. The more sensitive TaqMan assay estimated that 23% and 0.0003% of HIV-1 RNA values would be below 1 copy per milliliter and 1 copy per 3 L, respectively. This is in sharp contrast to the overestimation provided by the less sensitive Amplicor assay, whereby the corresponding predicted percentages were 51% and 1%. Both assays appropriately characterized suboptimal virologic response as the rightmost peaks of both distributions provided an excellent fit to the observed data. Our results based on a widely available 20 copies per milliliter sensitive assay reproduce those obtained using customized assays that quantified HIV-1 RNA values as low as 1 copy per milliliter. [ABSTRACT FROM AUTHOR]

The article presents a study on antiretroviral therapy exposure and insulin resistance in interagency of HIV in women. It examined 1,614 HIV-infected and 604 HIV-uninfected participants from a study between October 2000 and March 2007 on women's interagency HIV with use of homeostasis model assessment (HOMA)-estimated insulin resitance (IR) at 11,019 semiannual visits. Result shows that longer nucleoside reverse transcriptase inhibitor (NRTI) was linked with greater IR in HIV-infected women.

The article characterizes the changes in regional anthropometry associated with stavudien exposure and discontinuation. It shows that HIV-infected women demonstrate decreases in weight and body circumference measurements over time regardless of continuing or discontinuing stavudine. The lower limbs seems to be most affected by stavudine exposure.

The article presents a cohort study on HIV1-positive women with viral failure that aims to describe the prevalence of protease inhibitor (PI) and nonnucleoside reverse transcriptase inhibitor (NNRTI) resistance mutations. Relationships on the presence of these mutations and immunologic outcomes following PI/NNRTI on the patients are also described. It was found that in the population-based cohort, virologic failure with PI or NNRTI resistance was common.

Determines the association of race with clinical and laboratory outcomes following initiation of highly active antiretroviral therapy in HIV-1-infected women in the U.S. Efficacy of antiretroviral therapies; Differences in behavior or in biologically determined pathways of drug metabolism and transport; Challenges in investigating racial and ethnic differences in biomedical processes.

Whether hepatitis C virus coinfection might accelerate atherosclerosis in HIV-infected individuals is unclear. We examined the relationship of HIV and hepatitis C virus with carotid artery intima media thickness and the presence of carotid plaques in the Women's Interagency HIV Study. Hepatitis C virus infection was not associated with greater carotid artery intima media thickness after adjustment for demographic and traditional cardiovascular risk factors. Further follow-up is needed to clarify whether HIV/hepatitis C virus coinfection may be associated with a greater risk of carotid plaque.

Objective: To determine the incidence of diabetes mellitus (DM) in a nationally representative cohort of HIV-infected women and a comparison group of HIV-uninfected women., Design: A prospective study between October 2000 and March 2006 of 2088 participants from the Women's Interagency HIV Study who did not have evidence of DM at enrollment (1524 HIV infected and 564 HIV uninfected)., Methods: Incident DM was defined as either having fasting glucose > or = 1.26 g/l, reporting antidiabetic medication, or reporting DM diagnosis (with subsequent confirmation by fasting glucose > or = 1.26 g/l or reported antidiabetic medication); all were assessed at semi-annual study visits., Results: DM developed in 116 HIV-infected and 36 HIV-uninfected women over 6802 person-years. HIV-infected women reporting no recent antiretroviral therapy had a DM incidence rate of 1.53/100 person-years; those reporting HAART containing a protease inhibitor (PI) had a rate of 2.50/100 person-years and those reporting non-PI-containing HAART a rate of 2.89/100 person-years. None of these rates differed from the HIV-uninfected women (1.96/100 person-years) substantially or beyond levels expected by chance. Among HIV-infected women, longer cumulative exposure to nucleoside reverse transcriptase inhibitors (NRTI) was associated with an increased risk of DM incidence compared with no NRTI exposure: relative hazard (RH) 1.81 [95% confidence interval (CI), 0.83-3.93] for > 0 to 3 years exposure and RH 2.64 (95% CI, 1.11-6.32) for > 3 years exposure., Conclusion: Longer cumulative exposure to NRTI was associated with increased DM incidence in HIV-infected women. Regular DM monitoring is advisable because NRTI form the backbone of effective antiretroviral therapy.