Cardiovascular disease is now a leading cause of mortality in people with HIV (PWH). High blood pressure is the major driver of cardiovascular disease. Despite this, little is known about blood pressure in PWH during the early years of antiretroviral therapy (ART). In this prospective cohort study in Tanzania, the authors conducted unobserved blood pressure measurements at enrollment, 3, 6, 12, 18, and 24 months in 500 PWH initiating ART and 504 HIV-uninfected adults. The authors excluded measurements taken on antihypertensive medications. Although PWH had a significantly lower blood pressure before ART initiation, they had a significantly greater increase in blood pressure during the first 2 years of ART compared to HIV-uninfected controls. Blood pressure correlates in PWH differed from HIV-uninfected controls. In PWH, lower baseline CD4 + T-cell counts were associated with lower blood pressure, and greater increases in CD4 + T-cell counts on ART were associated with greater increases in blood pressure, both on average and within individuals. In addition, PWH with a systolic blood pressure (SBP) <90 mm Hg at the time of ART initiation had ~30% mortality in the following 3 months due to occult infections. These patients require careful investigation for occult infections, and those with tuberculosis may benefit from corticosteroids. | 1555 REIS Et al.
Background.HIV-positive individuals are at significantly increased risk of depression. In low- and middle-income countries, depression is frequently under-detected, hampered by a lack of data regarding available screening tools. The 5-item World Health Organization Well-Being Index (WHO-5) is widely used to screen for depression, yet its validity in African adults with HIV has yet to be examined.Methods.In this cross-sectional study, we enrolled HIV-positive adults presenting to an outpatient HIV clinic in Mwanza, Tanzania. Patients were administered the Patient Health Questionnaires (PHQ)-2/9 and WHO-5 questionnaires. The rate of positive screens was calculated. Fisher's exact test and Pearson's correlation coefficients between PHQ-2/9 and WHO-5 scores were calculated.Results.We enrolled 72 HIV-positive adults: rates of positive depression screen were 62.5%, 77.8%, and 47.2% according to PHQ-2, PHQ-9, and WHO-5, respectively. PHQ and WHO results for depression were significantly associated (Fisher's exact test: PHQ-2 v. WHO-5, p = 0.028; PHQ-9 v. WHO-5, p = 0.002). The level of correlation between PHQ and WHO results for depression was moderate (Pearson's correlation coefficient: PHQ-2 v. WHO-5 −0.3289; PHQ-9 v. WHO-5 −0.4463).Per Mantel–Haenszel analysis, screening results were significantly more concordant among patients in the following strata: men, age >40, Sukuma ethnicity, Christian, unmarried, self-employed, at least primary school education completed, and higher than the median income level.Conclusions.WHO-5 scores correlated well with those of the PHQ-9, suggesting that the WHO-5 represents a valid screening tool. The concordance of PHQ-9 and WHO-5 results was poorer in marginalized socioeconomic groups. Positive depression screens were exceedingly common among HIV-positive Tanzanian adults according to all three questionnaires.
Background More than 15 million people in sub-Saharan Africa receive ART. Treatment failure is common, but the role of HIV drug resistance in treatment failure is largely unknown because drug resistance testing is not routinely done. This study determined the prevalence and patterns of HIV drug resistance in patients with suspected virological failure. Materials and methods A single high viral load of >1000 viral RNA copies/mL of plasma at any point during ART was considered as suspected virological failure. HIV-1 RNA was extracted from plasma samples of these patients using the QIAamp Viral RNA kit. The protease and part of the RT regions of the HIV pol gene were characterized. Results Viral load was determined in 317 patients; 64 (20.2%) had suspected virological failure. We successfully genotyped 56 samples; 48 (85.7%) had at least one major resistance-associated mutation (RAM). Common mutations in RT were M184V (75%), T215Y (41.1%), K103N (39.3%), M41L (32.1%), D67DN (30.3%), G190A (28.6%) and A98G (26.8%). No RAMs were detected in ART regimens based on a ritonavir-boosted PI. Conclusions The Tanzanian national guidelines define ‘virological failure’ as two consecutive viral load measurement results, at 3 month intervals, above the WHO threshold (1000 copies/mL). Here, we show that a single viral load above the WHO threshold is associated with high rates of RAMs. This suggests that a single high viral load measurement could be used to predict virological failure and avoid delays in switching patients from first-line to higher genetic barrier second-line regimens.
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