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Objective: To investigate the prevalence of widespread pain among people with HIV (PWH) and describe associations with antiretroviral therapy (ART) and markers of HIV disease stage. Design: Cross-sectional analysis of cohort study in the United Kingdom and Ireland. Methods: Pain information was collected during the baseline visit (conducted from 2013 to 2015) through a self-completed manikin identifying pain at 15 sites from five body regions. Pain was classified as widespread if reported at at least four regions and at least seven sites, or regional otherwise. Chi-squared tests, Kruskal–Wallis tests and ordinal logistic regression were used to consider associations between pain extent and sociodemographic and HIV-related factors. Results: Among the 1207 participants (614 PWH ≥ 50 years, 330 PWH < 50 years, 263 HIV-negative controls ≥50 years), pain was most commonly reported at the upper (left: 28.9%, right: 28.0%) and lower (left: 25.7%; right: 24.5%) leg, upper (18.6%) and lower (29.7%) back and shoulders (left: 16.0%; right: 16.8%). Widespread pain was more commonly reported in PWH than in HIV-negative controls (PWH ≥ 50 years: 18.7%; PWH < 50 years: 12.7%; HIV-negative ≥50 years: 9.5%) with regional pain reported in 47.6, 44.8 and 49.8%, respectively (global P = 0.001). In multivariable analyses, pain extent was greater in those with lower educational attainment, those exposed to more ART drugs, and those with a higher current CD4+ cell count but longer exposure to immunosuppression. Conclusion: Widespread pain is commonly reported in PWH and is associated with longer duration of exposure to HIV, immunosuppression and ART. Our findings call for greater awareness, and interventions to support the management, of pain in PWH.

Associations between markers of liver and renal dysfunction and nucleotide reverse transcriptase inhibitor plasma exposure are ill-defined. As part of a large cohort study (Pharmacokinetic and Clinical Observations in People over Fifty), we analysed associations between alanine aminotransferase and estimated glomerular filtration rate results in people living with HIV on tenofovir disoproxil fumarate, emtricitabine, abacavir and lamivudine. While we found no associations between nucleotide reverse transcriptase inhibitor concentrations and alanine aminotransferase, lower estimated glomerular filtration rate values were associated with greater tenofovir, emtricitabine and lamivudine exposure, whereas abacavir showed no associations.

Increasing access to more tolerable ARV treatments has vastly extended the expected lifespan of People with HIV (PWH), with some models predicting that in developed nations approximately two-thirds of PWH will be older than 50 years by 2030. Longer lifespans increase the risk of age-related neuropathologies, such as the deposition of amyloid beta plaques (Aβ42), regarded as an important prognostic marker of Alzheimer’s Disease (AD). Frequently first detected during mid-life, Aβ42 may predate the manifestation of neurocognitive symptoms associated with AD by 1-2 decades. \ud \ud The etiological significance of Aβ42 deposition in PWH is an active area of investigation. There is little clarity thus far in the clinical and research literature on whether the presence of Aβ42 in PWH leads to elevated risk of developing AD in those with and without HIV Associated Neurocognitive Disorders (HAND). Biological measures of neuropathology, such as CSF serum assays and brain tissue staining, have great potential in determining the extent to which Aβ42 deposition patterns in PWH are HAND-specific, and in linking these deposits to clinical outcomes. In this way, they might provide insight into otherwise seemingly paradoxical findings, such as the observation that neither age nor HIV clinical variables (including ARV status and duration of HIV infection) were able to explain the roughly 5 times greater incidence of mild cognitive impairment (MCI) over a period of 14 months in neurocognitively asymptomatic PWH compared to seronegative controls. \ud \ud In the study by Morgello and colleagues in this issue of AIDS, the authors examined hippocampal and frontal cortical tissue samples from a large cohort of 197 PWH and 63 HIV seronegative controls who donated brain tissue to the Manhattan HIV Brain Bank. Using this approach, they were able to quantify the association of HIV status and the presence of amyloid deposits in brain regions that are typically affected in AD. Despite the study being relatively well-powered, they were unable to identify between- 3 group differences in the occurrence of Aβ42 deposits. Rather, within the PWH cohort, duration of HIV infection, and, somewhat paradoxically, undetectable HIV viral load, emerged as significant predictors of the likelihood of detecting Aβ42.