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• W2054296427 abstract "Background Anaemia has been linked with mortality in HIV infection. The mechanism of anaemia in the era of contemporary antiretroviral therapy is not understood. The aim of this study was to describe the association between anaemia and markers of immune activation and inflammation in a cohort of HIV-infected adults on stable antiretroviral therapy. Methods We performed a cross-sectional study of HIV-infected adults on antiretroviral therapy with HIV-1 RNA<1,000 copies/ml. Soluble and cellular markers of inflammation and immune activation were measured. Relationships between haemoglobin levels, anaemia (haemoglobin <13 g/dl for men and <12 g/dl for women) and mild anaemia (haemoglobin <14 g/dl for men and <13 g/dl for women) and these markers were explored using multivariable linear regression. Results Among the 147 participants, median age was 46 years, 78% were men, 68% were African American and 29% were Caucasian. Median body mass index (BMI) was 26.7 kg/m 2 , nadir and current CD4 + T-cell counts were 179 and 613 cells/mm 3 , respectively, and 78% had HIV-1 RNA<50 copies/ml (range 20–600 copies/ml). Median (IQR) haemoglobin was 14.3 (13.1– 15.1) g/dl; 14% were anaemic and 33% had at least mild anaemia. In multivariable analyses, mild anaemia was independently associated with female sex, older age, shorter duration of antiretroviral therapy, lower white blood cell count, higher platelet count, higher sCD14 and a greater number of CD14 dim CD16 + cells or ‘patrolling’ monocytes, which remained significant after further adjusting for race and BMI. Conclusions Having haemoglobin <14 g/dl for men and <13 g/dl for women was independently associated with monocyte activation (sCD14 and CD14 dim CD16 + cells) in HIV-infected adults on stable antiretroviral therapy." @default.
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• W2054296427 date "2014-07-01" @default.
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• W2054296427 title "Anaemia is Associated with Monocyte Activation in HIV-Infected Adults on Antiretroviral Therapy" @default.
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• W2054296427 doi "https://doi.org/10.3851/imp2940" @default.
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