BackgroundThere is growing evidence of an interaction between HIV-infection, anti-retroviral therapy (ART) and cardiovascular diseases (CVD). Epidemiological studies in Europe and North America have been observing a shift towards an increased incidence of coronary heart disease and acute myocardial infarctions in HIV-infected populations compared to the general population even after adjusting for traditional cardiovascular risk factors. Despite South Africa (and sub-Saharan Africa, SSA) being regarded as the epicentre of the global HIV epidemic, very little is known about the prevalence of cardiovascular risk factors and precursors of vascular disease in HIV-infected populations in this region. The knowledge gap is further widened by the paucity of data from prospective studies. We present the rationale, objectives and key methodological features of the EndoAfrica study, which aims to determine whether HIV-infection and ART are associated with altered cardiovascular risk and changes in vascular endothelial structure and function in adults living in the Western Cape Province of South Africa.MethodsIn this longitudinal study, comprehensive cardiovascular assessments of HIV-negative and HIV-positive (with and without ART) study participants are performed by clinical and biochemical screening for traditional cardiovascular risk factors and biomarkers of CVD. Vascular and endothelial function is determined by brachial artery flow-mediated dilatation (FMD), carotid-intima-thickness (IMT) measurements and quantitative retinal blood vessel analyses, complemented by vascular endothelial biomarker assays. Finally, we aim to statistically determine whether HIV-infection and/or ART are associated with increased cardiovascular risk and vascular endothelial dysfunction, and determine whether there is progression/regression in these endpoints 18 months after the baseline assessments.DiscussionThe EndoAfrica study provides a unique opportunity to recruit a cohort of HIV-infected patients and HIV-negative controls who will be comprehensively and longitudinally assessed for cardiovascular risk and disease profile with vascular endothelial function as a potentially important intermediate cardiovascular phenotype. To our knowledge, it is the first time that such a systematic study has been established in the context of SSA and South Africa.

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Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a cytokine processed by proprotein convertase furin and released into extracellular space as a shorter bioactive fragment called soluble TWEAK (sTWEAK). CD163 has been identified as a new potential scavenger receptor for TWEAK. Studies in last years suggests that sTWEAK and sCD163 levels could be the potential biomarkers of some diseases like atherosclerosis. Behcet's disease (BD) is a chronic and relapsing multisystemic inflammatory disorder with unknown etiology. Systemic vasculitis is the main pathology observed in BD. The aim of the study to examine the sTWEAK and sCD163 concentrations in BD. Methods: The study group consists of 50 patients with BD and 30 healthy control individuals who do not use any drugs and have any systematic illness. sTWEAK and sCD163 concentrations were determined by Enzyme Linked Immunosorbent Assay (ELISA) in serum samples of the study group. Results: sTWEAK levels were significantly higher in BD (807 pg/mL vs. 663 pg/mL, p¼0.012) and also sCD163 levels were significantly higher in BD (644 ng/mL vs. 501 ng/mL, p¼0.002). Both sTWEAK and sCD163 concentrations were higher in active patients with BD (832 pg/mL and 667 ng/mL, respectively). Predictive values of sTWEAK and sCD163 levels obtained by Receiver Operating Characteristic (ROC) Curve analysis were found to be statistically significant. Conclusions: sTWEAK and sCD163 levels were increased in patients with Behcet's Disease. These two molecules can take part in the pathogenesis of Behcet's Disease and might be used for evaluation of the clinical activity of the disease.

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Aim: Flow-mediated dilatation (FMD) and retinal vascular analysis (RVA) may assist in predicting cardiovascular disease (CVD) but are poorly characterised in South Africa. We recorded baseline FMD and retinal vascular widths in healthy participants, and investigated associations with cardiovascular risk factors. Methods: Endothelial function (measured with FMD), microvascular structure (evaluated via fundus image analysis) and major CVD risk factors were assessed in 66 participants from Cape Town. Results: Median FMD% was 9.6%, with higher values in females. Mean retinal arteriolar and venular widths were ~156 and ~250 µm, respectively. FMD was not associated with CVD risk factors. Hypertension was associated with narrower retinal arterioles and venules. Conclusions: We report novel baseline FMD data in healthy South African adults from the Western Cape, and show that retinal microvascular calibres are associated with blood pressure. Our baseline FMD and RVA data could serve as a reference for future studies in South Africa.