Key result
Concurrent HIV infection and type 2 diabetes was associated with significantly elevated levels of the endothelial dysfunction marker ADMA (0.67 μM) compared to HIV infection alone (0.60 μM, p=0.017).
Cross-Sectional (n=100)
Yes
Absolute Event Rate: 0.67% vs 0.6%
p-value: p=0.017
Concurrent HIV infection and type 2 diabetes is associated with significantly greater endothelial dysfunction than either condition alone, highlighting a high-risk cardiovascular phenotype.
Combined HIV-T2D effects on endothelial function remain unclear; leaves open synergistic CVD mechanisms for prospective study.
Increased incidence of cardiovascular diseases (CVD) in both HIV infection and type 2 diabetes (T2D) compared to the general population has been described. Little is known about the combined effect of HIV infection and T2D on inflammation and endothelial function, both of which may contribute to elevated risk of CVD. Cross-sectional study including 50 HIV-infected persons on combination anti-retroviral therapy (cART), with HIV RNA <200 copies/mL ( n = 25 with T2D (HIV + T2D+), n = 25 without T2D (HIV + T2D-)) and 50 uninfected persons ( n = 22 with T2D (HIV-T2D+) and n = 28 without T2D (HIV-T2D-)). Groups were matched on age and sex. High sensitive C-reactive protein (hsCRP) was used to determine inflammation (cut-off 3 mg/L). The marker of endothelial dysfunction asymmetric dimethylarginine (ADMA) was measured using high performance liquid chromatography. Trimethylamine-N-oxide (TMAO), a microbiota-dependent, pro-atherogenic marker was measured using stable isotope dilution LC/MS/MS. The percentage of HIV + T2D+, HIV + T2D-, HIV-T2D+, and HIV-T2D- with hsCRP above cut-off was 50%, 19%, 47%, and 11%, respectively. HIV + T2D+ had elevated ADMA (0.67 μM (0.63-0.72) compared to HIV + T2D- (0.60 μM (0.57-0.64) p = 0.017), HIV-T2D+ (0.57 μM (0.51-63) p = 0.008), and HIV-T2D- (0.55 μM (0.52-0.58) p < 0.001). No differences in TMAO between groups were found. However, a positive correlation between ADMA and TMAO was found in the total population (r s = 0.32, p = 0.001), which was mainly driven by a close correlation in HIV + T2D+ (r s = 0.63, p = 0.001). Elevated inflammation and evidence of endothelial dysfunction was found in HIV-infected persons with T2D. The effect on inflammation was mainly driven by T2D, while both HIV infection and T2D may contribute to endothelial dysfunction. Whether gut microbiota is a contributing factor to this remains to be determined.
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Hove‐Skovsgaard et al. (2017) conducted a cross-sectional in HIV infection and Type 2 Diabetes (n=100). Concurrent HIV infection and type 2 diabetes vs. HIV infection without type 2 diabetes, type 2 diabetes without HIV, and healthy controls was evaluated on Asymmetric dimethylarginine (ADMA) concentration (p=0.017). Concurrent HIV infection and type 2 diabetes was associated with significantly elevated levels of the endothelial dysfunction marker ADMA (0.67 μM) compared to HIV infection alone (0.60 μM, p=0.017).
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