ABSTRACT
Background: Dyslipidaemia is a known cause of cardiovascular mortality. Persons living with HIV are at high risk of developing cardiovascular disease due to lipid metabolism disorders associated with HIV or its therapy. Objective: This study evaluated concentrations of lipoproteins and apolipoprotein C-III and E, as a way of assessing cardiometabolic risks among HIV patients. Methods: We enrolled 50 HIV-negative persons and 100 HIV-positive patients, 50 on antiretroviral therapy (ART) and 50 treatment-naïve persons, from the Central Hospital and the Stella Obasanjo Hospital, Benin City, Edo State, Nigeria, between May 2015 and November 2015. Participants with a history of metabolic abnormalities were excluded. Apolipoproteins were assessed by enzyme-linked immunosorbent assay, while lipids were measured by spectrophotometry. Results: There were significant abnormalities in the lipid profile of patients with HIV. Triglycerides levels of HIV patients (ART-naïve: 1.44 ± 0.65 mmol/L; p < 0.001 and ART-experienced: 1.49 ± 0.70 mmol/L; p = 0.001) were significantly higher than among controls (0.95 ± 0.54 mmol/L). HIV patients had higher concentrations of apolipoprotein C-III than controls (p < 0.001) and higher low-density lipoprotein cholesterol levels (treatment-naïve: 2.83 mmol/L and ART-experienced patients: 3.59 mmol/L) than controls (2.50 mmol/L; p = 0.003). Conversely, HIV patients had significantly lowered high-density lipoprotein cholesterol levels compared to controls (p < 0.001). Conclusion: Dyslipidaemia was observed among HIV participants, irrespective of their ART experience. Therefore, it is crucial that the lipids of HIV patients be closely monitored to enable early intervention and decrease cardiovascular death. What this study adds: This study affirms that dyslipidemia is a complication of HIV or the prolonged use of ART.
ABSTRACT
BACKGROUND: Prostate cancer (PCa) may result from an interplay between many factors including exposure to trace elements. This study examined the association between cadmium exposure and PCa among Nigerian men and evaluated possible modification of this effect by zinc status. METHODS: This case-control study involved men with histologically confirmed PCa (n = 82), benign prostatic hyperplasia (BPH; n = 93) and controls (n = 98), aged between 40 and 80 years. Study participants were recruited from the main teaching hospital that draws clients from the entire Anambra State in South-Eastern Nigeria. Blood and urine samples were collected from these participants and were analyzed for trace elements using ICP-MS. Statistical models were used to assess the exposure risk for cadmium exposure as well as the mediating effect of zinc status. RESULTS: Among men with prostatic disorders (case-case analysis), every 10-fold increase in urinary cadmium was associated with increased risk of PCa (adjusted odds ratios: 2.526; 95% CI: 1.096-5.821). Men in the highest blood zinc quartile had lower odds of PCa compared to the lowest quartile (AOR: 0.19; 95% CI, 0.06-0.54; p-for trend = 0.001). Zinc-specific effect was observed in this group: every 10-fold increase in urinary cadmium was associated with increased risk of PCa among men with creatinine-adjusted urinary zinc levels below the median value (AOR: 8.46; 95% CI: 1.97 -36.39) but not in those above the median value (AOR: 1.55; 95% CI: 0.45 - 5.39). CONCLUSION: Higher exposure to cadmium may be associated with increased risk of PCa in Nigeria and probably other countries with high prevalence of Zn deficiency. These results point to the need to consider co-occurring trace metals in any effort to mitigate the toxicity of Cd in the environment.
