Hyperuricemia and Associated Cardiometabolic Factors: A Cross-sectional Study on Taxi-motorbike Drivers Working in Cotonou, Benin

Background: An elevated level of uric acid (UA), also known as hyperuricemia (HUA), contributes to the occurrence of cardiovascular diseases (CVDs). However, epidemiolocal features of HUA in populations of Benin are rare. Objectives: We identified clinical and metabolic factors associated with HUA in taxi-motorbike drivers (TMDs) of Cotonou. Methods: A total of 134 participants with a mean age of 39.3 years were analyzed using a retrospective cross-sectional study design. Data from a self-administered questionnaire and biochemical markers including, plasma UA, glucose, insulin, creatinine, and lipids were obtained from each participant. HUA was defined as plasma UA greater than 416 μmol/L. Insulin resistance (IR) was determined using the homeostatic model assessment (HOMA). Logistic regression analysis was performed to determine the association of various risk factors with HUA. Odds ratio (OR) and 95% confidence interval (CI) were calculated for HUA. Results: The overall prevalence of HUA was 19.4% (95% CI: 12.7-26.1) in TMDs. Multivariable logistic regression showed that IR (OR = 3.60, 95% CI: 1.27-10.22, P = 0.02), hypertension (OR = 2.75, 95% CI: 1.00-7.54, P = 0.05), and triglycerides (TG; OR = 4.25, 95% CI: 1.39-12.98, P = 0.01) were risk factors for HUA. Furthermore, creatinine was inversely associated with HUA (OR = 0.62, 95% CI: 0.41-0.94, P = 0.02). Conclusion: HUA was found in 19.4% of the patients. In addition, hypertension, IR, creatinine, and TG levels were independently associated with HUA in TMDs. Therefore, the monitoring of these markers may help prevent HUA

Hematological changes among Beninese motor-bike taxi drivers exposed to benzene by urban air pollution

Exposure to high-concentration of benzene in polluted air has been associated with bone marrow deficiency, aplastic anemia and leukemia. However, epidemiological studies have reported conflicting data following human exposure to benzene levels below 1 ppm (that is, 3.2 mg/m3). Therefore we investigated the influence of outdoor air benzene on peripheral blood cells among exposed motor-biketaxi drivers (MBTD) in which specific IgG antibodies against reactive benzene metabolites, such as hydroquinone (HQ) and para-benzoquinone (p-BQ) are identified and quantified for further use as biomarker of exposure. We compared 144 MBTD with 30 unexposed age and sex-matched controls. The mean age ± SD (95% CI) were: MBTD 39.5 ± 7.82 (38.2 - 40.7) and village residents 40.3 ± 10.56 (39.1-43.0). Personal benzene exposure was assessed using GABIE diffusive samplers. The levels of specific IgG antibodies to HQ and p-BQ were determined by ELISA. The peripheral blood cells were counted by an automated analyzer. Benzene, Toluene and Xylene levels were much higher in MBTD in comparison to the control group. Benzene exposure levels ranged from 0.012 to 0.550 ppm in MBTD. Their average exposure level per one week was 0.126±0.206 ppm. Accordingly, MBTD had significantly higher levels of specific IgG antibodies to HQ and p-BQ compared to the controls (p< 0.001). WBC, lymphocytes, eosinophils and platelets were significantly decreased in MBTD, whereas RBC and other blood cell numbers remained unchanged. Total WBC, lymphocytes and eosinophils counts were decreased among exposed MBTD compared to unexposed controls. We suggest the use of these blood parameters together with specific IgG antibodies to HQ and p-BQ as biomarkers in biological monitoring of low level benzene exposure. Larger studies are however required to validate this new approach of health survey in workers exposed to benzene.Key words: Benzene, motor-bike-taxi drivers, specific immune responses, peripheral blood cell count

BRIP1 coding variants are associated with a high risk of hepatocellular carcinoma occurrence in patients with HCV- or HBV-related liver disease

The molecular mechanisms of hepatocellular carcinoma (HCC) carcinogenesis are still not fully understood. DNA repair defects may influence HCC risk. The aim of the study was to look for potential genetic variants of DNA repair genes associated with HCC risk among patients with alcohol- or viral-induced liver disease. We performed four case-control studies on 2,006 European- (Derivation#1 and #2 studies) and African-ancestry (Validation#1 and #2 studies) patients originating from several cohorts in order to assess the association between genetic variants on DNA repair genes and HCC risk using a custom array encompassing 94 genes. In the Derivation#1 study, the BRIP1 locus reached array-wide significance (Chi-squared SV-Perm, P=5.00×10-4) among the 253 haplotype blocks tested for their association with HCC risk, in patients with viral cirrhosis but not among those with alcoholic cirrhosis. The BRIP1 haplotype block included three exonic variants (rs4986763, rs4986764, rs4986765). The BRIP1 'AAA' haplotype was significantly associated with an increased HCC risk [odds ratio (OR), 2.01 (1.19-3.39); false discovery rate (FDR)-P=1.31×10-2]. In the Derivation#2 study, results were confirmed for the BRIP1 'GGG' haplotype [OR, 0.53 (0.36-0.79); FDR-P=3.90×10-3]. In both Validation#1 and #2 studies, BRIP1 'AAA' haplotype was significantly associated with an increased risk of HCC [OR, 1.71 (1.09-2.68); FDR-P=7.30×10-2; and OR, 6.45 (4.17-9.99); FDR-P=2.33×10-19, respectively]. Association between the BRIP1 locus and HCC risk suggests that impaired DNA mismatch repair might play a role in liver carcinogenesis, among patients with HCV- or HBV-related liver disease