Preterm birth is a global epidemic and a leading cause of neonatal mortality in Sub-Saharan Africa. We evaluated the prevalence and risk factors of preterm birth among women attending the labor ward for delivery at a tertiary hospital in Ghana. This comparative cross-sectional study was conducted among a cohort of 209 pregnant women admitted to the labor ward of the Komfo Anokye Teaching Hospital (KATH). Pregnant women who delivered between 28 and 36 completed weeks of gestation were classified as preterm delivery whereas those who delivered after 37–42 completed weeks were described as term. Sociodemographic, clinical, and obstetric data were collected from patient's folder and hospital archives. Categorical variables were analyzed and expressed as frequencies and proportions. We determined the association between obstetric factors and preterm delivery with multiple logistic regressions. Significance level of the strength of association was determined at p-value < 0.05. of the 209 participants, the prevalence of preterm birth was 37.3% (78/209) whereas 62.7% (131/209) delivered at Term. Intrauterine growth restriction (IUGR) [aOR = 2.15, 95% CI = (1.819.55), p = 0.0390], HELLP (hemolysis, elevated liver enzymes and low platelet count) syndrome [aOR = 3.94, 95% CI = (1.64–9.48), p = 0.0020], early gestational obesity [aOR = 2.11, 95% CI = (1.31–11.92), p = 0.0480] and preeclampsia [aOR = 4.56, 95% CI = (1.63–12.76), p = 0.004] were identified as independent risk factors of preterm birth. Prevalence of preterm birth was high among women attending labor admission at the Komfo Anokye Teaching Hospital and this was independently influenced by IUGR, HELLP syndrome, early gestational obesity, and preeclampsia. Identifying early signs of adverse pregnancy outcomes would inform the need for management policy to prevent high prevalence of preterm births.

Background Soil-transmitted helminths (STHs) pose a formidable health risk to school-age children in resource-limited settings. Unfortunately, mass deworming campaigns have been derailed since the onset of the coronavirus disease 2019 pandemic. The present study assessed the cross-sectional associations between STHs, nutritional status and academic performance of schoolchildren in the Banda District of Ghana. Methods Schoolchildren (5–16 y of age; n=275) were recruited through both school and household visits by community health workers using a multistage cluster sampling technique. In addition to school microscopy, anthropometric records were also taken. Results The prevalence of geohelminthiasis was 40.4% (95% confidence interval 34.6 to 46.2). STHs targeted for elimination by the World Health Organization and national programmes were detected among schoolchildren. Children with intestinal parasite infection (53.7 [standard deviation {SD} 11.5]) had lower mean academic scores compared with uninfected children (59.6 [SD 16.9]) (p=0.034). In multiple regression analysis, intestinal parasite infection status and z-scores for weight-for-age showed a collective significant effect on the academic score (F1117=8.169, p<0.001, R2=0.125). Conclusions Schoolchildren with STHs had poorer academic performance compared with uninfected children, despite their nutritional status. In addition to school feeding programmes, school-based mass drug administration campaigns may be critical for improving learning outcomes in young schoolchildren.

Objectives: To assess variability and predictability of adiponectin, leptin, resistin and their ratios in non-obese and obese women with anovulatory polycystic ovary syndrome (aPCOS). Results: A total of 52 ovulatory controls (mean age=31.63±4.88 years, BMI=25.33±2.68 kg/m3); 54 non-obese [mean age=32.11±4.25 years, BMI=25.72±2.95 kg/m3] and 50 obese women with aPCOS [mean age= 33.64±4.14 years, BMI=39.19±2.99 kg/m3] were recruited. The aPCOS group had lower adiponectin [13.0(10.49-16.59) vs 18.42(15.72-19.92) µg/ml, p<0.0001], adiponectin: leptin ratio (A:L) [0.60(0.35-0.88) vs 1.19(0.92-1.37), p<0.0001], and adiponectin: resistin ratio (A:R) [0.30(0.21-0.43) vs 0.42(0.32-0.62), p<0.0001] but a higher leptin [20.02(14.54-26.80) vs 16.17(14.51-18.36) ng/ml, p<0.0001] and leptin: resistin ratio (L:R) [0.53(0.37-0.82) vs 0.40(0.27-0.48), p<0.0001] compared to the controls. The obese aPCOS group had lower adiponectin [11.04(5.66-13.25) vs 14.18(11.04-18.02), p<0.0001 and 18.42(15.72-19.92) µg/ml, p<0.0001], A:L [0.36(0.27-0.44) vs 0.78(0.61-1.16), p<0.0001 and 1.19(0.92-1.37), p<0.0001], and A:R [0.24(0.17-0.38) vs 0.40(0.23-0.58), p<0.0001 and 0.42(0.32-0.62), p<0.0001] but a higher leptin [26.80(14.28-32.09) vs 17.95(14.86-21.26), p<0.05 and 16.17(14.51-18.36) ng/ml, p<0.0001] and L:R [0.63(0.46-1.03) vs 0.41(0.30-0.61), p<0.0001 and 0.40(0.27-0.48), p<0.0001] compared to the non-obese aPCOS and control group, respectively. A:L showed the best discriminatory power in predicting aPCOS (AUC=0.83), followed by adiponectin alone (AUC=0.79), L:R and leptin alone (both AUC=0.69). Resistin alone had the poorest discriminatory power (AUC=0.48).

Abstract BackgroundSLC10A1 gene codes NTCP, a receptor through which the hepatitis B virus (HBV) gets access into hepatocytes - a stage of the viral cycle necessary for replication. Polymorphism variants of SLC10A1 play roles in HBV infection, viral clearance, treatment outcome, and complications, in diverse ethnic groups and countries. However, no such study has been conducted in the Ghanaian population, a country with HBV endemicity. Therefore, an exploratory study was conducted to investigate the presence of three (3) single nucleotide polymorphisms (SNPs) in the SLC10A1 gene (rs2296651, rs61745930, and rs4646287) and assessed the risk of HBV infection among the Ghanaian population.MethodPolymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used to determine the presence of the SNPs among 292 participants comprising 146 HBV infected persons as case-subjects and 146 HBV non-infected persons as control-subjects. ResultsThe minor allele frequency (T) of rs2296651 was present in a significantly high proportion of cases compared with the control group (12.6% vs. 3.1%, p < 0.0001). The homozygote recessive variant of rs61745930 was present in 2.7% of the control group and 5.5% of the case group. Moreover, the minor allele frequencies of rs4646287 were 9.6% and 8.6% among the control and the case group, respectively (p = 0.767). Under the dominant (CC) genetic model of inheritance, rs2296651 was found to be protective of HBV infection [OR = 0.18 (0.07–0.44)], whereas under the co-dominant and additive model, rs2296651 was a potential risk factor for HBV infection [OR = 5.2 (95%CI: 2.1–12.8); 3.5 (95%CI: 1.6–7.6], respectively. Variants of rs61745930 and rs4646287 were not associated with HBV infection (p > 0.05). Polymorphisms in SLC10A1, however, did not show any significant association with HBV infectivity (p > 0.05).ConclusionThe study highlights some polymorphism proof that variants rs2296651, rs61745930, and rs4646287 exist in HBV-infected individuals in Ghana. Variant rs2296651 was found to be associated with HBV infection. Nonetheless, polymorphisms in SLC10A1 were not associated with HBV infectivity among the Ghanaian population. Further investigation is warranted to assess the offensive role of the relationship between rs2296651 and HBV infectivity.

Objectives To assess the variability in adiponectin, leptin, and resistin between ovulatory women, and non-obese and obese women with polycystic ovary syndrome (PCOS). The study also explores the ratios of the adipokines and evaluated their predictability for PCOS. Results The PCOS group presented with lower adiponectin [13.0(10.49-16.59) vs 18.42(15.72-19.92) µg/ml, p<0.0001], adiponectin: leptin ratio [0.60(0.35-0.88) vs 1.19(0.92-1.37), p<0.0001], and adiponectin: resistin ratio [0.30(0.21-0.43) vs 0.42(0.32-0.62), p<0.0001] but a higher leptin [20.02(14.54-26.80) vs 16.17(14.51-18.36) ng/ml, p<0.0001] and leptin: resistin ratio [0.53(0.37-0.82) vs 0.40(0.27-0.48), p<0.0001] compared to the ovulatory group. The obese PCOS group presented with lower adiponectin [11.04(5.66-13.25) vs 14.18(11.04-18.02) µg/ml, p<0.0001 and 18.42(15.72-19.92) µg/ml, p<0.0001], adiponectin: leptin ratio [0.36(0.27-0.44) vs 0.78(0.61-1.16), p<0.0001 and 1.19(0.92-1.37), p<0.0001], and adiponectin: resistin ratio [0.24(0.17-0.38) vs 0.40(0.23-0.58), p<0.0001 and 0.42(0.32-0.62), p<0.0001] but a higher leptin [26.80(14.28-32.09) vs 17.95(14.86-21.26) ng/ml, p<0.05 and 16.17(14.51-18.36) ng/ml, p<0.0001] and leptin: resistin ratio [0.63(0.46-1.03) vs 0.41(0.30-0.61), p<0.0001 and 0.40(0.27-0.48), p<0.0001] compared to the non-obese PCOS and ovulatory control group, respectively. Adiponectin: leptin ratio presented with the best discriminatory power in predicting PCOS (AUC=0.83) followed by adiponectin alone (AUC=0.79), and leptin: resistin ratio and leptin alone (both AUC=0.69). Resistin alone presented with the poorest discriminatory power (AUC=0.48).