Maternal demographic and placental risk factors in term low birth weight in Ghana

Background: Several studies report on factors that associate preterm birth and intrauterine growth restriction with low birth weight (LBW). However, few studies discuss risk factors that associate with LBW for full-term births. No such studies exist that involve a population from Ghana. Method: We used a nested case-control study approach to examine maternal socio-demographic and placental factors that contribute significantly to term LBW in Ghana. We assessed also the incidence of LBW in general at a major teaching hospital facility in Ghana. Results: Univariate and multivariate logistic regression analysis were used to investigate maternal sociodemographic and placental factors that associate with LBW. Following the preliminary univariate analysis, a stepwise logistic regression analysis showed that unstable income source, single motherhood, combined effect of pre-eclampsia and anaemia; ORs of 5.366 (95% CI: 1.986 to 14.497), 21.390 (95% CI: 3.610 to 126.734) and 3.246 (95% CI: 1.074 to 9.814), respectively, and placental weight and irregular insertion of the umbilical cord (variables scaled by a factor of 10-2 to aid interpretation) ORs 0.28 (95% CI: 0.115 to 0.683), 0.010 (95% CI: 0.001 to 0.173 respectively) on the chorionic plate, were risk factors for LBW. The socio-demographic and placental factors reveal a core role of maternal and infant nutritional deficiencies in term LBW in Ghana. The general prevalence of LBW in the Hospital facility was 6.2%. Conclusion: We conclude that poor maternal and infant nutrient supply is key factors in term LBW in Ghana. These factors are amenable to appropriate nutritional and educational interventions. a, Tettey Yaob, Gyasi Richard, Obed Samuel, Farnell Damian Joseph John, Quaye Isaac Kweku

HUMAN IMMUNODEFICIENCY VIRUS, HEPATITIS B VIRUS AND SYPHILIS INFECTIONS AMONG LONGDISTANCE TRUCK DRIVERS IN, A PORT CITY IN GHANA

Background: Although the high prevalence of human immunodeficiency virus (HIV), hepatitis B virus (HBV) and syphilis infections among longdistance truck drivers has been well documented globally, such data are sparse from Africa, and there has been no such data from Ghana. This study carried out between the months of January and June 2013 sought to determine the sero-prevalence and risk factors of HIV, HBV and syphilis infections among long distance truck drivers at the Tema sea port, Ghana. Materials and Methods: Of a total of 800 eligible drivers, 106 (13.25%) drivers consented to take part in the study. Subjects voluntarily completed a risk factor questionnaire and provided blood specimen for testing for HIV, syphilis and the surface antigen of HBV (HBsAg). Results: The mean age of the drivers was 40.56 ± 11.56 years. The sero-prevalence of HIV was 0.94%, 14.2% had HBsAg and reactive syphilis serology was 3.8%. On multivariate analysis, the main determinants of HBV infection were; multiple sexual partnership (OR, 6.36; 95% CI: 1.35– 29.79), patronage of commercial sex workers (OR, 6.85; 95% CI: 0.88 – 52.89), cross-border travelers (OR: 6.89-fold, 95% CI: 0.86 - 55.55) and prolonged duration of trips for more than two weeks (OR: 4.76; 95% CI: 0.59 – 38.02). The main determinant of syphilis infection on multivariate analysis was being a Muslim (OR, 2.19; 95% CI: 0.22 – 21.74). Conclusion: The data indicate a lower sero-prevalence of HIV but a higher sero-prevalence of syphilis. However, the sero-prevalence of HBV infection is comparable to that of the general population

Injury-related mortality among adolescents: findings from a teaching hospital's post mortem data

<p>Abstract</p> <p>Background</p> <p>Injuries are noted to be an important cause of death among adolescents. There is however limited data on the injury related deaths among adolescents in Ghana.</p> <p>Findings</p> <p>Using data from post-mortem records derived from the Department of Pathology of the Korle-Bu Teaching Hospital (KBTH), Accra Ghana from 2001 to 2003, the causes of injury related deaths among adolescents 10 to 19 years were analyzed by gender and age groups 10 to 14 and 15 to 19 years. There were 151 injury-related deaths constituting 17% of the autopsies performed among adolescents in the study period. The male-to-female ratio was 2.1:1. Drowning was the most common cause of death (37%) in the study population. This was followed by road traffic accidents (RTA) (33%). Over 70% of the RTA victims were pedestrians knocked downed by a vehicle. Deaths from electrocution, poisoning, burns, stab/gunshot, hanging and other miscellaneous causes (example blast injury, traumatic injury from falling debris, fall from height) made up the remaining 30% of the injury related mortality. Among males and in both age categories, drowning was the leading cause of death. In females, the highest mortality was from road traffic accidents accounting for almost half (49%) of the deaths; significantly more than that occurring in males (25%, p = .004).</p> <p>Conclusions</p> <p>Findings from Korle-Bu Teaching Hospital post-mortem data on adolescents show that drowning and road traffic accidents are the leading causes of injury-related mortality. Appropriate injury reducing interventions are needed to facilitate a decrease in these preventable deaths.</p

Unexpected elevated alanine aminotransferase, asparte aminotransferase levels and hepatitis E virus infection among persons who work with pigs in accra, ghana

<p>Abstract</p> <p>Background</p> <p>Several studies have suggested that elevated serum alanine aminotransferase (ALT) and asparte aminotransferase (AST) may be markers of hepatitis E virus (HEV) infection. Thus, individuals with elevated ALT and AST may have ongoing subclinical infection of HEV. We estimated the prevalence of anti-HEV antibodies and serum ALT and AST levels among persons who work with pigs in Accra, Ghana.</p> <p>Results</p> <p>Three hundred and fifty- persons who work with pigs provided blood samples for unlinked anonymous testing for the presence of antibodies to HEV, ALT and AST levels. The median age of participants was 32.85 ± 11.38 years (range 15-70 years). HEV seroprevelance was 34.84%. Anti-HEV IgG was detected in 19.26% while anti-HEV IgM was detected in 15.58% of the persons who tested positive. On multivariate analysis, the independent determinants of HEV infection were, being employed on the farm for less than six months [odds ratio (OR) 8.96; 95% confidence interval (95% CI) 5.43-14.80], having piped water in the household and/or on the farm (OR 13.33; 95% CI 5.23-33.93) and consumption of alcohol (OR 4.91: 95% CI 2.65-9.10). Levels >3× the expected maximum were found for both ALT and AST among individuals who tested positive for anti-HEV IgG (ALT, 210.17 ± 11.64 U/L; AST, 127.18 ± 11.12 U/L) and anti-HEV IgM (ALT, 200.97 ± 10.76 U/L; AST, 120.00 ± 15.96 U/L).</p> <p>Conclusion</p> <p>Consistent with similar studies worldwide, the results of our studies revealed a high prevalence of HEV infection, ALT and AST values in pig handlers.</p

Atlas of prostate cancer heritability in European and African-American men pinpoints tissue-specific regulation.

Although genome-wide association studies have identified over 100 risk loci that explain ∼33% of familial risk for prostate cancer (PrCa), their functional effects on risk remain largely unknown. Here we use genotype data from 59,089 men of European and African American ancestries combined with cell-type-specific epigenetic data to build a genomic atlas of single-nucleotide polymorphism (SNP) heritability in PrCa. We find significant differences in heritability between variants in prostate-relevant epigenetic marks defined in normal versus tumour tissue as well as between tissue and cell lines. The majority of SNP heritability lies in regions marked by H3k27 acetylation in prostate adenoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines. We find a high degree of similarity between European and African American ancestries suggesting a similar genetic architecture from common variation underlying PrCa risk. Our findings showcase the power of integrating functional annotation with genetic data to understand the genetic basis of PrCa.This work was supported by NIH fellowship F32 GM106584 (AG), NIH grants R01 MH101244(A.G.), R01 CA188392 (B.P.), U01 CA194393(B.P.), R01 GM107427 (M.L.F.), R01 CA193910 (M.L.F./M.P.) and Prostate Cancer Foundation Challenge Award (M.L.F./M.P.). This study makes use of data generated by the Wellcome Trust Case Control Consortium and the Wellcome Trust Sanger Institute. A full list of the investigators who contributed to the generation of the Wellcome Trust Case Control Consortium data is available on www.wtccc.org.uk. Funding for the Wellcome Trust Case Control Consortium project was provided by the Wellcome Trust under award 076113. This study makes use of data generated by the UK10K Consortium. A full list of the investigators who contributed to the generation of the data is available online (http://www.UK10K.org). The PRACTICAL consortium was supported by the following grants: European Commission's Seventh Framework Programme grant agreement n° 223175 (HEALTH-F2-2009-223175), Cancer Research UK Grants C5047/A7357, C1287/A10118, C5047/A3354, C5047/A10692, C16913/A6135 and The National Institute of Health (NIH) Cancer Post-Cancer GWAS initiative Grant: no. 1 U19 CA 148537-01 (the GAME-ON initiative); Cancer Research UK (C1287/A10118, C1287/A 10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007 and C5047/A10692), the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065 and 1U19 CA148112—the GAME-ON initiative), the Department of Defense (W81XWH-10-1-0341), A Linneus Centre (Contract ID 70867902), Swedish Research Council (grant no K2010-70X-20430-04-3), the Swedish Cancer Foundation (grant no 09-0677), grants RO1CA056678, RO1CA082664 and RO1CA092579 from the US National Cancer Institute, National Institutes of Health; US National Cancer Institute (R01CA72818); support from The National Health and Medical Research Council, Australia (126402, 209057, 251533, 396414, 450104, 504700, 504702, 504715, 623204, 940394 and 614296); NIH grants CA63464, CA54281 and CA098758; US National Cancer Institute (R01CA128813, PI: J.Y. Park); Bulgarian National Science Fund, Ministry of Education and Science (contract DOO-119/2009; DUNK01/2–2009; DFNI-B01/28/2012); Cancer Research UK grants [C8197/A10123] and [C8197/A10865]; grant code G0500966/75466; NIHR Health Technology Assessment Programme (projects 96/20/06 and 96/20/99); Cancer Research UK grant number C522/A8649, Medical Research Council of England grant number G0500966, ID 75466 and The NCRI, UK; The US Dept of Defense award W81XWH-04-1-0280; Australia Project Grant [390130, 1009458] and Enabling Grant [614296 to APCB]; the Prostate Cancer Foundation of Australia (Project Grant [PG7] and Research infrastructure grant [to APCB]); NIH grant R01 CA092447; Vanderbilt-Ingram Cancer Center (P30 CA68485); Cancer Research UK [C490/A10124] and supported by the UK National Institute for Health Research Biomedical Research Centre at the University of Cambridge; Competitive Research Funding of the Tampere University Hospital (9N069 and X51003); Award Number P30CA042014 from the National Cancer Institute.This is the final version of the article. It first appeared from Nature Publishing Group via http://dx.doi.org/0.1038/ncomms1097