| Aflatoxin Exposure and Viral Hepatitis in the Etiology of Liver Cirrhosis in The Gambia, West Africa Mark H. Kuniholm,1* Olufunmilayo A. Lesi,2,3* Maimuna Mendy,4 Aliu O. Akano,5,6 Omar Sam,5 Andrew J. Hall,7 Hilton Whittle,4 Ebrima Bah,2 James J. Goedert,8 Pierre Hainaut,9 and Gregory D. Kirk1 1Infectious Disease Program, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA; 2International Agency for Research on Cancer, Gambia Hepatitis Intervention Study, Banjul, The Gambia; 3Department of Medicine, Lagos University Teaching Hospital, Lagos, Nigeria; 4Medical Research Council Laboratories, Banjul, The Gambia; 5Department of Medical Services, Royal Victoria Teaching Hospital, Government of The Gambia, Banjul, The Gambia; 6Department of Radiodiagnosis, National Hospital, Abuja, Nigeria; 7London School of Hygiene and Tropical Medicine, London, United Kingdom; 8Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA; 9International Agency for Research on Cancer, Gambia Hepatitis Intervention Study, Lyon, France Abstract
Background: Cirrhosis of the liver is thought to be a major cause of morbidity and mortality in sub-Saharan Africa, but few controlled studies on the etiology of cirrhosis have been conducted in this region. Objectives: We aimed to elucidate the association between environmental and infectious exposures and cirrhosis in The Gambia. Methods: Ninety-seven individuals were diagnosed with cirrhosis using a validated ultrasound scoring system and were compared with 397 controls. Participants reported demographic and food frequency information. Blood samples were tested for hepatitis B surface antigen (HBsAg) , hepatitis B e antigen (HBeAg) , hepatitis C virus (HCV) antibody, HCV RNA, and the aflatoxin-associated 249ser TP53 mutation. Results: HBsAg seropositivity was associated with a significant increase in risk of cirrhosis [odds ratio (OR) = 8.0 ; 95% confidence interval (CI) , 4.4–14.7] as was the presence of HBeAg (OR = 10.3 ; 95% CI, 2.0–53.9) and HCV infection (OR = 3.3 ; 95% CI, 1.2–9.5) . We present novel data that exposure to aflatoxin, as assessed both by high lifetime groundnut (peanut) intake and by the presence of the 249ser TP53 mutation in plasma, is associated with a significant increase in the risk for cirrhosis (OR = 2.8 ; 95% CI, 1.1–7.7 and OR = 3.8 ; 95% CI, 1.5–9.6, respectively) . Additionally, aflatoxin and hepatitis B virus exposure appeared to interact synergistically to substantially increase the risk of cirrhosis, although this was not statistically significant. Conclusions: Our results suggest that the spectrum of morbidity associated with aflatoxin exposure could include cirrhosis. Key words: aflatoxin, Africa, hepatitis B virus, liver cirrhosis, p53, The Gambia, ultrasound. Environ Health Perspect 116:1553–1557 (2008) . doi:10.1289/ehp.11661 available via http://dx.doi.org/ [Online 10 July 2008]
Address correspondence to G.D. Kirk, 615 N. Wolfe St., E-6533, Baltimore, MD 21205 USA. Telephone: (410) 502-2038. Fax: (410) 955-1383. E-mail: gkirk@jhsph.edu *These authors contributed equally to this work. We thank the staff of the Gambia Liver Cancer Study and the staff and participants at the Bansang, Medical Research Council, and Royal Victoria hospitals for their contributions. This work was supported by the National Cancer Institute, National Institutes of Health, contract N02-CP40521. The authors declare they have no competing financial interests. Received 5 May 2008 ; accepted 10 July 2008.
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