The Additive Effect of Hepatitis B Virus and Aflatoxin B1 to Liver Disease Burden: A Case Study in Kitui, Makueni and Machakos Counties, Kenya

Journal of Health and Medical Sciences

ISSN 2622-7258

Published: 23 August 2019

The Additive Effect of Hepatitis B Virus and Aflatoxin B1 to Liver Disease Burden: A Case Study in Kitui, Makueni and Machakos Counties, Kenya

Pius Mutisya Kimani, Yeri Kombe, Fred W. Wamunyokoli, Charles F. L. Mbakaya, James K. Gathumbi

Institute of Tropical Medicine and Infectious Diseases JKUAT, Center for Public Health Research KEMRI, Jomo Kenyatta University of Agriculture and Technology, Rongo University, University of Nairobi

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10.31014/aior.1994.02.03.52

Pages: 312-331

Keywords: Hepatitis B Virus, Aflatoxin B1, Additive Effect to Liver Disease, Kitui, Makueni, Machakos

Abstract

There are various causes of liver disease, including viruses, trauma, and toxins. Hepatitis B virus (HBV) is a major etiological agent for liver disease in lower eastern Kenya. This had compounded an already existing problem of aflatoxinB1 induced hepatoxicity associated with contaminated grain which had been reported over the years in parts of the region including Kitui, Makueni and Machakos counties. A study was carried out to evaluate the additive effects of hepatitis B virus (HBV) and dietary AFB1 in liver disease among the subjects. Liver disease bio markers HBSAg and AFB1 lysine albumen adducts were used in this study. The investigation was conducted as a case-control study where blood samples from appropriately selected subjects were collected and analyzed for exposure to dietary AFB1 and HBV. A non-probability purposive sampling method was used to choose and divide the study area into strata with 19 clusters. The sample size (n) for the human case-control study was determined as per the Schelsselman formula (1982), as 283 each for both cases and controls A computer software SPSS® version 18.0 was used to analyze the data statistically. For case subjects, 52.29% (n=148) of serum samples were positive for HBsAg with level range of 500 to 9800 Iu/mL and a mean of 3.204 х 103 Iu/mL {95%; CI= (2.76 to 3.65)х 103}, p≤ 0.05. For controls, 24% (n=68) of serum sample was positive for HBsAg with a level range of 50 to 990 Iu/mL and a mean of 347.57 Iu/mL (95%; CI= (278.35 to 416.80), p≤ 0.05. For AFB1 lysine albumin adducts, case subjects had 55.83% (n=158) of positive serum sample with a level range of 15.5 to 135.0 pg/mg and a mean of 42.93 pg/mg (95%; CI= (39.36 to 46.51) p≤ 0.05, while the controls with 31.0% (n=88) of positive serum sample had a lower AFB1 serum albumin adducts level range of 3.5 to 60.5 pg/mg with a mean of 14.30 pg/mg (95%; CI= (12.23 to 16.36), p≤ 0.05. Case subjects had higher means for both HBsAg and AFB1 lysine albumin adducts than controls, suggesting an additive effect on liver disease among the subjects. In control subject samples, lower HBsAg suggested either a carrier state or a recent exposure and recovery from HBV. In control serum samples, lower mean AFB1 lysine albumin adducts suggested a lower level of dietary aflatoxin B1 exposure among those subjects. The case and control cohorts, the higher total number of serum samples testing positive for HBsAg, 30.83% (n=175) and AFB1 lysine albumin adducts 36.13% (n=205) out of the total sample (N=566), implied that the causal factors for the liver disease were endemic in the region. There was a higher dietary AFB1 exposure to residents than HBV exposure. It is concluded that AFB1 induced hepatoxicity was more prevalent than HBV infection among the study subjects.

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