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

The purpose of this study was, therefore, to evaluate the additive effects of the elevated levels of both HBsAg and AFB1 lysine albumin adducts and determine whether the two etiological factors for liver disease are endemic in Kenya. Liver disease can be brought on by a number of factors, such as viruses, trauma, and poisons. In lower eastern Kenya, the hepatitis B virus (HBV) is a prominent cause of liver illness. AflatoxinB1-induced hepatotoxicity caused by tainted grain has already been an issue, and reports of it had been made over the years in Kitui, Makueni, and Machakos counties, among other places in the region. 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 x 103 Iu/mL {95%; CI= (2.76 to 3.65) x 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. It is concluded that, even though both dietary AFB1 toxicity and HBV infection were endemic in the area, comparatively dietary AFB1 toxicity was much more prevalent in the region than hepatitis B infections and that the two factors had an additive effect to liver disease.