Determining if the two etiological causes for liver disease are endemic in Kenya and evaluating the additive impact of the high levels of both HBsAg and AFB1 lysine albumin adducts were the goals of this study. Many things, including infections, trauma, and chemicals, can cause liver damage. The hepatitis B virus (HBV) is a common cause of liver disease in lower eastern Kenya. In the past, reports of contaminated grain causing AflatoxinB1-induced hepatotoxicity in Kitui, Makueni, and Machakos counties, among other sites in the region, have been made. The combined effects of dietary AFB1 and hepatitis B virus (HBV) on participants' liver illness were investigated in a study. In this investigation, the biomarkers of liver disease AFB1 lysine albumen adducts and HBSAg were employed. Blood samples from suitably chosen patients were taken as part of the investigation's case-control research, and they were then examined for evidence of exposure to dietary AFB1 and HBV. The study region was selected and divided into strata with 19 clusters using a non-probability purposive sampling technique. Using the Schelsselman formula (1982), the sample size (n) for the human case-control study was calculated to be 283 for both the cases and controls. To do a statistical analysis on the data, SPSS® version 18.0 was utilised on a computer. With a 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, HBsAg was detected in 52.29% (n=148) of serum samples from case participants. 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, 24% (n=68) of the blood samples from controls tested positive for HBsAg. Case subjects had a higher percentage of positive serum samples for AFB1 lysine albumin adducts, 55.83% (n=158), with levels ranging from 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, compared to controls, who had a lower percentage of positive serum samples—31.0% (n=88), with levels In comparison to controls, case subjects had greater means for both HBsAg and AFB1 lysine albumin adducts, which may have an additive influence on the individuals' liver disease. Lower HBsAg in samples from control subjects indicated either a carrier state or recent exposure to and recovery from HBV. Lower mean AFB1 lysine albumin adducts in control serum samples revealed a lower degree of dietary aflatoxin B1 exposure in those participants. The greater overall percentage of serum samples that tested positive for HBsAg, 30.83% (n=175), and AFB1 lysine albumin adducts, 36.13% (n=205) out of the total sample (N=566), suggested that the region's endemic liver disease risk factors were the case and control cohorts. Conclusion: Although both dietary AFB1 toxicity and HBV infection were widespread in the region, dietary AFB1 toxicity was significantly more common than hepatitis B infections, and the two variables contributed to liver illness in an additive manner.
Author(s) Details:
Pius Mutisya Kimani,
Institute of Tropical Medicine and Infectious Diseases, JKUAT, Kenya.
Yeri Kombe,
Center for Public Health Research, KEMRI, Kenya.
Fred W. Wamunyokoli,
Department of Biochemistry, Jomo Kenyatta University of Agriculture and Technology, Kenya.
Charles F. L. Mbakaya,
Department of Science and Technology, Rongo University, Kenya.
James K. Gathumbi
Department of Animal Pathology, University of Nairobi, Kenya.
Please see the link here: https://stm.bookpi.org/CODHR-V3/article/view/7900
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