Aflatoxins in Infants with Extrahepatic Biliary Atresia
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- Category: Vol. 83, March 2015
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Aflatoxins in Infants with Extrahepatic Biliary Atresia, MAGD A. KOTB
Abstract
Background: Aflatoxin B 1 induced hepatitis was reported to be associated with characteristic features of centrizonal scarring, hepatic venous occlusion, ductular proliferation and cholestasis, focal syncytial giant cell giant cell transformation of hepatocytes, and pericelluar fibrosis which is congruent to biopsy findings in extra hepatic biliary atresia (EHBA).
Aim of Work: Is to study aflatoxins B1, B2, M1 and M2 in infants with EHBA.
Material and Methods: Aflatoxins B1, B2, M1 and M2 were analyzed in sera and post-Kasai portoenterostomy sac-rificed portahepatis liver tissue of 24 neonates and infants with EHBA, sera and breast milk of their mothers. Levels were compared to 17 infants with idiopathic neonatal hepatitis and their mothers' sera and milk. Two-dimensional thin layer chromatography and high performance liquid chromatography were employed for assessment of aflatoxins. Study commenced by July, 2001 and ended July, 2004, in New Children Hospital, Cairo University.
Results: All infants with EHBA were exclusively breast fed. All post-portoenterostomy cores were loaded with afla-toxins B1, (mean ± SD=2.88±0.88 ppb), and only 2 had B2 (mean ± SD=2.58±0.63 ppb). Their serum contained higher levels of B 1 (mean ± SD=3.8±1.73 ppb) (p=0.02). All their mothers had aflatoxin B 1 in their sera (mean ± SD=5.6±6.9 ppb) and aflatoxin M1 in their expressed breast milk (mean ± SD=1.6±1.02 ppb), and their aspartate and alanine transam-inases, serum bilirubin levels, albumin and prothrombin time were within normal range. None of the idiopathic neonatal hepatitis group had any detectable aflatoxins B1, B2, or M1 in their sera or in their mothers' sera or milk. Aflatoxin M2 was not detected in any of studied infants' sera, or their mothers or their milk. Infants with aflatoxin B2 had worse outcome.
Conclusion: Porta hepatis adjacent liver tissue was heavily loaded with aflatoxin B 1 in all infants with EHBA. Though EHBA infants and their mothers had very high blood levels of aflatoxin B1, mothers did not have any symptoms. Only two infants had elevated aflatoxin B2 levels. Cytotoxic afla-toxin M1 was transmitted to infants through breast milk.