Assessing risks of hepatobiliary disorders in children under combined exposure to persisting herpes and technogenic chemicals

Abstract

Chronic persistent viral infection leads to developing immune deficiency and may induce lesions in many organs, the hepatobiliary system included. This, in its turn, may facilitate the onset of diseases of the digestive system under exposure to technogenic chemicals, especially those able to produce hepatotoxic effects. In this study, our aim was to examine risks of developing hepatobiliary disorders in children under combined exposure to persisting herpes infection and technogenic chemicals. We conducted a clinical examination of 324 children aged between 6 and 17 years living either in a large industrial city or on a territory where the sanitary-hygienic situation was favorable. The examination included a clinical checkup, laboratory diagnostic tests identifying herpes markers, chemical analyses aimed at establishing levels of technogenic chemicals in blood, and ultrasound scanning of hepatobiliary organs. We established that exposure to airborne technogenic chemicals created elevated levels of aromatic hydrocarbons and formaldehyde in 64.9–97.6 % of the exposed children; elevated manganese and chromium levels, in 20.8–34.6 % of them. Markers of cytomegalovirus (CMV) and Epstein Barr virus (EBV) were detected in 75 % of the exposed children; each second child had HSV-1 or HSV-2; each third child had human herpesvirus 6. Hepatobiliary disorders occurring under combined exposure to persistent herpes and echnogenic chemicals were represented by structural liver changes in 30.8 % of the examined children; abnormally shaped gallbladder or reactive changes in its walls and dyscholia, in 15.7–48.8 %. These disorders entail elevated levels of direct bilirubin and greater ALT against imbalance of oxidant and antioxidant systems and manifest themselves as biliary pathology in 69.5 % of cases. Exposed children with persistent herpes infection have 1.2–2.3 times higher likelihood of developing structural changes in the liver and gallbladder pathology and up to 4.3 times higher risks of biliary dysfunction and chronic gastroduodenitis.