PubMed · 8868765
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P Aldershon. Ethics. Body language.. https://pubmed.ncbi.nlm.nih.gov/8868765/
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Extrahepatic biliary atresia (EHBA) and choledochal cysts (CDC) are important causes of obstructive jaundice in pediatric patients. Viruses in general, and reoviruses in particular, have long been considered as possible etiologic agents responsible for inciting the inflammatory process that leads to these infantile obstructive cholangiopathies. In an effort to determine whether reovirus infection is associated with these disorders, we used a sensitive and specific reverse-transcriptase polymerase chain reaction (RT-PCR) technique designed to amplify a portion of the reovirus L1 gene segment from extracts of liver and/or biliary tissues. These tissues were obtained at the time of liver biopsy or surgical procedures from 23 patients with EHBA, 9 patients with CDC, and 33 patients with other hepatobiliary diseases. Hepatic and biliary tissues obtained at autopsy from 17 patients who died without known liver or biliary disease were also analyzed. Reovirus RNA was detected in hepatic and/or biliary tissues from 55% of patients with EHBA and 78% of patients with CDC. Reovirus RNA was found also in extracts of hepatic and/or biliary tissue from 21% of patients with other hepatobiliary diseases and in 12% of autopsy cases. The prevalence of reovirus RNA in tissues from patients with EHBA and CDC was significantly greater than that in patients with other hepatobiliary diseases (chi2 P = .012 EHBA vs. OTHER, P = .001 CDC vs. OTHER), or AUTOPSY cases (chi2 P = .006 EHBA vs. AUTOPSY, P < .001 CDC vs. AUTOPSY).
BACKGROUND: Intercellular adhesion molecule-1 (ICAM-1) is strongly expressed on the bile ducts and hepatic parenchyma of livers with biliary atresia. A soluble, circulating form of this membrane protein has been found to be elevated in a number of inflammatory hepatic disorders. However, its expression in biliary atresia is unknown. The purpose of this study was to assess the presence of soluble ICAM-1 in infants with biliary atresia in relation to disease activity, degree of cholestasis, and standard liver function tests. MATERIALS AND METHODS: A total of nine patients (n = 9) with biliary atresia (seven) and neonatal hyperbilirubinemia (two) were studied (age range 6 weeks-9 years). Control samples were obtained from three healthy infants (2-10 months). Serum was collected from each patient and stored at -80 degrees C until assayed. Levels of sICAM-1 were measured in duplicate utilizing an ELISA method (Bioscource International). Standard liver function tests (conjugated bilirubin, gamma-glutamyl transpeptidase, alkaline phosphatase, alanine aminotransferase) were determined at the same time. Results are expressed as the means +/- SEM with statistical analysis by Mann-Whitney test. RESULTS: sICAM-1 levels were significantly elevated in all patients with biliary atresia (997 +/- 56 ng/ml) when compared to controls (P < 0.001). No correlation was found between sICAM-1 levels and conjugated bilirubin, gamma-glutamyl transpeptidase, alkaline phosphatase, and alanine aminotransferase levels or with clinical assessment of disease severity. CONCLUSIONS: sICAM-1 is markedly elevated in biliary atresia reflecting the immunopathology of the disease process but does not appear to correlate with markers of liver function. sICAM-1 may be useful in assessing the effects of immunomodulatory therapy.
In 3 (9 %) of 34 children with biliary atresia, US revealed gallbladder contraction following an oral feed, given on admission, but not with subsequent feeds. Surgery revealed a Kasai type IIIa biliary atresia with a patent communication between the gallbladder and duodenum. We propose that the bile ducts may initially have been patent, but then gradually became obliterated secondary to inflammation. These cases may explain the development of one type of biliary atresia.