Sixty-nine patients with chronic hepatitis C (CH-C) were treated with interferon therapy, and serum collagen type IV (s-collagen IV) levels were measured by enzyme immunoassay to analyze the responsiveness to interferon therapy. Classified by the improved pattern of serum alanine aminotransferase levels after interferon administration, 23 patients were judged as sustained responders, 23 as transient responders, and 23 as non-responders. Fibrotic grades of the liver sample correlated statistically with the levels of s-collagen IV (P < 0.01). Pre-therapy s-collagen IV levels of sustained responders were significantly lower than those of the other responders, and only sustained responders showed a significant decrease of s-collagen IV levels after interferon therapy, in accordance with histologic improvement. Multivariate analysis showed that s-collagen IV and hepatitis C virus genotype were the most important factors affecting the response to interferon therapy of all variates. Thus, s-collagen IV is one of the most useful aids for the evaluation of liver fibrotic grade in CH-C and a potent predicting indicator for the responsiveness to interferon therapy.
Portal hypertension in the presence of chronic hepatitis is generally thought to develop during the progression of the chronic hepatitis to cirrhosis. Before the establishment of assays for diagnosing hepatitis C virus infection, such a case of portal hypertension without liver cirrhosis could be misdiagnosed as idiopathic portal hypertension. It had not fully determined whether portal hypertension might precede the onset of cirrhosis in type C chronic hepatitis. This report presents two cases of women with chronic hepatitis C who developed severe thrombocytopenia; each showed splenomegaly and hypersplenism due to portal hypertension. Angiographic study and histological analysis were conducted to determine the cause of the portal hypertension. Histological evaluation showed an intrahepatic presinusoidal block pattern and fibrotic changes in the periportal area, but no evidence of liver cirrhosis or of other incidental complications such as idiopathic portal hypertension. Both of these patients exhibited normal platelet counts after splenectomy. Thus, type C chronic hepatitis can lead to portal hypertension, as demonstrated in these two patients.
Three sisters with cystic dilatation of the intrahepatic bile ducts (Caroli's disease) are reported. The index case, a 41-year-old woman with remittent high fever and right upper quadrant abdominal pain, was diagnosed as Caroli's disease with hepatic lithiasis and cholangitis based on findings of ultrasonography, computed tomography and endoscopic retrograde cholangiography. Her two older sisters were also examined and found to have the same disease without clinical symptoms. Their symptoms, locations of the dilated ducts and complications all varied. The hereditary mode of Caroli's disease in 13 families (32 cases) reported in the world literature including our study was examined. While Caroli's disease is thought to be an autosomal recessive disease, a conclusion on the hereditary mode of transmission could not be made in this study because of an insufficient investigation of family members, especially the parents.
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