Overlap syndrome of primary sclerosing cholangitis and autoimmune hepatitis

We report a 46-year-old patient with the typical biochemical, histological and cholangiographic findings of primary sclerosing cholangitis (PSC) whose clinical and laboratory findings would also qualify her for the diagnosis of definite autoimmune hepatitis (AIH), according to the aggregate score of the International Autoimmune Hepatitis Group. We suggest that this patient may represent an example of the overlapping syndrome of PSC and AIH. Eur J Gastroenterol Hepatol 13:203-206 (C) 2001 Lippincott Williams & Wilkins

Histopathology of chronic hepatitis C in relation to epidemiological factors

Background/Aims: To evaluate the clinicopathological features of chronic hepatitis C, 170 liver biopsies were studied and histological grade and stage (degree of fibrosis) of hepatitis were correlated with epidemiological features and characteristic histological findings. Methods/Results: Normal liver was found in 3 (1.8%), minimal chronic hepatitis in 40 (23.5%), mild chronic hepatitis in 104 (61.2%) and moderate chronic hepatitis in 23 (13.5%) cases. Cirrhosis was observed in 24 (14.1%) patients and was more frequently encountered among patients more than 40 years old (34.4% vs 2.8%, p<10(-6)) and rarely among intravenous drug users in comparison with post-transfusion and sporadic cases (3% vs 25% and 20% respectively, p<0.005). Minimal chronic hepatitis was more frequently observed among patients 40 years old or younger (30.3% vs 11.5%, p<0.01)), while moderate chronic hepatitis was significantly more common in older age groups (24.6% vs 7.3%, p<0.005). Multiple regression analysis revealed that only age was statistically related to histological grade and stage of hepatitis (p<10(-5)). The frequency of the histological features more likely seen in chronic hepatitis C, including steatosis (57.6%), lymphoid follicles and/or aggregates (F/A) (47.1%) and bile duct lesions (22.9%), increased with hepatitis grade and the latter two features were more often encountered in moderate chronic hepatitis (p<0.005); in addition, both lesions statistically coexisted (p<0.005). No correlation was found between histological findings and possible source of infection. Conclusions: More than half of the chronic hepatitis C patients presented mild histological lesions. Age was proven to be the only independent epidemiological factor related to histological grade and stage of hepatitis. Lymphoid F/A and bile duct damage are important diagnostic findings associated with hepatitis activity

Cholestatic syndrome with bile duct damage and loss in renal transplant recipients with HCV infection

Background/Aims: Bile duet cells are known to be susceptible to hepatitis B and C virus, while it has been recently suggested that hepatitis B virus (HBV) and hepatitis C virus (HCV) infection may have a direct role in the pathogenesis of vanishing bile duct syndrome (VBDS) after liver transplantation. We report the development of a cholestatic syndrome associated with bile duct damage and loss in four HCV-infected renal transplant recipients. Methods: All four patients were followed up biochemically, serologically and with consecutive liver biopsies, Serum HCV RNA was quantitatively assessed and genotyping was performed, Results: Three patients were anti-HCV negative and one was anti-HCV/HBsAg positive at the time of transplantation and received the combination of methylprednisolone, azathioprine and cyclosporine A. Two patients became anti-HCV positive 1 year and one patient 3 years posttransplantation. Elevation of the cholestatic enzymes appeared simultaneously with seroconversion, or 2-4 years later, and was related to lesions of the small-sized interlobular bile ducts. Early bile duct lesions were characterized by degenerative changes of the epi;helium. Late and more severe bile duct damage was associated with bile duct loss. The progression of the cholestatic syndrome coincided with high HCV RNA serum levels, while HCV genotype was la and Ib. Two patients tone with HBV co-infection! developed progressive VBDS and died of liver failure 2 and 3 years after biochemical onset. One patient, despite developing VBDS within a 10-month period, showed marked improvement of liver function after cessation of immunosuppression because of graft loss. The fourth patient, who had mild biochemical and histological bile duct changes, almost normalized liver function tests after withdrawal of azathioprine. Conclusion: A progressive cholestatic syndrome due to bile duct damage and loss may develop in renal transplant patients with HCV infection. The occurrence of the lesions after the appearance of anti-HCV antibodies and the high HCV RNA levels are indicative of viral involvement in the pathogenesis. Withdrawal of immunosuppressive therapy may have a beneficial effect on the outcome of the disease

Fibrosing cholestatic hepatitis in renal transplant recipients with hepatitis C virus infection

patitis B virus (HBV) infection in liver allograft recipients characterized by a rapid progression to liver failure. Only sporadic cases have been reported in other immunocompromised groups infected with HBV and in a few transplant recipients with hepatitis C virus (HCV) infection. We present the occurrence of FCH in 4 NOV-infected renal transplant recipients within a series of 73 renal transplant recipients with HCV infection followed up closely serologically and with consecutive liver biopsies. All 4 patients received the triple-immunosuppressive regimen (azathioprine, cyclosporine A, methylprednisolone). The interval from transplantation to the appearance of liver dysfunction was 1 to 4 months and to histological diagnosis, 3 to 11 months. The biochemical profile was analogous to a progressive cholestatic syndrome in 3 patients, whereas the fourth patient had only slightly increased alanine aminotransferase and gamma-glutamyl transferase (gamma GT) levels, Liver histological examination showed the characteristic pattern of FCH in 2 patients, whereas the other 2 patients had changes compatible with an early stage; All patients were anti-NOV negative at the time of transplantation, whereas 2 patients, 1 with incomplete and 1 with complete histological FCH features, seroconverted after 3 and 31 months, respectively. The patients were HCV RNA positive at the time of the first liver biopsy and showed high serum HCV RNA levels (14 to 58 x 10(6) Eq/mL, branched DNA). HCV genotype was 1b in 3 patients and 3a in 1 patient. After histological diagnosis; immunosuppression was drastically reduced. Two patients died of sepsis and liver: failure 16 and 18 months posttransplantation, whereas the seroconverted patients showed marked improvement of their liver disease, which was histologically verified in 1 patient. In conclusion, FCH can occur in HCV-infected renal transplant recipients, It seems to develop as a complication of a recent HCV infection during the period of maximal immunosuppression and is associated with high HCV viremia levels. There are indications that drastic reduction of immunosuppression may have a beneficial effect on the outcome of the disease. Copyright (C) 1999 by the American Association for the Study of Liver Diseases