SUMMARY BackgroundRecently, a new enteropathy has been described: olmesartan-associated enteropathy. However, the association has been questioned: a phase 3 trial and a cohort study found no association between gastrointestinal events and olmesartan.

To examine the effects of interferon (IFN) therapy on clinical, biochemical, and histological features in patients with compensated hepatitis C virus (HCV)-related cirrhosis, we have conducted a randomized, controlled trial of IFN therapy versus observation. Eight centers included a total of 99 patients with biopsy-proven cirrhosis. IFN-␣2b, 3 million units three times per week, or no antiviral therapy was given for 48 weeks. Twenty-three patients dropped out. End-of-treatment biochemical response was not observed in any of the 39 controls but was observed in 6 of the 47 treated patients (P F .02); sustained biochemical response was obtained in only 2 treated patients. Controls and treated patients did not significantly differ with regard to the changes in serum level of albumin, bilirubin, ␣-fetoprotein, in plasma prothrombin, in histological activity, or liver collagen content. During trial or follow-up (160 ؎ 57 weeks), hepatocellular carcinoma developed in 9 controls and 5 treated patients (NS); decompensation of cirrhosis occurred in 5 controls and 7 treated patients. Seven controls and 10 treated patients died. In conclusion, in patients with compensated HCV-related cirrhosis, a 48-week course of IFN therapy is safe and is able to induce end-of-treatment biochemical response in a significant proportion of patients. However, a 48-week course of IFN therapy usually fails to achieve sustained response and, within the limit of this study, did not significantly improve the 3-year outcome. Therefore, a longer course of IFN therapy or combination therapy with ribavirin should be evaluated in patients with HCV-related cirrhosis. (HEPATOLOGY 1999;29:1870-1875.)Cirrhosis is a common complication of chronic hepatitis C, affecting approximately 20% of patients followed up for more than 10 years. 1 Currently identified risk factors for cirrhosis in hepatitis C virus (HCV)-infected patients are age at contamination, duration of infection, degree of histological activity, and alcohol consumption. 2,3 Natural history of HCVrelated cirrhosis is jeopardized by a high incidence of hepatocellular carcinoma (up to 5% per year) 4-7 and hepatic decompensation (up to 25% at 4 years). 4,6,7 Mortality rate is about 15% to 20% at 4 years. HCV-related cirrhosis accounts for 30% of liver transplantation in adults. 1 A treatment able to halt the progression of liver disease once cirrhosis is established but not yet complicated would be of great interest. Current data on the efficacy of interferon (IFN) therapy in patients with HCV-related cirrhosis are conflicting. Cirrhosis is a marker of a poor response to IFN therapy. 8 However, when genotype and serum viral load are taken into account, it is unclear that cirrhosis has any independent value in predicting a poor response to IFN therapy. 8 It has been recently suggested that IFN therapy can prevent the subsequent development of hepatocellular carcinoma, 9 but this contention is not supported by all studies. [5][6][7] In addition, the effects of IFN therapy on mortality rate and probab...

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In an analysis of data from the CESAME cohort in France, patients with anal and/or perianal Crohn's disease have a high risk of anal cancer, including perianal fistula-related cancer, and a high risk of rectal cancer.

Liver repopulation constitutes an attractive approach for the treatment of liver disorders or of diseases requiring abundant secretion of an active protein. We have described previously a model of selective repopulation of a normal liver by Fas/CD95-resistant hepatocytes, in which we achieved up to 16% hepatocyte repopulation. In the present study, we investigated the therapeutic efficacy of this strategy. With this aim, apolipoprotein E (ApoE) knockout mice were transplanted with Fas/CD95-resistant hepatocytes which constitutively express ApoE. Transplanted mice were submitted to weekly injections of non-lethal doses of the Fas agonist antibody Jo2. After 8 weeks of treatment, we obtained up to 30% of the normal level of plasma ApoE. ApoE secretion was accompanied by a drastic and significant decrease in total plasma cholesterol, which even fell to normal levels. Moreover, this secretion was sufficient to markedly reduce the progression of atherosclerosis. These results demonstrate the efficacy of this repopulation approach for correcting a deficiency in a protein secreted by the liver.