Abstract

Celiac hepatitis is a gluten‑dependent liver disease that usually eliminates after 12 months of a strict gluten‑free diet. What is important is that liver histology also improves after a gluten‑free diet. Hypertransaminasemia (in 13—60% of cases) is common at the untreated celiac disease (CD). Conversely, CD presents in 9% of patients with unexplained hypertransaminasemia. Patients with CD have a higher risk of both subsequent liver disease and death caused by cirrhosis compared to the general population. Pathogenetic mechanisms underlying CD, have not been sufficiently studied. The permeability of the intestinal mucosa appears to be considerably higher in patients with CD and hypertransaminasemia than in patients with CD and normal liver tests. The normalization of intestinal permeability and transaminase levels after following a gluten‑free diet demonstrates that this phenomenon is gluten‑dependent. It has been suggested that increased intestinal permeability promotes the admission of toxins, microbial and other antigens, cytokines, and/or other mediators of liver damage into the portal circulation (and hence to the liver). However, liver damage is not usually observed in other intestinal pathologies associated with increased intestinal permeability. A liver biopsy is rarely performed in celiac hepatitis. Mild and/or non‑specific histological changes are observed. Severe liver fibrosis and cirrhosis occur rarely.
 Primary biliary cholangitis and autoimmune hepatitis may be associated with CD. The incidence of CD in patients with primary biliary cholangitis is 1—7%, while the incidence of primary biliary cholangitis in patients with CD is 0.1—3%. CD is revealed in 4—6% of patients with autoimmune hepatitis, both type 1 and type 2. Cases of primary sclerosing cholangitis combined with CD have been reported, too.
 No correlation has been found between CD and chronic hepatitis C. Treatment of hepatitis C with interferon‑a and/or ribavirin may activate occult or latent CD. The incidence of CD in patients with non‑alcoholic fatty liver disease ranges from 3% to 7%.
 The prevalence of CD in patients after liver transplantation for a variety of reasons ranges from 3% to 4.3%.
 Liver‑caused mortality is increased in patients with CD, although the absolute risk of mortality from liver failure is low.

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