Celiac disease and viral B hepatitis: lessons for clinical practice.
Year: 2010
Type: article
Abstract: C disease (CD) is a chronic inflammatory disease of the gut occurring in genetically susceptible individuals after the ingestion of gluten. It is characterized by a flattened mucosa, villous atrophy, and crypt hyperplasia in the small intestine, by the classic malabsorption syndrome (diarrhea, steatorrhea, weight loss), or by seemingly less severe symptoms such as iron deficiency anemia, osteopenic bone disease, amenorrhea, and infertility (1). The elimination of gluten from the diet generally leads to a return to normality of the morphological changes (2). Intestinal damage is caused by an interaction between the deamidated glutamine residues of gliadin and HLADQ2 (DQA1*05/DQB1*2) or DQ8 (DQA1*03/ DQB1*0302) molecules (3), with consequent T-cell response and production of autoantibodies against type 2 transglutaminase (anti-tTG2-Ab). HLA phenotype is also considered the most important genetic marker of nonresponders to the hepatitis B (HBV) vaccination. In particular, the immune response to the HBV vaccine is largely determined by the presence of the immunogenetic peptides via the HLA-DR and DQ molecules (4, 5), with the DR3-DQ2 and DR7-DQ2 haplotypes generally having a lower response rate (6-9). In 2000, the World Health Organization estimated that 2 billion people worldwide had serological evidence of past or present infection with HBV and that 350 million of these people were chronically infected and at risk for HBV-related liver disease (10). HCV infection is endemic to most parts of the world, although there is considerable geographic variation (11). Estimates indicate that 2.2% of the global population is infected with HCV (12). HCV is the most common chronic blood-borne infection in the U.S. and is a major cause of cirrhosis and hepatocellular carcinoma (13). An interesting chapter in clinical practice is the possible association between CD and viral hepatitis. Recently, researchers have hypothesized that nonintestinal inflammatory chronic diseases, such as HBV and HCV, may be the immunologic trigger for the development of CD (14, 15). However, the association between chronic viral hepatitis and the development of CD is still a matter of debate. In a recent study, Leonardi and La Rosa found no cases of CD in a retrospective cohort of patients carrying HBV, and no CD cases appeared during treatment with interferon (16). This study, although limited by the small size of patients studied, is interesting because it may be representative of what has been observed in Italy. HBV prevalence in Italy is higher than in the rest of Europe (17), and a high prevalence of CD is estimated as well (18). A more interesting question is: if it does not seem to be an association between CD and viral hepatitis in Italy, what is happening in other regions of the world that have a high incidence of viral hepatitis (19-21) and an increased incidence of CD (22, 23)? Until further, large, epidemiological studies investigate this question, the answer is still open.
Source: Europe PMC (PubMed Central)
Author: Antonio Tursi
Language: English
Subfield: Gastroenterology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2234072871