Celiac Disease and Viral B Hepatitis: Lessons for Clinical Practice

Celiac 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).