Secretor status and human leucocyte antigens in coeliac disease.

Abstract

The ability to secrete blood group antigens into body fluids and secretions is controlled by a single gene on chromosome 19. By means of erythrocyte Lewis (Le) antigen phenotype secretor status can be inferred. An increase prevalence of non-secretors of blood group antigens among coeliac patients has recently been described. Blood was collected from 112 coeliac patients and 103 controls and tested for secretor status. Secretor status was correlated with human leucocyte antigens (HLA) in coeliac patients, thus evaluating a proposed interaction of susceptibility genes--that is, the secretor gene on chromosome 19 and HLA-linked genes on chromosome 6. Case notes for coeliacs were reviewed with regard to clinical outcome. Of 112 coeliacs who had either Le(a) or Le(b) antigens, 36 (32%) were non-secretors Le(a+, b-), compared with 27% (28) of 103 disease-free controls (P = 0.313). Recessive Lewis phenotype Le(a-, b-) was found in 9% of coeliacs versus 2% of controls. Prevalence of HLA-A1, B8, DR3, and DQ2 was unrelated to secretor status in coeliac versus patients. An increased prevalence of complications and coeliac-associated abnormalities was found in the non-secreting and recessive coeliac groups. This study shows no firm relationship between the non-secretor state and coeliac disease, nor any difference in the distribution of HLA markers among secretor and non-secretor coeliacs. It is unlikely, therefore, that the secretor gene is the much sought-after second coeliac gene.