Advertisement
Research Article Free access | 10.1172/JCI107755
Digestive and Hereditary Diseases Branch, National Institute of Arthritis, Metabolism and Digestive Diseases, Washington, D. C.
Dermatology Service, Walter Reed General Hospital, Washington, D. C.
Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Find articles by Gebhard, R. in: JCI | PubMed | Google Scholar
Digestive and Hereditary Diseases Branch, National Institute of Arthritis, Metabolism and Digestive Diseases, Washington, D. C.
Dermatology Service, Walter Reed General Hospital, Washington, D. C.
Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Find articles by Falchuk, Z. in: JCI | PubMed | Google Scholar
Digestive and Hereditary Diseases Branch, National Institute of Arthritis, Metabolism and Digestive Diseases, Washington, D. C.
Dermatology Service, Walter Reed General Hospital, Washington, D. C.
Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Find articles by Katz, S. in: JCI | PubMed | Google Scholar
Digestive and Hereditary Diseases Branch, National Institute of Arthritis, Metabolism and Digestive Diseases, Washington, D. C.
Dermatology Service, Walter Reed General Hospital, Washington, D. C.
Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Find articles by Sessoms, C. in: JCI | PubMed | Google Scholar
Digestive and Hereditary Diseases Branch, National Institute of Arthritis, Metabolism and Digestive Diseases, Washington, D. C.
Dermatology Service, Walter Reed General Hospital, Washington, D. C.
Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Find articles by Rogentine, G. in: JCI | PubMed | Google Scholar
Digestive and Hereditary Diseases Branch, National Institute of Arthritis, Metabolism and Digestive Diseases, Washington, D. C.
Dermatology Service, Walter Reed General Hospital, Washington, D. C.
Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20014
Find articles by Strober, W. in: JCI | PubMed | Google Scholar
Published July 1, 1974 - More info
In the present study the relation between the gluten-sensitive intestinal lesion observed in dermatitis herpetiformis (DH) and in gluten-sensitive enteropathy (coeliac sprue) (GSE) was analyzed. Jejunal IgA synthesis in DH was estimated from the extent of incorporation of [14C]leucine into IgA in jejunal biopsy specimens during short-term in vitro culture. Patients with DH have significantly elevated incorporation values as compared to normal control individuals (18,880±13,614 vs. 5,830±3,190 cpm/mg tissue protein/ 90 min) (P < 0.02) and the degree of elevation correlates well with the degree of morphologic abnormality. Thus patients with DH are similar to patients with GSE where elevated local mucosal IgA synthesis has also been observed.
By using both morphologic and immunologic criteria for evaluating intestinal status, patients with DH and intestinal disease were distinguished from patients with DH free of intestinal disease. Of the eight patients in the former group, seven carried HL-A8 (87.5%), an incidence which is strikingly similar to that observed in patients with GSE alone (88.5%). In contrast, of the seven patients in the latter group (without gastro-intestinal disease) two had HL-A8, an incidence (27%) not significantly different from that in the normal population (20%) (P > 0.1).
Thus, both in respect to local mucosal increase in IgA synthetic rates and in respect to the association with HL-A8, the intestinal lesion of DH is similar to that of GSE.