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The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 11 4062-4067
Copyright © 1999 by The Endocrine Society


Original Studies

High Prevalence of Manifestations of Gastric Autoimmunity in Parietal Cell Antibody- Positive Type 1 (Insulin-Dependent) Diabetic Patients1

Christophe E. M. De Block, Ivo H. De Leeuw, Luc F. Van Gaal and the Belgian Diabetes Registry

Department of Endocrinology-Diabetology, University of Antwerp, University Hospital Antwerp (C.E.M.D.B., I.H.D.L., L.F.V.G.), B-2650 Edegem; and the Belgian Diabetes Registry, B-1090 Brussels, Belgium

Address all correspondence and requests for reprints to: Christophe De Block, M.D., Department of Endocrinology-Diabetology, University of Antwerp, University Hospital Antwerp, Wilrijkstraat 10, B-2650 Edegem, Belgium. E-mail: christophe.deblock{at}uia.ua.ac.be

Previous studies have shown a high prevalence of gastric parietal cell antibodies (PCA) in type 1 diabetes, which can be accompanied by (sub)clinical autoimmune gastric disease. This study aimed to determine the grade of associated autoimmunity and to assess the pattern of prevalence of PCA by gender, age, duration of disease, age at onset of diabetes, and human leukocyte antigen (HLA) type in an adult type 1 diabetic population. Furthermore, to examine the clinical significance of being PCA positive, manifestations of gastric autoimmune disease were studied in PCA-positive and PCA-negative patients.

The population studied consisted of 497 type 1 diabetics (men/women, 252/245; mean age, 40.8 ± 12.1 yr; mean duration of disease, 16.4 ± 10.4 yr; mean age at onset, 26.9 ± 13.5 yr; mean hemoglobin A1c, 8.1 ± 1.6%). Associated autoantibodies were present in 39% and PCA were present in 20.9% of the subjects, particularly in older patients. Gender, duration, and age at onset of diabetes did not influence the appearance of PCA. Antithyroid peroxidase antibodies (aTPO) were more frequent in PCA-positive patients than in those without PCA (33.6% vs. 22.4%; P = 0.025), suggesting an association between gastric and thyroid autoimmunity. We could demonstrate an association between PCA and the HLA DR5 haplotype (P = 0.001) as well, but not with HLA DR3 and/or DR4. In the PCA-positive group, iron deficiency anemia was detected in 15.4%, and pernicious anemia was found in 10.5% of subjects. These autoimmune gastric manifestations were significantly more prevalent in PCA-positive diabetics than in PCA-negative subjects, in whom the percentages were 6.9% and 0.5%, respectively (P = 0.01 and P < 0.0001). PCA were prevalent in 84.6% of patients with pernicious anemia. A gastroscopic and anatomopathoplogical examination performed in a subgroup of 30 patients with gastric symptoms revealed atrophic gastritis in 13 of 14 PCA-positive patients and in 9 of 16 PCA-negative subjects (P = 0.04). PCA were present in 59.1% of patients with atrophic gastritis.

In conclusion, a high prevalence of parietal cell antibodies and associated autoimmune gastric disease is present in PCA-positive type 1 diabetics, recommending its screening. Early detection of PCA and iron deficiency anemia, pernicious anemia, and atrophic gastritis and the subsequent care could reduce the morbidity of type 1 diabetes.




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