Autoimmune Gastropathy in Type 1 Diabetic Patients With Parietal Cell Antibodies

Histological and clinical findings

  1. Christophe E.M. De Block, MD, PHD1,
  2. Ivo H. De Leeuw, MD, PHD1,
  3. Johannes J.P.M. Bogers, MD, PHD2,
  4. Paul A. Pelckmans, MD, PHD3,
  5. Margareta M. Ieven, PHARM, PHD4,
  6. Eric A.E. Van Marck, MD, PHD2,
  7. Kristien L. Van Acker, MD, PHD1 and
  8. Luc F. Van Gaal, MD, PHD1
  1. 1Department of Endocrinology-Diabetology, Faculty of Medicine, University of Antwerp, University Hospital Antwerp, Edegem, Belgium
  2. 2Department of Pathology, Faculty of Medicine, University of Antwerp, University Hospital Antwerp, Edegem, Belgium
  3. 3Department of Gastroenterology and Hepatology, Faculty of Medicine, University of Antwerp, University Hospital Antwerp, Edegem, Belgium
  4. 4Department of Microbiology, Faculty of Medicine, University of Antwerp, University Hospital Antwerp, Edegem, Belgium

    Abstract

    OBJECTIVE—Approximately 15–20% of type 1 diabetic patients exhibit parietal cell antibodies (PCAs) targeting gastric H+/K+ATPase. We examined whether iron deficiency anemia, pernicious anemia, and autoimmune gastritis, which may predispose to gastric tumors, were more frequent in PCA+ than in PCA- patients.

    RESEARCH DESIGN AND METHODS—Gastric biopsies from 88 consecutively recruited type 1 diabetic patients (51 men and 37 women, 47 PCA+ and 41 PCA-, aged 42 ± 13 years) were evaluated using the updated Sydney system. Immunostaining was done for parietal cells, B- and T-cells, enterochromaffin-like (ECL) cells, and Helicobacter pylori (HP). PCAs were assayed by indirect immunofluorescence, H+/K+ATPase antibodies by enzyme immunoassay, and HP by serology, urea breath test, and histology. Pentagastrin tests were performed in 42 subjects.

    RESULTS—Autoimmune gastritis (AG) was present in 57% of PCA+ and 10% of PCA- cases (OR 12.5, P < 0.0001). PCA positivity (β = 1.44; P = 0.04) and hypergastrinemia (β = 0.01; P = 0.026), but not HP, age, diabetes duration, sex, and HLA-DQ type were risk factors for AG. Iron deficiency anemia (OR 3.9, P = 0.015), pernicious anemia (OR = 4.6, P = 0.022), and hypochlorhydria (OR = 20.0, P = 0.0002) were more frequent in AG+ individuals. HP infection was present in 47 patients but did not influence corpus histology or gastrinemia. (Pre)malignant lesions were found in 26% of PCA+ subjects: ECL cell hyperplasia in 7 AG+ patients, comprising 1 with a gastric carcinoid tumor, and corpus intestinal metaplasia in 11 AG+ patients, including 1 with linitis plastica.

    CONCLUSIONS—PCA+ type 1 diabetic patients should be screened for autoimmune gastritis, iron deficiency, and pernicious anemia. Particularly hypergastrinemic PCA+ patients with autoimmune gastritis are at increased risk for (pre)malignant gastric lesions.

    Footnotes

    • Address correspondence and reprint requests to Dr. Christophe De Block, Department of Endocrinology-Diabetology, University Hospital Antwerp, Wilrijkstraat 10, B-2650 Edegem, Belgium. E-mail: cdeblock{at}uia.ua.ac.be.

      Received for publication 22 May 2002 and accepted in revised form 18 August 2002.

      A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

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