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Adrenal medullitis in type I diabetes.

F M Brown1, A M Smith, S Longway

  • 1Joslin Diabetes Center, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02215.

The Journal of Clinical Endocrinology and Metabolism
|December 1, 1990
PubMed
Summary

Cell-mediated immunity may target the adrenal medulla in type I diabetes (IDDM). This autopsy study found increased lymphocytic infiltrates and fibrosis in IDDM subjects, suggesting adrenal medullitis in 20% of cases.

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Area of Science:

  • Immunology
  • Endocrinology
  • Pathology

Background:

  • Type I diabetes (IDDM) is an autoimmune disease primarily affecting pancreatic beta cells.
  • The potential involvement of other endocrine glands, such as the adrenal medulla, in the autoimmune process of IDDM remains less understood.

Purpose of the Study:

  • To investigate the presence of cell-mediated immunity against the adrenal medulla in individuals with type I diabetes.
  • To determine if the adrenal medulla is an immunological target in type I diabetes.

Main Methods:

  • Retrospective autopsy study of adrenal glands from 44 IDDM subjects and 29 non-diabetic controls.
  • Immunohistochemistry using UCHL1 (T-lymphocytes) and L26 (B-cells) antibodies.
  • Scoring of lymphocytic infiltrates and fibrosis in adrenal medullary tissue.

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Main Results:

  • A moderate to severe lymphocytic infiltrate (UCHL1) was observed in 20% of IDDM subjects versus 3% of controls (P < 0.04).
  • Mild to severe fibrosis was significantly more prevalent in IDDM subjects (52%) compared to controls (16%) (P = 0.003).
  • Overall, 39% of IDDM subjects showed significant lymphocytic infiltrate or fibrosis, compared to 7% of controls (P = 0.003).

Conclusions:

  • The findings suggest that the adrenal medulla may be an immunological target in type I diabetes.
  • Adrenal medullitis, characterized by lymphocytic infiltration and fibrosis, was observed in 20% of IDDM subjects.
  • Further research is warranted to elucidate the role of adrenal medullitis in the pathogenesis of type I diabetes.