Type 1 diabetes and autoimmune polyglandular syndrome: a clinical reviewType 1 diabetes and autoimmune polyglandular syndrome: a clinical review
Faculty of Medicine and Health Sciences
Laboratory Experimental Medicine and Pediatrics (LEMP)
The Netherlands journal of medicine. - Amsterdam
67(2009):11, p. 376-387
University of Antwerp
Type 1 diabetes mellitus (T1DM) results from autoimmune destruction of insulin-producing â cells and is characterisedby the presence of insulitis and â-cell autoantibodies. Up to one third of patients develop an autoimmune polyglandular syndrome. Fifteen to 30% of T1DM subjects have autoimmune thyroid disease (Hashimotos or Graves disease), 5 to 10% are diagnosed with autoimmune gastritis and/or pernicious anaemia (AIG /PA ), 4 to 9% present with coeliac disease (CD), 0.5% have Addisons disease(AD ), and 2 to 10% show vitiligo. These diseases are characterised by the presence of autoantibodies against thyroid peroxidase (for Hashimotos thyroiditis), TSH receptor (for Graves disease), parietal cell or intrinsic factor (for AIG /PA ), tissue transglutaminase (for CD), and 21-hydroxylase (for AD ). Early detection of antibodies and latent organ-specific dysfunction is advocated to alert physicians to take appropriate action in order to prevent full-blown disease. Hashimotos hypothyroidism may cause weight gain, hyperlipidaemia, goitre, and may affect diabetes control, menses, and pregnancy outcome. In contrast, Graves hyperthyroidism may induce weight loss, atrial fibrillation, heat intolerance, and ophthalmopathy. Autoimmune gastritis may manifest via iron deficiency or vitamin B12 deficiency anaemia with fatigue and painful neuropathy. Clinical features of coeliac disease include abdominal discomfort, growth abnormalities, infertility, low bone mineralisation, and iron deficiency anaemia. Adrenal insufficiency may cause vomiting, anorexia, hypoglycaemia, malaise, fatigue, muscular weakness, hyperkalaemia, hypotension, and generalised hyperpigmentation. Here we will review prevalence, pathogenetic factors, clinical features, and suggestions for screening, follow-up and treatment of patients with T1DM and/or autoimmune polyglandular syndrome.