The presence of thyrogastric antibodies in first degree relatives of type 1 diabetic patients is associated with age and proband antibody status

A quarter of type 1 diabetic patients have thyrogastric autoantibodies (thy roid peroxidase and gastric parietal cell antibodies). Clinical, immune, an d genetic risk factors help predict antibody status. First degree relatives of these patients may also frequently exhibit these antibodies. We assesse d the prevalence of thyrogastric antibodies and dysfunction in first degree relatives in relation to age, gender, human leukocyte antigen-DQ type, bet a -cell antibody (islet cell, glutamic acid decarboxylase-65, and tyrosine phosphatase antibodies), and proband thyrogastric antibody status. Sera from 272 type 1 diabetic patients (116 men and 156 women; mean age, 27 +/- 18yr; duration, 10 +/-9 y), 397 first degree relatives (192 men and 20 5 women; parents/siblings/offspring, 48/222/127; age, 22 +/- 10 yr), and 10 0 healthy controls were tested for islet cell antibodies and gastric pariet al cell antibodies by indirect immunofluorescence and for tyrosine phosphat ase, glutamic acid decarboxylase-65, and thyroid peroxidase antibodies by r adiobinding assays. Glutamic acid decarboxylase-65 antibodies were present in 68% and 5%, islet cell antibodies were present in 36% and 2.5%, tyrosine phosphatase antibod ies were present in 45% and 0.5%, thyroid peroxidase antibodies were presen t in 21% and 4.5%, and gastric parietal cell antibodies were present in 18% and 11% of diabetic patients and relatives, respectively. The presence of thyroid peroxidase antibodies in relatives was determined by age (beta =0.2 2; P=0.0001) and proband thyroid peroxidase antibodies status (beta=-2.6; P =0.002; odds ratio=11.1). Gastric parietal cell antibody positivity in rela tives was associated with age (beta =0.04; P=0.026). Gastric parietal cell antibody-positive compared with gastric parietal cell antibody-negative rel atives were more likely to have gastric parietal cell antibody-positive pro bands (P=0.01; odds ratio=3.0). beta -Cell antibody status and human leukoc yte antigen-DQ type did not influence thyrogastric antibody status in relat ives. (Sub)clinical dysthyroidism was found in 3%, iron deficiency anemia w as present in 12% (26% gastric parietal cell antibody-positive and 9% gastr ic parietal cell antibody-negative subjects; P=0.009), and pernicious anemi a was found in 0.5% (5%, gastric parietal cell antibody-positive and 0% gas tric parietal cell antibody-negative subjects; P=0.012) of relatives. They had less thyroid dysfunction (P<0.0001) and pernicious anemia (P=0.018) tha n diabetic probands. In conclusion, thyrogastric antibodies and dysfunction are more prevalent i n type 1 diabetic patients than in first degree relatives. The presence of these antibodies in relatives is associated with age and proband antibody s tatus, but not with <beta>-cell antibodies or human leukocyte antigen-DQ ty pe.