Thyroid autoantibodies in black and in white children and adolescents with type 1 diabetes mellitus and their first degree relatives.
Genetic susceptibility is an important issue in understanding the mechanism of the autoimmune endocrinopathies and in assessing the risk of these conditions in pediatric patients. To this end, we evaluated autoantibodies to thyroid antigens, thyroglobulin (TgA) and microsomal antigen (TMA), in white and in American black juvenile patients with Type I diabetes mellitus (DM) to determine the predictive value of thyroid autoantibodies for the development of autoimmune thyroid disease. Sera from 159 patients (77 black and 82 white) with Type I DM were evaluated. A greater number of whites (41/82 or 50%) than blacks (12/72 or 16%) had thyroid autoantibodies (p less than 0.01). Fourteen patients (4 black and 10 white) exhibited hypothyroidism, and all had both TgA and TMA. Three patients (all black) had Graves' disease, one of whom had both TgA and TMA. Families of each racial group that had a diabetic child (proband) with thyroid autoantibodies (seropositive) or without thyroid autoantibodies (seronegative) were assessed for TgA and TMA as well as autoimmune thyroid disease. The prevalence of thyroid autoantibodies among siblings of seropositive probands was significantly greater than among the siblings of seronegative probands (p less than 0.01). The white sibling population showed a closer association of thyroid autoantibody prevalence with increasing age (p less than 0.05) than the blacks. Significantly more parents of probands than control parents exhibited thyroid autoantibodies (p less than 0.01). The general pattern of inheritance of either racial group showed that if one or both parents had thyroid autoantibodies, their progeny developed a significantly higher prevalence of thyroid autoantibodies than those of the seronegative parents. While there was no increase in overt thyroid disease among siblings of seropositive probands, a risk of developing autoimmune thyroid disease is probably imparted to these siblings by virtue of the thyroid autoantibodies.
Burek
C L
CL
Department of Immunology & Infectious Diseases, Johns Hopkins University School of Hygiene & Public Health, Baltimore, MD 21205.
Rose
N R
NR
Guire
K E
KE
Hoffman
W H
WH
D000293:Adolescent; D000974:Antibodies, Antinuclear / Q000032:analysis; D001323:Autoantibodies / Q000032:analysis*; D001327:Autoimmune Diseases / Q000235:genetics / Q000276:immunology*; D044383:Black People / Q000235:genetics; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics / Q000276:immunology*; D004198:Disease Susceptibility / Q000276:immunology; D005190:Family; D020022:Genetic Predisposition to Disease; D006111:Graves Disease / Q000235:genetics / Q000276:immunology*; D006801:Humans; D018828:Immunoglobulins, Thyroid-Stimulating; D010290:Parents; D012307:Risk Factors; D013961:Thyroid Gland / Q000276:immunology*; D013967:Thyroiditis, Autoimmune / Q000235:genetics / Q000276:immunology*; D044465:White People / Q000235:genetics
D000974:Antibodies, Antinuclear; D001323:Autoantibodies; D018828:Immunoglobulins, Thyroid-Stimulating; C056626:thyroid microsomal antibodies