Brief Report Conjugal Graves Disease

Hyperthyroid Graves disease is an autoimmune disorder characterized by thyrotoxicosis, diffuse goiter, and an-tibodies directed against the thyrotropin (TSH) recep-tor, thyroglobulin (Tg), and thyroid peroxidase (TPO). The TSH receptor antibody is believed to stimulate the generation of cAMP in the thyroid, resulting in the increased synthesis and release of the thyroid hor-mones. The abnormal function of the immune system found in patients with this disease is strongly linked to a genetic predisposition. The incidence of thyroid dis-ease among monozygotic twins is approximately 50%. This lack of complete concordance suggests that envi-ronmental factors, including infectious agents such as Yersinia enterocolitica (1) and a retrovirus (2), may be involved in regulating disease expression. The presence of autoimmune thyroid disease in nonconsanguineous household members also raises this possibility. We re-port the clinical and laboratory features of a family in which the parents developed thyrotoxicosis secondary to Graves disease. All their children developed thyroid disease. Methods Serum T4, T3, and TSH concentrations were mea-sured using a radioimmunoassay. Antithyroglobulin (an-ti-Tg) and antimicrosomal (anti-M, TPO) antibodies were assayed using hemagglutination tests. Thyroid up-take of radioactive iodine (131I) tests and thyroid scans were done when feasible. This family included a father, mother, three daughters and one son. All patients except the son were diagnosed and treated by LEB. There was no intermarriage