title: Thyroid autoimmunity in endemic goitre caused by excessive iodine intake.
abstract: The pathophysiology of endemic goitre caused by excessive iodine intake is not well defined. By interacting with the immune system, iodine excess may trigger the development of autoimmune thyroid disease such as lymphocytic Hashimoto's thyroiditis (LT). In an attempt to examine this further, we compared the presence of thyroid autoantibodies in 29 goitrous children, from an iodine excess area, and in 26 healthy children, from an iodine sufficient area, of north central China. Serum was tested for antimicrosomal (MAb), anti-thyroglobulin (TgAb), second colloid antigen antibodies (CA2-Ab) and TSH binding inhibitory immunoglobulins (TBII). Affinity chromatographically purified IgG was tested for thyroid growth-stimulating activity (TGI) by two different methods: a sensitive cytochemical bioassay (CBA) using guinea-pig thyroid explants and a mitotic arrest assay (MAA) employing a continuous rat thyroid cell line (FRTL-5). We found no increased prevalence of LT in patients with endemic iodine goitre. The levels of MAb, TgAb and CA2-Ab did not differ significantly between the two groups of children. Further, TBII were not present in either group. Thyroid growth-stimulating immunoglobulins (TGI) were the major autoantibodies found in children with goitres caused by iodine excess. In the CBA, 12 of 20 (60%) goitrous children and 0 of 12 (0% P less than 0.05) healthy children were positive for TGI. Similar results were found in the MAA, and a good correlation between results of the CBA and MAA was found (P = 0.003). Maximal TGI activity in dose-response CBA showed a good relation with clinical goitre size (r = 0.63; P less than 0.05) indicating a possible pathophysiological role for these antibodies. We conclude that endemic iodine goitre is not associated with Hashimoto's lymphocytic thyroiditis. Nevertheless, autoimmune growth factors such as TGI may play a primary role in the pathogenesis of thyroid growth in this condition.
authors.affiliation: Department of Medicine, Westmead Hospital, Sydney, Australia.
authors.forename: S C
authors.initials: SC
authors.lastname: Boyages
authors.forename: A M
authors.initials: AM
authors.lastname: Bloot
authors.forename: G F
authors.initials: GF
authors.lastname: Maberly
authors.forename: C J
authors.initials: CJ
authors.lastname: Eastman
authors.forename: M
authors.initials: M
authors.lastname: Li
authors.forename: Q D
authors.initials: QD
authors.lastname: Qian
authors.forename: D R
authors.initials: DR
authors.lastname: Liu
authors.forename: R D
authors.initials: RD
authors.lastname: van der Gaag
authors.forename: H A
authors.initials: HA
authors.lastname: Drexhage
mesh_terms: D000293:Adolescent; D001323:Autoantibodies / Q000032:analysis; D001324:Autoantigens / Q000276:immunology; D001327:Autoimmune Diseases / Q000276:immunology* / Q000473:pathology; D002648:Child; D002681:China; D003102:Colloids; D003593:Cytoplasm / Q000276:immunology; D006043:Goiter, Endemic / Q000209:etiology / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000502:physiology; D018828:Immunoglobulins, Thyroid-Stimulating; D007455:Iodine / Q000506:poisoning*; D008938:Mitosis; D013954:Thyroglobulin / Q000276:immunology; D013959:Thyroid Diseases / Q000276:immunology* / Q000473:pathology; D013961:Thyroid Gland / Q000276:immunology / Q000473:pathology
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D003102:Colloids; D007074:Immunoglobulin G; D018828:Immunoglobulins, Thyroid-Stimulating; C056626:thyroid microsomal antibodies; D013954:Thyroglobulin; D007455:Iodine