title: Comparison of atrophic and goitrous auto-immune thyroiditis in children: clinical, laboratory and TSH-receptor antibody studies.
abstract: We studied the clinical features, laboratory and thyroid functions and thyrotropin (TSH)-receptor and thyroid-stimulation antibodies in 21 patients with atrophic auto-immune thyroiditis (AAT) and 48 patients with goitrous auto-immune thyroiditis (GAT) of childhood onset. The clinical features of patient with AAT were cessation of growth and obesity, while asymptomatic enlargement of the thyroid gland was the sole symptom in most patients with GAT. Although the ages at diagnosis were comparable in both groups, the estimated ages at onset were much lower in patients with AAT than in those with GAT. Patients with AAT exhibited more severe hypothyroidism when evaluated by serum thyroxine (T4), tri-iodothyronine (T3), TSH, cholesterol levels and basal metabolic rates. The 24 h 123I-thyroidal uptake was significantly lower in patients with AAT than in those with GAT. None of the 19 patients with AAT possessed TSH-binding inhibitor immunoglobulins (TBII). On the other hand, 3 of the 32 GAT patients tested, possessed weak to potent TBII activities. Three TBII-positive patients with GAT also possessed thyroid-stimulation blocking antibodies. These findings suggest that: 1. Pathogenesis of AAT in children whose onset of hypothyroidism was before puberty is not due to TSH-receptor blocking antibodies, which are often found in patients with AAT of postpubertal onset. 2. AAT in children is considered not to be due to the later stage of GAT. 3. Some patients with GAT possessed TSH-receptor blocking antibodies. The aetiology and pathogenesis of AAT in children have yet to be elucidated.
authors.affiliation: Department of Paediatrics, Hokkaido University School of Medicine, Sapporo, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Matsuura
authors.forename: J
authors.initials: J
authors.lastname: Konishi
authors.forename: K
authors.initials: K
authors.lastname: Yuri
authors.forename: S
authors.initials: S
authors.lastname: Harada
authors.forename: K
authors.initials: K
authors.lastname: Fujieda
authors.forename: Y
authors.initials: Y
authors.lastname: Nohara
authors.forename: Y
authors.initials: Y
authors.lastname: Mikami
authors.forename: K
authors.initials: K
authors.lastname: Kasagi
authors.forename: Y
authors.initials: Y
authors.lastname: Iida
authors.forename: A
authors.initials: A
authors.lastname: Hosoda
mesh_terms: D000328:Adult; D000367:Age Factors; D000906:Antibodies / Q000032:analysis*; D001284:Atrophy; D001327:Autoimmune Diseases / Q000097:blood / Q000150:complications*; D001835:Body Weight; D002352:Carrier Proteins / Q000097:blood; D002648:Child; D004341:Drug Evaluation; D005260:Female; D005500:Follow-Up Studies; D006042:Goiter / Q000097:blood / Q000150:complications*; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000097:blood; D011989:Receptors, Thyrotropin / Q000276:immunology*; D012737:Sex Factors; D013954:Thyroglobulin / Q000276:immunology*; D013960:Thyroid Function Tests; D013963:Thyroid Hormones; D013966:Thyroiditis / Q000097:blood / Q000150:complications / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D013974:Thyroxine / Q000627:therapeutic use; D000097810:Thyroid Hormone-Binding Proteins
chemical_list: D000906:Antibodies; D002352:Carrier Proteins; D008565:Membrane Proteins; D011989:Receptors, Thyrotropin; D013954:Thyroglobulin; D013963:Thyroid Hormones; D013974:Thyroxine; D000097810:Thyroid Hormone-Binding Proteins