Three neonates born to three mothers with primary myxedema who have thyrotropin-binding inhibitor immunoglobulin (TBII) were continually examined after birth.One neonate showed a high TSH level in mass-screening for congenital hypothyroidism and developed transient hypothyroidism.Her TBII disappeared at 114 days of age, and she remained euthyroid after discontinuation of thyroxin replacement at 146 days of age. The other two neonates were euthyroid, though they had positive TBII.In three mothers, the doses of IgGs that inhibited 125I-TSH binding to the level of 50% were compared. The potency of IgG from the mother whose neonate developed hypothyroidism was stronger than that of IgG from the other two mothers. And the elevation of cAMP induced by bovine TSH in suspension culture with porcine thyroid follicles was significantly reduced in the presence of IgG from the three mothers when compared with normal IgG. The thyroid-stimulation blocking activity was more potent in the mother whose neonate developed hypothyroidism than in the other two mothers. This study suggests that the thyroid function of neonates born to primary myxedema with blocking type TBII is influenced by the potency of TSH-binding inhibitor and thyroid-stimulation blocking activity of the mother.
A girl, 12 years of age, developed Graves' disease compounded with rheumatic fever and idiopathic thrombocytopenic purpura. Thrombocytopenia improved under short-term treatment with steroids and her mitral valvular insufficiency, due to the rheumatic fever, disappeared 4 years later. Initially, she had been treated with propylthiouracil (PTU) for 28 months. She suffered a relapse 9 months after stopping PTU and so she was given further PTU therapy. However, hypothyroidism developed 11 months after the initiation of therapy and continued, though further PTU treatment was discontinued. She now receives 1-thyroxine and maintains a euthyroid state.At the onset of the patient's hyperthyroidism, the TSH-binding inhibitor immunoglobulin (TBII) and the thyroid stimulating antibodies (TSAb) were found to be positive. During the remission period, only the thyroid stimulation blocking immunoglobulin (TSBI) was weakly positive. At relapse, only TBII was mildly positive. When hypothyroidism developed, both TBII and TSBI were positive, and TSAb was negative in all testings of her diluted IgGs.The patient's TBII and thyroid dysfunction were unaffected by high-dose intravenous gammaglobulin therapy or by treatment with prednisolone 0.5 mg/kg/day for 2weeks.In conclusion, the emergence of TSBI during or after anti-thyroid drug therapy might possibly lead to hypothyroidism in patients with Graves' disease.
i i m i . Chiba U n l v e r s i t v School of W d i c i n e , DeDaKtWnt of P e d i a t r i c s . 1-8-1, Inohana, Chiba c i t y , Japan 280. Immunoglobulin G (IgG) f r a c t i o n s from t h r e e m t h e r s w i t h primary myxedema, who d e l i v e r e d neonates, 6 p a t i e n t s w i t h g o i t r o u s H a s h i m t o ' s d i s e a s e and one a d o l e s c e n t g i r l w i t h p r imary rnyxedema were t e s t e d f o r t h e i r a b i l i t y t o a l t e r TSH stimu l a t i o n of CAMP production i n p o r c i n e t h y r o i d f o l l i c l e s of suspension c u l t u r e and t h e binding of TSH t o its r e c e p t o r i n S m i t h ' s assay.The r e s u l t s suggested t h e presence o f a t l e a s t tho t y p e s of IgG: 1) one i n h i b i t s TSH-stimulated CAMP responses a n d TSH binding to its r e c e p t o r s ; 2 ) t h e o t h e r i n h i b i t s TSHs t i m u l a t e d CAMP responses b u t does n o t i n h l b i t TSH binding t o l t s r e c e p t o r s . The former was d e t e c t e d i n a l l t h r e e m t h e r s and t h e t h y r o i d stimulation-blocking a c t i v i t y of t h e IgG was most s l g n l f i c a n t I n t h e m t h e r of t r a n s i e n t n e o n a t a l hypothyroidism. The l a t t e r was d e t e c t e d i n 5 p a t i e n t s w l t h g o i t r o u s t h y r o i d itis. The accumulation o f CAMP by 1 mu/& TSH decreased w i t h i n c r e a s i n g q u a n t i t i e s o f both IgGs ( t h e dose range 1-15 mg/ml). The p r e s e n t s t u d y s u g g e s t s t h a t one of t h e IgGs which i r h~b i t s TSH-stimulated CAMP responses may be r e s p o n s i b l e f o r t h y r o i d dysfunction i n primary rnyxedema and a l s o f o r t r a n s L e n t n e o n a t a l hypothyroidism. Howver, t h e c l i n i c a l s i g n i f i c a n c e o f a n o t h e r blocking IgG which does n o t i n h i b i t TSH b i n d m g t o ~t s r e c e p t o r s should be c l a r i f i e d . Each of t h r e e c h i l d r e n i n a family was found t o be hypot h y r o i d a t b i r t h a s p a r t of t h e neonatal hypothyroid s c r e e n i n g program. T h e i r mother had developed Graves d i s e a s e a t age 8 y e a r s but became hypothyroid a t age 25 -3 y e a r s before t h e s t c h i l d . Serum o b t a i n e d 6 y e a r s a f t e r t h e s t c h i l d was born, i n h i b i t e d TSH binding t o human t h y r o i d c e l l membranes i n v i t r o . At b i r t h each c h i l d was found t o have increased TSH c o n c e n t r a t i o n . In r e t r o s p e c t t h y r o i d microsomal a u t o a n t i b o d i e swere p r e s e n t a t 1:6400 a t 2 months of age i n f i r s t boy and a t 1:6400 a t 3 days of age i n t h i r d c h i l d . The o l d e s t two c h i l d r e n have been followed 3 months o f f thyroxine therapy and continue t o have normal t h y r o i d f u n c t i o n (T4, unbound 1 4 , T3 and TSH).In p a t i e n t s with congenital hypothyroidism i n whom t h e mother has autoimmune t h y r o i d i t i s o r t h e r e i s a family h i s t o r y of t h y r o i d i t i s , t h e p o s ...
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