Basal TSH levels were found to be elevated in 6 patients with documented growth hormone deficiency and hypothyroidism. TRH (200 mug/m2 administered intravenously) led to an exaggerated TSH response. This is in contrast to the results in other GH-deficient children, with either a delayed rise of TSH (hypothalamic hypothyroidism due to TRH deficiency, n = 22), an absent TSH response (pituitary hypothyroidism due to TSH deficiency, n = 7), or a normal increase of TSH (isolated GH deficiency, n = 20). Elevated plasma TSH in the presence of hypothyroidism as seen in 6 of our patients with idiopathic hypopituitarism or craniopharyngioma, indicates an intact feedback action between the pituitary and the thyroid gland. TSH, however, seems to be inadequate for the maintenance of normal thyroid function. It is suggested that in certain patients with hypothalamic disorders, TSH is secreted in a biologically less active form.

14 years ago, a 5.7-year-old healthy girl was treated with desiccated thyroid for a goiter and elevated TSH levels. The goiter disappeared and TSH levels were normalized. However, hyperthyroidism appeared. Without therapy, the goiter reappeared and hyperthyroidism aggravated. Based on hormone values, TSH-induced hyperthyroidism was diagnosed. After exclusion of neoplastic TSH secretion, treatment with dextrothyroxine (DT₄) was initiated at age of 10 years and continued during the last 10 years (except for short periods). The girl became euthyroid, has no goiter and normal TSH values. Since thyrotrophs and peripheral tissues are probably normally sensitive to T₄, we postulate that her hypothalamopituitary-thyroid control is operating on a higher set point level for T₄.

H.KRAwczY~KA K.W6JCWE.ULWOWICTY.CUW 71 Endocrine Unit and the 1.Depsrtaent of Ped i a t r i c a , C h i l d r e n c s Hospital i n

B1-995) Ih J.A.,a 6 y e a r -o l d g i r l with small g o i t r e had e l e v a t e d l e v e l s o f T4, T 3 a s well cis TSH. Her high and w e i e h t were a t t h e 10th p e r c e n t i l e , bone age was delayed a b o u t 2 y e a r s but c l i n i c a l l y she was eutilyroid. Treatment w i t h t,h. r e s u l t e d i n T8H suppresion but s i n g s o f hyperthyroidism appeared. During t h e n e x t 3 y e a r s without any t r e a t m e n t T4, T 3 and bass1 TSH were s t i l l e l e v a t e d and TRH s t i m u l a t e d TSh i n c r e a s e d t o t h e hypothyroid range. A t t h e age o f 9 y e a r s c l i n i c a l symptams of hyperthyroidism were e v i d e n t , Hypothalamo-pituitary s t u d i e s were normal, t h e r e was no evidence f o r n i t u i t a r v tumor. A a r t i s s e l e c t i v e i t u i t a r y r e s i s t a n c e t o t h, was s u E p o s e d ,~i n c e 19SOPthe p a t i e n t~~-%~~~4 i n a dose o f 0.5mdd. Grsdual d e c r e a s e o f TSH l e v e l s was accompanied by r e d u c t i o n i n t h e s i z e of g o i t r e and a m e l i o r a t i o n o f c l i n i c a l symptoms o f hyperthyroidism, confirmed by n o r m a l i s a t i o n of WR, Temporary i n t e r r u pt i o n o f D-T4 t h e r a p y r e s u l t e d i n t h e i n c r e a s e o f a l l c l i n i c a l and biochemical a b a o r m a l i t i e s . To our knowl i d g e t h i s i s t h e f i ? s t case o f h e r t h roidism due t o 1 2 2 D-ri::. W h i l s t t h e l a s t 10 y e a r s ' l i t e r a t u r e u n a n i n o u s l y p o i n t s o u t t h e i n c r e a s e d p r e v a l e n c e o f s e r u a HCllA i n c h i l d r e n and y o u n g s t e r s u i l h i n s u l i n -d e p e n d e n t d i a l i e t c s n e l l i t u s (IOUH), t h e p r e d i c t i v e v a l u e o f o v e r t t h y r o i d d i s e a s e or such a b i o h u m o r a l n a r k c r i n t h e s e p a t i e n t s w i d e l y v a r i e s a c c o r d i n g t o t h e d i f f e r e n t A u t h a r s t sucl, a p a t t e r n was n o t c o n f i r m e d a t Lllc n c x l t e s t s . C o n c l u s i o n s : based on a l o n g i t u d i n a l s t u d y , o u r d a t a c o n f i r m t h a t t h e i n c r e a s e d p r e v a l e n c e o f HCllA i n IDOH c h i l d r e n i s n o t a s s o c i a t e d t o h i g h r i s k o f o v e r t t h yr o i d d i s e a s e . a t l e a s 1 i n Europc.C. Couprie", P.F. Bougneres, J.L. Chaussain. CONTINUOUS SUBCUTANEOUS GLUCAGON INFUSION IS AN EFFECTIVE MEAN OF INCREASING BLOOD GLUCOSE (BG) IN fNPERINSULINEMIC INFANTS.flyperinsulinemic infants develop severe hypoglycemia due to a major suppression of glucose production by the iiver. Treatnient of this condition is made difficult in a subset of patients by the limited efficacy of drugs, such as diazoxide or corticosteroids. The need for maintaining a large supply of glucose in these patients requires continuous nasogastric feeding and sometinies prolonged peripheral or central venous catheterization. We have used the subcutaneous infusion of glucagon via a small insulin pump in an attempt to maintain...