Severe hypothyroidism due to autoimmune atrophic thyroiditis--predicted target height and a plausible mechanism for sexual precocity.

Autoimmune thyroiditis, the most frequent cause of acquired hypothyroidism in childhood and adolescents, is characterized by raised levels of the specific antibodies to thyroperoxidase (TPOAb) and thyroglobulin (TgAb). We report a girl aged 10 years and 9 months who presented with arrested growth and breast development (thelarche). She also exhibited myxedema of the face and legs, prominent striae on the thighs, dry, cold skin, and hypertrichosis on her back. There was no goiter, no history of thyroid pain and no family history of thyroid disease. She complained occasionally of a transient headache. The patient's height was below the 3rd percentile, while her body weight was at the 50th percentile and bone age was normal. Laboratory tests proved severe hypothyroidism (fT4 0 ng/dl, fT3 0.99 pg/ml, TSH >100 microIU/ml plus an increased titer of TPOAb). Thyroid ultrasound supported the diagnosis of thyroiditis. Pituitary PRL and FSH levels and peripheral estradiol were all elevated. L-Thyroxine therapy, instituted following diagnosis, improved the growth velocity to 11 cm/year and the FSH and E2 levels were normalized to prepubertal values. Complete regression of the breast development was observed within 4 months. However, 4 months later a true (central), isosexual LHRH-dependent puberty started. The pubertal features at the time of the original diagnosis might be explained by: 1. the direct action of elevated TRH on gonadotropes to stimulate gonadotropin secretion and on lactotrophes to stimulate PRL secretion, and 2. TSH action on LH and mostly FSH receptors (homologous to TSH receptors) in the ovary, stimulating the secretion of estradiol.