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PERCENTAGE OF DIALYZABLE ESTRADIOL-17β (DE 2 ) FROM BIRTH TO ADULTHOOD AND IN SEXUAL PRECOCITY AND PREMATURE THELARCHE

An 11 y o girl had unilateral ankle bowing during the pre-menarchial growth spurt while on normal dietary vitamin D. Generalized rickets on x-ray, slight decrease in serum Ca (8.8 - 9.7) and increase in P (5.4 - 6.3 mg%) and alk.phos. (8.4 BLU) were associated with failure to increase phosphate clearance with parathormone (pth). Malabsorption was excluded by appropriate studies. Rickets healed completely and 47 calcium absorption was normal during 2 years on vit D2 50,000 IU/day, yet laminas dura were absent and remained so after adult height was reached. Restudy at age 15 years showed failure of increase in phosphate clearance, and CAMP (Δ 2.2 nanomoles/mg creat; vs 36 ± 0.7 SEM controls) with I.V. pth. Basal pth 640 pg/ml (normal 135 - 350) was elevated and decreased to normal 211 following Ca infusion, ruling out primary hyperparathyroidism. We suggest that renal unresponsiveness to pth and failure to lower renal tubular cell P interfered with conversion of 25-OH-D2 → 1,25-OH-D2 with resulting hypocalcemia, rickets, and hyperparathyroldism during the stress of pubertal growth. This represents a novel explanation of pubertal onset rickets with hyperparathyroidism in absence of renal disease and is probably the basis of so called pseudo hypo-hyperparathyroidism.

Subacute thyroiditis in an ectopic thyroid gland has not been reported. Our patient presented at age 4 10/12 with a mass in the left upper anterior neck. Scan 2 years previously when euthyroid revealed uptake only in the mass. On our evaluation she was euthyroid with enlargement of the mass, measuring 3.5 × 2 cm. RIA T4 and T3 were 8.1 ng (NL 5.1 - 11.5) and 191 ng/100 ml (NL adult 60 - 160)respectively. TSH was 60 μU/ml. During subsequent 4 mos of replacement therapy, the mass was not palpable. During 3 mos following stopping replacement therapy, sequential T3 72, 97, 115; and T4 1.8, 4.2, 6.8 increased. TSH decreased 120, 56, 42. 24 RAI uptake was 28% (slightly elevated). We conclude that pathological release of thyroid hormones occurring in subacute thyroiditis suppresses TRH-induced TSH release during initial phase of SAT. During recovery, the elevated RAI uptake is accompanied by high TSH levels which decrease as T3 and T4 return to normal.