Plasma Prolactin and Thyrotropin and the Response to Thyrotropin-Releasing Factor in Children with Primary and Hypothalamic Hypothyroidism*

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Abstract
The plasma concentration of PRL and TSH were determined in 41 infants and children with primary hypothyroidism without galactorrhea. These results were compared to those in children with idiopathic hypothalamic (tertiary) hypothyroidism (28 children), hypopituitarism due to a mass lesion (18 children), and hyperthyroidism (15 children). The mean basal PRL concentration was 25.4 ± 3.1 (SE) ng/ml in children with primary hypothyroidism, 13.9 ± 2.1 ng/ml in those with idiopathic hypothalamic hypopituitarism, and 16.3 ± 2.5 ng/ml in those with hypopituitarism secondary to tumors involving the hypothalamus and/or pituitary. The PRL values in primary hypothyroidism were significantly different from the latter two groups (P < 0.01) and from those in normal children (5.0 ± 0.6 ng/ml; P < 0.001). The PRL levels in children with hyperthyroidism were similar to those in normal children. The mean basal concentration of plasma TSH was 382 ± 85.5 μU/ml in children with primary hypothyroidism and correlated significantly with the mean basal plasma PRL levels (P < 0.02). There was a 2-fold rise in TSH after iv administration of TRF (200 μg) to 11 patients with primary hypothyroidism. The peak rise in TSH after TRF was similar in the normal children and in those with tertiary hypothyroidism, but the pattern of response differed. In both primary and tertiary hypothyroidism, there was a delay in return of plasma TSH to baseline values. No increase in plasma TSH concentration after TRF occurred in children with hyperthyroidism. The peak PRL concentration after TRF administration was significantly higher in patients with primary hypothyroidism than in those with tertiary hypothyroidism or in normal children. Both plasma TSH and PRL decreased significantly within 2–3 months of thyroid hormone therapy. The TSH response to TRF decreased in two patients by 2–3 weeks after treatment and one patient had no TSH rise after TRF after 3 months of L-T4 therapy. The PRL rise after TRF decreased significantly only in the patient on more prolonged treatment. These studies suggest that increased TRF secretion as well as increased pituitary sensitivity to TRF results in increased release of PRL and TSH in primary hypothyroidism. In contrast, the higher PRL levels observed in children with hypothalamic hypopituitarism and tertiary hypothyroidism can be attributed to decreased secretion of PRL release inhibitory factor.

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