Transient Neonatal Hyperthyrotropinemia: A Factitious Syndrome due to the Presence of Heterophilic Antibodies in the Plasma of Infants and Their Mothers*

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Abstract
The long term effects of hydrocortisone, estradiol, insulin, and T3 and T4 on GH and PRL secretion by cell cultures of human somatotropic and mixed somatotropic-lactotropic adenomas have been investigated. Twenty-four-hour secretion of GH was consistently stimulated by hydrocortisone in a dose-dependent manner over the range 2 × 10-8-10-5 M. Peak effects (4- to 16-fold) occurred around 9 days, declining slightly thereafter but persisted for 27 days at which time they represented 3- to 400-fold increases over controls, which had declined throughout. The degree of stimulation by hydrocortisone was less (3- to 4-fold) in those cultures where basal GH secretion remained stable. Transfer of cells from hydrocortisone-supplemented to basal medium led to a prompt decline in GH secretion that paralleled that in the controls. The addition of T3 (2 × 10-9 M) and T4 (1 × 10-7 M), insulin (20 µU⁄ml), or estradiol (3.7 × 10-10 M) did not change the GH response to hydrocortisone. Intravenous administration of hydrocortisone to an acromegalic suppressed serum GH, and the adenoma cells were similarly suppressed when subsequently cultured with varying doses of hydrocortisone. This in vitro suppressive effect was confined to this one adenoma and reversed after 5 days, so that a dosedependent stimulation of GH secretion was observed. PRL secretion was reduced approximately 50% within 1 day by increasing doses of hydrocortisone from one of three mixed adenomas and normal lactotrops from an acromegalic. Estradiol (3.7 × 10-10 M) stimulated PRL secretion 4-fold from a mixed adenoma and partially reversed the suppressive effect of hydrocortisone on another adenoma over 17 days. Insulin had no effect on GH and PRL secretion, whereas T3 and T4 together suppressed both. It is concluded that hydrocortisone has marked long term timulatory effects on GH secretion by human adenoma cells and occasionally suppresses PRL secretion. Estradiol can stimulate PRL secretion at low doses, whereas insulin has no effect on GH or PRL, and T3 and T4 inhibited both. The cell culture system described allows examination of these interrelationships over the longer term.

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