The hypothalamic-pituitary axis was investigated in 11 adult patients with pituitary dysfunction: 8 with deficiency of all anterior hypophyseal hormones except prolactin and 3 with preservation of several hormones. The etiology of the hypopituitarism was diverse and included primary or metastatic intracranial neoplasms (4), head trauma (1), birth trauma (l), surgical stalk section (2) and idiopathic disease (3). Basal prolactin was elevated in 6 and normal in the remainder. Thyrotropin (TSH)-releasing hormone (TRH) administration increased plasma prolactin in all patients (mean ±sem, 201.1 ± 80.0%, p < 0.05) while TSH rose in 7 of 9 patients not taking thyroid hormone replacement. In contrast, chlorpromazine elicited a normal prolactin rise in only 1 of 8 subjects tested. In 9 patients oral l-dopa (500 mg) decreased prolactin 59.2 ± 7.5% (p < 0.01) by 90–240 min. Thus considerable pituitary function is demonstrable in many adult patients with hypopituitarism. Normal or elevated basal plasma prolactin concentration will identify these patients. In addition, they maintain prolactin and usually TSH responsivity to TRH. The ability of l-dopa to suppress plasma prolactin levels in these subjects may be related to augmented circulating PIF activity, a direct pituitary effect of l-dopa, or both.
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Woolf et al. (1974) studied this question.