Effects of TRH and Bromocriptine in Acromegaly: In Vivo and in Vitro Studies
In patients with acromegaly, disturbances involving the regulation of growth hormone (GH) have been reported. Thyroliberin (TRH), which does not modify GH plasma levels in normal subjects, is able to induce release of GH in 55–70% of patients with acromegaly (Schalch et al., 1972; Irie and Tsushima, 1972). Administration of dopaminergic drugs in cases of acromegaly often results in reduction of GH hypersecretion, whereas this effect is absent in normal persons (Liuzzi et al., 1972, 1974; Camanni et al., 1975). The physiological significance of such abnormalities is currently unclear. In particular, it has not yet been demonstrated that these pharmacological effects are related to action of the drugs directly on the adenomatous somatotropic cell. Indeed, it is conceivable that administration of TRH or dopaminergic drugs at supraphysiological doses primarily induces modifications in the neurohormonal output of the hypothalamus. In this hypothetical situation, the abnormal GH regulation encountered in acromegaly would reflect only disturbed hypothalamo-pituitary regulation.
KeywordsGrowth Hormone Pituitary Cell Acromegalic Patient Growth Hormone Response Growth Hormone Release
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- Goodyer, C. G., Marcovitz, S., Guyda, H., Giraud, C. J. P., Hardy, J., Gardiner, R. J., and Martin, J. B., 1978, Comparative study of human fetal, normal adult and acromegalic pituitary function, in: The Endocrine Society 60th Annual Meeting Program and Abstracts, Abstracts No. 143, p. 146, The Endocrine Society, Bethesda, Maryland.Google Scholar
- Rodbard, D. C., and Lewald, J. E., 1970, Computer analysis of radioligand assay and radioimmunoassay data, Acta Endocrinol. (Copenhagen) 147: 79.Google Scholar
- Schalch, D. S., Gonzalez-Barcena, D., Kastin, A. J., Schally, A. V., and Lee, L. A., 1972, Abnormalities in the release of TSH in response to thyrotropin-releasing hormone (TRH) in patients with disorders of the pituitary, hypothalamus and basal ganglia, J. Clin. Endocrinol. Metab. 35: 609.PubMedCrossRefGoogle Scholar