Thyrotrophin and prolactin responses to thyrotrophin-releasing hormone in patients with Parkinson's disease
- 1 March 1982
- journal article
- research article
- Published by Oxford University Press (OUP) in Acta Endocrinologica
- Vol. 99 (3) , 344-351
- https://doi.org/10.1530/acta.0.0990344
Abstract
The thyrotropin (TSH) and prolactin (Prl)-releasing effects of TRH were investigated in 20 subjects with Parkinson''s disease (PD), unmedicated, on chronic treatment with a combination levodopa-benserazide (Madopar) or levodopa-carbidopa (Sinemet) or withdrawn from therapy. Administration of TRH (200 .mu.g i.v.) induced in unmedicated patients TSH and Prl responses significantly lower than those of sex- and age-matched controls. In patients on Madopar therapy the TSH and Prl responses to TRH were greater than in unmedicated patients and comparable to those of controls, while in patients on Sinemet therapy the pituitary responses were undistinguishable from those of unmedicated subjects. Withdrawal of Madopar therapy resulted in a marked diminution of the TSH response but did not affect the Prl response to TRH. Withdrawal of Sinemet therapy did not alter the TSH and Prl responses to TRH. Concomitant evaluation of growth hormone (GH) levels in none of the subjects evidenced non-specific changes in plasma GH following TRH. Since TSH and Prl responses to TRH are inhibited by an enhancement of the dopaminergic tone, it would appear that the latter is preserved in the tuberoinfundibular system of unmedicated subjects and subjects on chronic Sinemet therapy, but is defective in subjects on chronic Madopar therapy.This publication has 6 references indexed in Scilit:
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