Surgical cure of prolactinoma reverses abnormal prolactin repsonse to carbidopa/L-dopa.
To determine whether the abnormalities in dopaminergic regulation of PRL secretion in patients with prolactinomas persist after resection of the adenoma, we evaluated PRL inhibitory responses to L-dopa alone and L-dopa given after pretreatment with the dopa decarboxylase inhibitor carbidopa before and after transsphenoidal selective resection of prolactinomas in 23 women. Eighteen women were cured by surgery (normal PRL, menses, no galactorrhea), while 5 women were not cured. Preoperatively, the PRL inhibitory responses to L-dopa cured, 4 .3 +/- 3.8%; uncured, 50.1 +/- 5.5% of baseline) was blunted by pretreatment with the decarboxylase inhibitor carbidopa (cured, 79.1 +/- 4.1%; uncured, 76.8 +/- 9.2%). Postoperatively, this blunting disappeared in the cured patients (L-dopa, 49.1 +/- 3.5%; carbidopa/L-dopa, 56.3 +/- 5.1%), but the blunting persisted in the uncured patients (L-dopa, 49.3 +/- 7.9%; carbidopa/L-dopa, 69.3 +/- 4.2%). The return to normal of the carbidopa/L-dopa test in cured prolactinoma patients after surgery is evidence that in these individuals, preoperative abnormalities of secretion are due to either intrinsic abnormalities of the tumor or alteration of hypothalamic function secondary to tumor secretion. In those patients not cured by surgery, dynamic tests of function remain abnormal, findings attributable to either incomplete tumor resection or the presence, in some patients, of underlying hypothalamic dysregulation.
D000236:Adenoma / Q000378:metabolism / Q000601:surgery; D002230:Carbidopa; D004298:Dopamine / Q000502:physiology; D005260:Female; D006801:Humans; D007031:Hypothalamus / Q000503:physiopathology; D007980:Levodopa; D010911:Pituitary Neoplasms / Q000378:metabolism / Q000601:surgery*; D011388:Prolactin / Q000378:metabolism*; D011863:Radioimmunoassay
D007980:Levodopa; D011388:Prolactin; D002230:Carbidopa; D004298:Dopamine