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Surgical cure of prolactinoma reverses abnormal prolactin repsonse to carbidopa/L-dopa.

作者信息

Molitch M E, Goodman R H, Post K D, Biller B J, Moses A C, King L W, Feldman Z T, Reichlin S

出版信息

J Clin Endocrinol Metab. 1982 Dec;55(6):1118-23. doi: 10.1210/jcem-55-6-1118.

DOI:10.1210/jcem-55-6-1118
PMID:7130339
Abstract

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.

摘要

相似文献

1
Surgical cure of prolactinoma reverses abnormal prolactin repsonse to carbidopa/L-dopa.
J Clin Endocrinol Metab. 1982 Dec;55(6):1118-23. doi: 10.1210/jcem-55-6-1118.
2
Loss of central nervous system component of dopaminergic inhibition of prolactin secretion in patients with prolactin-secreting pituitary tumors.泌乳素分泌型垂体瘤患者中多巴胺能对泌乳素分泌的抑制作用的中枢神经系统成分缺失。
J Clin Invest. 1978 Apr;61(4):973-80. doi: 10.1172/JCI109022.
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Dynamic tests of prolactin secretion in hyperprolactinemic states: carbidopa-L-dopa and indirectly acting dopamine agonists.
J Clin Endocrinol Metab. 1982 Feb;54(2):429-35. doi: 10.1210/jcem-54-2-429.
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Carbidopa inhibits the growth hormone- and prolactin-suppressive effect of L-dopa in acromegalic patients.卡比多巴可抑制左旋多巴对肢端肥大症患者生长激素和催乳素的抑制作用。
J Clin Endocrinol Metab. 1978 Sep;47(3):647-52. doi: 10.1210/jcem-47-3-647.
5
Dopaminergic mechanisms regulating prolactin secretion in patients with prolactin-secreting pituitary adenoma. Long-term studies after selective transsphenoidal surgery.多巴胺能机制对分泌催乳素的垂体腺瘤患者催乳素分泌的调节。选择性经蝶窦手术后的长期研究。
Metabolism. 1982 Nov;31(11):1100-4. doi: 10.1016/0026-0495(82)90159-7.
6
[Various aspects of dopaminergic function in patients with prolactin-secreting hypophyseal adenoma].
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Effects of CNS dopamine augmentation on stimulated prolactin secretion.
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In vitro effect of dopamine and L-dopa on prolactin and growth hormone release from human pituitary adenomas.多巴胺和左旋多巴对人垂体腺瘤催乳素和生长激素释放的体外作用。
J Clin Endocrinol Metab. 1979 Nov;49(5):737-41. doi: 10.1210/jcem-49-5-737.
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Functional characterization of hypothalamic hyperprolactinemia.
J Clin Endocrinol Metab. 1982 Nov;55(5):897-901. doi: 10.1210/jcem-55-5-897.
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Evaluation of two inhibitory tests (nomifensine and L-dopa + carbidopa) for the diagnosis of hyperprolactinaemic states.两种抑制试验(诺米芬辛和左旋多巴+卡比多巴)用于诊断高催乳素血症状态的评估。
Clin Endocrinol (Oxf). 1980 Dec;13(6):525-33. doi: 10.1111/j.1365-2265.1980.tb03420.x.

引用本文的文献

1
Hyperprolactinemia.高催乳素血症
Pituitary. 2008;11(2):141-6. doi: 10.1007/s11102-008-0107-5.
2
Hyperprolactinemia: neuroendocrine and diagnostic aspects.高催乳素血症:神经内分泌及诊断方面
J Endocrinol Invest. 1989 Oct;12(9):653-68. doi: 10.1007/BF03350030.
3
Enlarged adenomectomy for enclosed prolactinomas: a preliminary study of 26 cases.扩大性腺瘤切除术治疗包裹性泌乳素瘤:26例初步研究
Acta Neurochir (Wien). 1990;103(3-4):92-8. doi: 10.1007/BF01407512.