Reduction of Central Dopamine Release in Hyperprolactinemia
- Author:
Bong Soo CHA
;
Young Duk SONG
;
Sung Kil LIM
;
Kyung Rae KIM
;
Hyun Chul LEE
;
Kap Bum HUH
;
Su Youn NAM
;
Eun Jig LEE
;
Bong Chul CHUNG
;
Jung Han KIM
;
Sei Chang OH
- Publication Type:Original Article
- Keywords:
Prolactinoma;
Idiopathic hyperprolactinemia
- MeSH:
3,4-Dihydroxyphenylacetic Acid;
Brain;
Diagnosis;
Dopamine;
Epinephrine;
Female;
Follicular Phase;
Galactorrhea;
Humans;
Hyperprolactinemia;
Infertility;
Lactotrophs;
Methoxyhydroxyphenylglycol;
Norepinephrine;
Pregnancy;
Prolactinoma;
Reference Values
- From:Journal of Korean Society of Endocrinology
1996;11(3):277-284
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Background: Prolactin(PRL) secretion is tonically inhibited by doparnine that originates from the hypothalamic tuberoinfundibular tract and reaches the lactotroph via the hypophyseal portal vessel. Hyperprolactinemia associated with oligomenorrhea-amenorrhea, galactorrhea and/or infertility is mainly due to PRL-secreting pituitary adenoma(PA). The diagnosis of idiopathic hyperprolac- tinemia(IHP) is made, when hyperprolactinemia is sustained and all causes of hyperprolactinemia are excluded without radiological abnormality. It is not known, whether IHP and PA are two distinct entities or two subsequent phases of the same disease. The etiology of both disorders remains unresolved. We investigated that PRL hypersecretion in patients with IHP and PA may be the result of a defect in the central nervous system(CNS)-dopamine release, and that there may be some differences in pathogenesis of both diseases. Methods: We measured 24 hour-urinary dopamine, norepinephrine, epinephrine, and serum and 24 hour-urinary VMA(vanillyl rnandelic acid), HVA(homovanilic acid), DOPAC(3,4-dihydroxy phenylaceticacid), MHPG(3-methoxy 4-hydroxy phenylglycol) in 10 normal controls, 9 patients with IHP, and 17 patients with PA in the early follicular phase. Results: Urinary HVA and DOPAC concentrations, the major metabolites of CNS dopaminergic activity, were signficantly lower in both patients with IHP and PA compared with those in normal controls(p 0.05), whereas they were not different in both disease groups. Dopamine, norepine-phrine, epinephrine, MHPG concentrations were similar to those of the normal controls. Although VMA concentrations of both disease groups were significantly higher than those of normal controls, all of them were within normal range. Conelusion: Although our data are unable to establish the precise biochemical defect responsible for central dopamine deficiency in pathogensis of IHP and PA, we can support the presence of a pathological reduction of brain dopamine activity in IHP and PA.
