抄録
In order to clarify the mechanism (s) which causes galactorrhea and amenorrhea in patients with Galactorrhea-Amenorrhea Syndrome (GAS) (Group A, n=20), composed of Chiari-Frommel Syndrome (CFS) (Subgroup I, n=3), Argonz-del Castillo Syndrome (ADCS) (Subgroup II, n=5) and Drug-induced Galactorrhea-Amenorrhea (DIG) (Subgroup III, n=12), we analysed basal plasma prolactin (PRL) and gonadotropin levels and their responsiveness to TRH and LH-RH, respectively in GAS patients. In addition, another group of galactorrheic patients without amenorrhea (Group B, n= 29) was selected, and further divided into three subgroups; subgroup I (n=7) with persisting postpartum lactation, subgroup II (n=7) of idiopathic galactorrhea, and subgroup III (n=15) induced by drug administration.
There were found unexpectedly high frequencies of normoprolactinemic patients (<23.7ng/ml) in 40% of GAS (66.7% in CFS, 40% in ADCS, and 33.3% in DIG). The PRL responsiveness to TRH, evaluated by %ΔPRL (peak PRL-basal PRL/basal PRL×100), tended to be high in ADCS and DIG (group after discontinuation of drugs) compared with those of normal subjects (n=12) and patients with primary hypothyroidism (n=21). PRL response was almost normal in CFS or DIG (group during drug administration).
Basal level of plasma gonadotropin in GAS was comparable to that of normal subjects. However, responsiveness of gonadotropin to LH-RH in GAS tended to be high compared with that of normal subjects.
The patients in group B (subgroup demonstrated almost parallel responses of PRL and gonadotropin, respectively, to those of corresponded subgroups in group A.
From the present results, we concluded that; 1) It seems likely that frequency of normoprolactinemic patients in GAS (Group A) is surprisingly high. 2) A still unclarified mechanism (s) for the occurrence of galactorrhea, not explained solely by plasma radioimmunoassayable PRL level and/or hyperresponsiveness of PRL to stimuli, may operate on a considerably large number of group A patients. 3) Decreased gonadotropin secretion at pituitary level seems not to be a main cause of menstrual abnormality in group A patients. 4) The same mechanism (s) as in group A patients may cause galactorrhea in group B patients.
