PubMed Health⌕ Search

Biomedical subjects

T Kinugasa

Publications and source records attributed to T Kinugasa.

At least 55 records · Page 3Linked to original sources
PubMed1978

Absence of positive feedback effect of oestrogen on LH release in patients with testicular feminization syndrome.

The response of serum LH to exogenous oestrogen administration was studied in 5 patients with testicular feminization syndrome (TFS). The serum LH levels were elevated in all the patients, while serum testosterone levels were within the normal male range. Serum FSH levels were elevated in 4 patients and normal in one patient. Intravenous administration of 100 microgram of LH-RH provoked a further increase in both LH and FSH. Following intravenous injection of 20 mg of conjugated oestrogen (Premarin), the LH levels were serially determined until 120 h in TFS patients, 5 normal males, and 10 normal females during the mid-follocular phase (D7-9). Both TFS patients and normal males showed no LH release following oestrogen injection in contrast to normal females who displayed a significant increase in LH with a peak at 48 to 56 h after the injection. These results seem to suggest that the insensitivity of the hypothalamus to androgen in TFS patients do not affect the sex differentiation of the hypothalamus. The possible role of oestradiol conversion from testosterone in the hypothalamus is discussed.

Adolescent↗
PubMed1978

The time course change after castration in short-loop negative feedback control of LH by HCG in women.

The time course of change in the suppressive effect of human chorionic gonadotrophin (HCG) on luteinizing hormone (LH) and/or LH-beta following castration was studied by a specific LH-beta radioimmunoassay. At 14-50 days after castration 8 women were given 10 000 IU of HCG in a single intramuscular injection (group 1), 5 women were given 2000 IU of HCG in the same way (group 2), and 5 were injected with saline as controls (group 5). In addition, 5 women 6-15 months (group 3) and 7 women 3-8 years (group 4) after castration were given 10 000 IU of HCG. The serum concentrations of HCG in groups 1, 2, 3 and 4 reached peak levels of 209.4, 44.1, 210.6 and 238.6 uU/ml, respectively, 4 h after the HCG injection. The serum LH concentration in group 1 was reduced significantly (P less than 0.01) by HCG administration, but the reductions in the LH levels in groups 2, 3 and 4 after HCG injection were not significantly different from that of the controls. These findings suggest that the threshold of the short-loop negative feedback control of LH in women changes with time after castration.

Adult↗
PubMed1977

Responses of serum gonadotrophins to LH-releasing hormone and oestrogens in Japanese women with polycystic ovaries.

In order to define the abnormality in gonadotrophin secretion in Japanese women with polycystic ovaries (PCO) who rarely show virilization and markedly enlarged ovaries, basal levels of LH and FSH, and responses of serum gonadotrophins to LH-releasing hormone (LH-RH) or oestrogens were determined by radioimmunoassay. Eleven patients with PCO diagnosed by laparotomy or laparoscopy and 30 normal women in the follicular phase were studied. The mean (+/- SD) basal level of LH was significantly higher in patients with PCO than in normal controls (PCO 28.6 +/- 2.4 vs. normal 10.9 +/- 3.0 mIU/ml), while the mean FSH level in PCO patients was not significantly different from that in the normal controls (9.7 +/- 0.7 vs. 11.4 +/- 2.6 mIU/ml). The mean LH/FSH ratio in PCO patients was significantly higher than that in normal controls (3.2 +/- 0.9 vs. 1.0 +/- 0.3). Exaggerated response of LH to LH-RH was observed in PCO patients, while the FSH response was comparable with the normal controls. Ten out of 11 patients with PCO showed LH release exceeding the basal level after bolus iv injection of 20 mg conjugated oestrogens (Premarin), and virtually the same mean net increase in LH from the basal level was obtained in both PCO patients and normal controls. Since the abnormalities in gonadotrophin secretion in Japanese women with PCO are not different from those reported in patients with PCO in Europe and USA, it seems likely that lower incidence of markedly enlarged ovaries and virilization in Japanese patients may be caused by the difference in ovarian response to gonadotrophin.

Adult↗
PubMed1976

[Studies on the measurements of LH-releasing hormone (LH-RH) by radioimmunoassay (RIA) (author's transl)].

The radioimmunoassay for LH-RH would aid greatly in the assessment of hypothalamic function. The anti-LH-RH was prepared by immunizing rabbits with LH-RH conjugate of BSA. 125I-LH-RH was prepared by the lactoperoxidase method and Sephadex G-10 column chromatography. The double antibody RIA technique was employed. On the assay of biological materials, LH-RH was extracted by methanol because LH-RH was rapidly destroyed in the serum, and this breakdown could not be prevented by benzamidine or 2,3-dimercaptopropranol. Sensitivity of this RIA system ranged from 10 tp 104 pg/ml, and the coefficient of variations of intra- and interassay were 12.9% and 9.% respectively. The serum LH-RH levels of men in a normal gonad state were below 10 pg/ml, and those of women in a normal gonad state in the early follicular or luteal phase were below 50 pg/ml. Whereas those of postmenopausal or castrated women were increased, and were highest in women with several gonadal disturbed states. The disappearance curve of LH-RH in women was characterized by two exponentials, t(1/2) of the initial component was 4.9 min, and that of the second component 24.6 min. Urinary excretion of exogenously administered LH-RH was also studied.

Amenorrhea↗
PubMed1976

Impaired LH release following exogenous estrogen administration in patients with amenorrhea-galactorrhea syndrome.

Serum gonadotropin levels were determined in 10 patients with the amenorrhea-galactorrhea syndrome before and following acute iv administration of synthetic LH-releasing hormone (LHRH) or conjugated estrogens, in order to clarify the hypothalamic derangements in the gonadotropin secretion in patients with hyperprolactinemia. The basal prolactin (PRL) levels were elevated in all the patients, and blunted responses to 500 mug of iv synthetic thyrotropin-releasing hormone (TRH) injection were found in 9 out of the 10 patients. The basal levels of LH and FSH were subnormal in 2 and 3 patients, respectively, while those in the remaining patients were normal or slightly elevated. Normal or excessive responses of gonadotropins to 100 mug of iv LHRH were observed in most patients, 9 for LH and 10 for FSH out of 10 patients. In 10 normal cyclic women at the mid-follicular phase (D7-9) and 10 hypothalamic amenorrhea patients without galactorrhea, LH release was found 48 to 72 h after the iv injection of 20 mg conjugated estrogens (Premarin). This LH release following Premarin injection was completely abolished in the patients with amenorrhea-galactorrhea. These data seem to indicate that in patients with hyperprolactinemia, tonic secretion of gonadotropin is maintained fairly well, while of the positive feedback effect of Premarin on the release of LH is impaired. It is suggested that impaired LH release may be partly responsible for anovulation and amenorrhea in patients with hyperprolactinemia.

Abortion, Spontaneous↗
PubMed1975

Assessment of gonadotrophin secretion in women with anorexia nervosa.

The LH and FSH secretions in 21 patients with anorexia nervosa were assessed by radioimmunoassay. On a single iv injection of 100 mug LH-releasing hormone (LH-RH), 8 patients showed LH response comparable to that of normal cyclic women in the follicular phase, and 5 patients showed excessive response. Although the remaining 8 patients showed almost no LH response, infusion of 400 mug LH-RH or daily im injections of LH-RH restored gonadotrophin responsiveness to LH-RH in all patients tested. The initial rise in LH during clomiphene citrate treatment was observed in 3 out of 5 patients, but the second peak of LH was found in only one patient. The initial suppression of LH following iv injection of conjugated oestrogen (Premarin) was observed in 9 out of 10 patients but a rebound increase comparable to that in normal cyclic women in the mid-follicular phase was found in only 3 patients. These results seem to suggest that impaired hypothalamic function is the cause of gonadotrophin deficiency and the resultant anovulation in most patients with anorexia nervosa.

Adolescent↗