Haemostatic changes during continuous oestradiol-progestogen treatment of postmenopausal women

Citations ,fiom the Literature crrAdremqic

mechanism in menopausal hot flushes

Freedman RR; Woodward S; Sabharwal SC Lufayette

Clinic, 951 East Lafayette.

Detroit,

MI 48207; USA

OBSTET GYNECOL 1990 76/4 (573-578) It has been hypothesized that hot Bushes are triggered within the hypothalamus by cu2-adrenergic receptors on noradrenergic neurons. We administered intravenous clonidine (an as-adrenergic agonist) and yohimbine (an oz-adrenergic antagonist) to nine menopausal women with hot flushes and to an asymptomatic comparison group. Hot flushes were defined objectively by skin conductance responses recorded from the sternum; finger temperature recordings and symptom reports were also evaluated. The subjects were prescreened using ambulatory skin conductance monitoring. A significantly greater number of hot flushes occurred during yohimbine sessions than in corresponding placebo sessions (six verus zero). Clonidine significantly increased the amount of peripheral heating needed to provoke a hot flush (40.6 versus 33.6 mins) and reduced the number of hot flushes that did occur (two versus eight). No hot flushes occurred in the asymptomatic women. These findings support the role of a central oz-adrenergic mechansims in the initiation of hot flushes.

Haemoatatic changes during continuous oestradiol-progestogen treatment of postmenopausal women

Sporrong T; Mattsson L-A; Samsioe G; Stigendal L; Hellgren M Department

of Obstetrics and Gynecology.

East Hospital, 416 85

Goteborg; S WE

BR J OBSTET GYNAECOL 1990 97/10 (939-944) To identify changes in haemostatic balance during continuous oestradiol-progestogen treatment, 60 postmenopausal women with climacteric complaints, mean age 55.4 years (range 44-68) were randomly allocated to receive one of four hormone replacement regimens for one year. All four formulations were administered daily and continuously, each contained 2 mg of 17-oestradiol in combination with either norethisterone acetate, I mg (group A) or 0.5 mg (group B) or megestrol acetate, 5 mg (group C) or 2.5 mg (group D). No significant changes occurred during treatment within or between the groups in platelet count, fibrinogen and 2-antiplasmin. Activated partial thromboplastin time was shortened (P < 0.05) in group D and a decline in factor VII activity and antigen (P < 0.001) and in ATIH activity (P < 0.05) was noted in group A. Protein C tended to decline in all treatment groups but statistically significant changes were noted only in groups A and C. Two women developed crural thrombosis during the observation period

Hnmmne implants and tachyphylaxis Garnett T; Studd JWW; Henderson A; Watson N; Savvas M; Leather A Dulwich Hospital Menopause

Clinic, East Dulwieh Grove, Lon-

don SE22 8PT; GBR

BR J OBSTET GYNAECOL 1990 97/10 (917-921) The serum oestradiol levels of 1388 women treated with hor-

285

mone implants at a menopause clinic were reviewed in 1988. Thirty-eight (3%) were found to be above 1750 pmolil. Of these 38 women with supraphysiological oestradiol levels 23 had started therapy for menopausal symptoms and 15 for the premenstrual syndrome (PMS). Of the 23 women treated for menopausal symptoms 11 had a history of psychiatric referral for depression and nine had undergone a surgical menopause. Nine of the 15 women with PMS had a history of psychiatric referral for depressive symptoms. We conclude that the women who attain supraphysiological levels of oestradiol on implant therapy have a high frequency of psychopathology or surgical menopause and may require higher oestradiol levels for adequate control of symptoms.

ACTS stimulation tests and plasma dehydroepiandrosterone sulfate levels in women with hiism Siegel SF; Finegold DN; Lanes R; Lee PA Children’s Hospital, 3705 Fifth Ave, Pittsburgh,

PA 15213-3417;

USA

NEW ENGL J MED 1990 323113(849-854) Background: Hirsutism in women is a clinical manifestation of excessive production of androgens. The source of the excess androgen may be either the ovaries or the adrenal glands, and distinguishing between these sources may be difftcult. Methods: To determine whether measurements of plasma dehydroepiandrosterone (DHEA) sulfate and ACTH stimulation tests, both widely used in the evaluation of hirsutism in women, provide useful information, we performed both tests in 22 normal women and 31 female patients with hirsutism. The hormones measured in plasma during the ACTH stimulation tests were progesterone. 17-hydroxypregnenolone, 17-hydroxyprogesterone, DHEA, androstenedione, 1I-deoxycortisol, and cortisol. Results: The women with hirsutism were divided into four groups based on their individual responses to ACTH stimulation: patients with a possible 3&hydroxy-Delta5-steroid dehydrogenase deficiency, those with a possible 21-hydroxylase deficiency, those with a possible 1lb-hydroxylase deficiency, and those with no apparent defect in steroidogenesis. The results in 19 patients (61 percent) suggested subtle defects in adrenal steroidogenesis. There was no significant correlation between the basal plasma DHEA sulfate levels and the hormonal response to ACTH, nor were the basal of hormones predictive of the levels after ACTH stimulation. Eleven patients had significantly elevated basal levels of plasma DHEA sulfate; only 5 of these 11 had responses to ACTH suggestive of compromised steroidogenesis. Thirteen patients who had responses suggestive of defective steroidogenesis had DHEA sulfate levels within the normal range. Conclusions: A substantial proportion of women with hirsutism have mild defects in adrenal steroidogenesis, revealed by an ACTH stimulation test, that are indicative of late-onset (nonclassic) congenital adrenal hyperplasia. Measurements of basal steroid levels are not helpful in differentiating among the causes of increased androgen production in such patients and may be misleading. Int J Gynecol Obstet 35