Urogenital disorders associated with oestrogen deficiency: the role of promestriene as topical oestrogen therapy

2010 ◽  
Vol 26 (9) ◽  
pp. 644-651 ◽  
Author(s):  
Isabel Santos ◽  
Steve Clissold
Keyword(s):  
Oestrogen Therapy ◽  
Oestrogen Deficiency

FEEDBACK CONTROL OF FSH IN THE MALE: ROLE OF OESTROGEN

1973 ◽  
Vol 74 (3) ◽  
pp. 449-460 ◽  
Author(s):  
Patrick C. Walsh ◽  
Ronald S. Swerdloff ◽  
William D. Odell
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Oestrogen Therapy ◽  
Serum Concentrations ◽  
Elderly Men ◽  
Normal Range ◽  
Oestrogen Treatment ◽  
Serum Lh ◽  
Higher Doses

ABSTRACT Serum follicle stimulating hormone (FSH) and luteinizing hormone (LH) were measured by radioimmunoassay in a group of elderly men following castration and oestrogen therapy. Prior to orchiectomy, mean serum concentrations of LH and FSH were within the normal range. Two days following castration, serum LH concentrations increased in all eight patients; higher levels of LH were subsequently measured in all but one patient after periods of time ranging from 49 to 210 days. Serum FSH levels, measured in three patients following castration, increased in a pattern parallel to LH changes. Ethinyl oestradiol (EOe) in doses ranging from 5 to 300 μg/day was administered to ten men who had been castrated 3 to 72 months earlier. Oestrogen treatment suppressed both LH and FSH in a parellel manner in nine of ten patients. LH was first suppressed to intact levels in one of eight patients treated with 20 μg/day of EOe, in two of six patients treated with 50 μg/day, and in one patient by 80 μg/day. FSH was not suppressed to precastration levels until 50 μg/day of EOe was administered; this dose suppressed three of six patients. Higher doses of EOe (150–300 μg/day) suppressed both LH and FSH to levels below the sensitivity of the assay. These data fail to demonstrate any differential effect of oestrogen on LH and FSH release.

scholarly journals Factors influencing bone loss in anorexia nervosa: assessment and therapeutic options

RMD Open ◽  
2019 ◽  
Vol 5 (2) ◽  
pp. e001009 ◽  
Author(s):  
Isabelle Legroux ◽  
Bernard Cortet
Keyword(s):  
Anorexia Nervosa ◽  
Bone Loss ◽  
Mineral Density ◽  
Related Factors ◽  
Oestrogen Treatment ◽  
Oestrogen Deficiency ◽  
Resumption Of Menses ◽  
Main Factor

Decreased mineral density is one of the major complications of anorexia nervosa. The phenomenon is even more pronounced when the disease occurs during adolescence and when the duration of amenorrhoea is long. The mechanisms underlying bone loss in anorexia are complex. Oestrogen deficiency has long been considered as the main factor, but cannot explain the phenomenon on its own. The essential role of nutrition-related factors—especially leptin and adiponectin—has been reported in recent studies. Therapeutic strategies to mitigate bone involvement in anorexia are still a matter for debate. Although resumption of menses and weight recovery appear to be essential, they are not always accompanied by a total reversal of bone loss. There are no studies in the literature demonstrating that oestrogen treatment is effective, and the best results seem to have been obtained with agents that induce bone formation—such as IGF-1—especially when associated with oestrogen. As such, bone management in anorexia remains difficult, hence, the importance of early detection and multidisciplinary follow-up.

The road to ovulation: the role of oestrogens

2001 ◽  
Vol 13 (8) ◽  
pp. 543 ◽  
Author(s):  
J. K. Findlay ◽  
K. Britt ◽  
J. B. Kerr ◽  
L. O'Donnell ◽  
M. E. Jones ◽  
...  
Keyword(s):  
Somatic Cells ◽  
Follicular Cells ◽  
Targeted Disruption ◽  
Phenotypic Differentiation ◽  
The Road ◽  
Oestrogen Deficiency ◽  
Proliferation And Differentiation ◽  
Recent Developments ◽  
Follicular Dynamics

Oestrogens have been known for many years to have a direct influence on folliculogenesis. Oestradiol-17β‚ (E2) and its analogues have both proliferative and differentiative effects on somatic cells of follicles. Nevertheless, definitive proof of an obligatory role for oestrogen in folliculogenesis and elucidation of the mechanisms subserving its different actions in follicular cells remains elusive. Several recent developments permit a re-examination of the roles and actions of E2 in the follicle. They are: (i) the discovery of a second form of the oestrogen receptor, ERβ; (ii) the advent of genetically modified mice with deletions in the ERα(αERKO) ERβ‚ BERKO) and the double ER deletions (αβERKO); and (iii) a mouse model of oestrogen deficiency (ArKO) by targeted disruption of the cyp 19gene encoding the aromatase enzyme. Recent information derived from these models is reviewed to re-assess the roles and actions of oestrogens in follicular dynamics and the phenotypic differentiation of ovarian somatic cells in the ovary. The data demonstrate that oestrogen is obligatory for normal folliculogenesis and that the phenotype of the ovarian somatic cells depends on the steroid milieu. The ArKO mouse provides a model to test the roles of the respective ERs in proliferation and differentiation using specific agonists and antagonists, and to study regulation of the differentiation of ovarian and testicular somatic cells.

scholarly journals Should psychiatrists be prescribing oestrogen therapy to their female patients?

2013 ◽  
Vol 202 (1) ◽  
pp. 9-13 ◽  
Author(s):  
Michael C. Craig
Keyword(s):  
Neuropsychiatric Disorders ◽  
Oestrogen Therapy ◽  
Female Patients ◽  
Putative Role

SummarySome studies have indicated that oestrogen therapy may be beneficial in the treatment of a number of neuropsychiatric disorders. However, it has been suggested that psychiatrists fail to prescribe oestrogen therapy to their patients, as they are ‘not aware of or ‘do not believe’ studies supporting their use. This paper reappraises the putative role of hormone treatments, particularly oestrogen therapy, in psychiatry.

Direct evidence of hypertension and the possible role of post-menopause oestrogen deficiency in the pathogenesis of berry aneurysms

1985 ◽  
Vol 232 (2) ◽  
pp. 67-72 ◽  
Author(s):  
T. Stober ◽  
S. Sen ◽  
T. Anst�tt ◽  
G. Freier ◽  
K. Schimrigk
Keyword(s):  
Direct Evidence ◽  
Oestrogen Deficiency ◽  
Post Menopause

Hormone replacement therapy for osteoporosis: clinical and pathophysiological aspects

1994 ◽  
Vol 3 (3) ◽  
pp. 209-224 ◽  
Author(s):  
JE Compston
Keyword(s):  
Hormone Replacement Therapy ◽  
Replacement Therapy ◽  
Hormone Replacement ◽  
Pathogenetic Role ◽  
Duration Of Therapy ◽  
Risks And Benefits ◽  
Oestrogen Deficiency ◽  
Reduce Fracture Risk

The pathogenetic role of oestrogen deficiency in osteoporosis was first postulated by Fuller Albright in 1941 and has subsequently become well established. Hormone replacement therapy prevents menopausal bone loss and is the only treatment which has convincingly been shown to reduce fracture risk at both the spine and hip. The mechanisms by which oestrogens affect bone, however, are poorly understood and many aspects of treatment remain ill-defined, in particular with respect to the duration of therapy and its long-term risks and benefits.

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