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Journal articles on the topic 'Oestrogen deficiency'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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1

Robinson, Dudley, and Linda Cardozo. "The pathophysiology and management of postmenopausal urogenital oestrogen deficiency." British Menopause Society Journal 7, no. 2 (June 1, 2001): 67–73. http://dx.doi.org/10.1258/136218001100321263.

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Increasing life expectancy has led to an increasingly elderly population and it is now common for women to spend a third of their lives in the oestrogen-deficient postmenopausal state. Oestrogen is known to have an important physiological impact on the female lower urinary tract and the loss of endogenous oestrogen is associated with the development of urogenital atrophy and lower urinary tract dysfunction, offering a rationale for prevention and treatment. Whilst the role of systemic hormone replacement therapy and the use of topical oestrogens in the management of urogenital atrophy has been firmly established, the use of oestrogens in urinary incontinence remains more controversial. Oestrogen therapy alone has been shown to have little effect in management of genuine stress incontinence, although it may have a synergistic role when used with an α-adrenergic agonist. When considering the irritative urinary symptoms associated with urinary urgency and urge incontinence, oestrogen may be beneficialalthough this may simply reflect a reversal of urogenital atrophy rather than a direct effect on the lower urinary tract. Finally, oestrogens would appear to be efficacious in the management of recurrent lower urinary tract infections, with the most convincing evidence being in support of local vaginal administration.
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2

Laron, Z., R. Kauli, and A. Pertzelan. "Clinical evidence on the role of oestrogens in the development of the breasts." Proceedings of the Royal Society of Edinburgh. Section B. Biological Sciences 95 (1989): 13–22. http://dx.doi.org/10.1017/s0269727000010514.

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SynopsisGirls start their puberty including breast development around age 8. Though the best correlation found is that with oestradiol, most girls still have at the onset of breast development oestrogen levels in the normal range for adult males. Therefore, it seems that oestrogen receptor sensitivity plays an important role in breast development. An important insight into the hormonal interplay in breast development was obtained when comparing the effect of exogenous oestrogens in forty-five girls with four different aetiologies of oestrogen deficiency: gonadal dysgenesis (GD). 17-alpha hydroxylase deficiency (17-OHase def), isolated gonadotrophin deficiency (IGnD) and multiple pituitary hormone deficiencies (MPHD). None of the girls had any breast development in the absence of oestrogens. Treatment with oestrogen was given in an identical manner to all. In GD, in whom the hypothalamic-pituitary functions were normal, treatment led to full development of breasts in a relatively short period. In IGnD and MPHD, breast development was incomplete even after years of oestrogen treatment. The conspicuous difference of the hormonal status between GD and IGnD and MPHD is that the latter two groups lack gonadotrophins, while in GD and 17-OHase def. these hormones are pathologically elevated. Thus the gonadotrophins seem to play an important role in mammary gland development. In the girl with 17-OHase def., it was also found that cortisol is necessary for normal breast development. A girl with hyperprolactinaemia due to a microadenoma had delayed puberty including slow breast development. Upon bromocriptine treatment the prolactin fell, the oestrogens rose and puberty including breast development occurred. Patients with Laron-type dwarfism (isolated IGF-I deficiency) have been found to have normal breast development.
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3

Sturdee, D. W. "Clinical symptoms of oestrogen deficiency." Current Obstetrics & Gynaecology 7, no. 4 (December 1997): 190–96. http://dx.doi.org/10.1016/s0957-5847(97)80032-7.

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4

Cattanach, John. "OESTROGEN DEFICIENCY AFTER TUBAL LIGATION." Lancet 325, no. 8433 (April 1985): 847–49. http://dx.doi.org/10.1016/s0140-6736(85)92209-3.

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5

Ginsberg, J., and P. Hardiman. "Oestrogen deficiency and estradiol implants." BMJ 300, no. 6716 (January 6, 1990): 44–45. http://dx.doi.org/10.1136/bmj.300.6716.44-a.

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6

Gangar, K., D. Fraser, M. Whitehead, and M. Cust. "Oestrogen deficiency and oestradiol implants." BMJ 300, no. 6716 (January 6, 1990): 44–45. http://dx.doi.org/10.1136/bmj.300.6716.44-b.

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7

Ginsburg, J., and P. Hardiman. "Oestrogen deficiency and oestradiol implants." BMJ 299, no. 6706 (October 21, 1989): 1031. http://dx.doi.org/10.1136/bmj.299.6706.1031-a.

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8

Gangar, K. F., M. P. Cust, and M. I. Whitehead. "Oestrogen deficiency and oestradiol implants." BMJ 299, no. 6710 (November 18, 1989): 1279–80. http://dx.doi.org/10.1136/bmj.299.6710.1279-c.

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9

Cattanach, John F. "Oestrogen deficiency following pelvic inflammatory disease." Medical Journal of Australia 153, no. 7 (October 1990): 433–34. http://dx.doi.org/10.5694/j.1326-5377.1990.tb125522.x.

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10

Rozenberg, S., C. Antoine, B. Carly, and F. Liebens. "MANAGING OESTROGEN DEFICIENCY AFTER BREAST CANCER." Maturitas 63 (May 2009): S6—S7. http://dx.doi.org/10.1016/s0378-5122(09)70024-6.

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11

Smith, EP, and KS Korach. "Oestrogen receptor deficiency: consequences for growth." Acta Paediatrica 85, s417 (October 1996): 39–43. http://dx.doi.org/10.1111/j.1651-2227.1996.tb14292.x.

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12

Nich, Christophe, Jean Langlois, Arnaud Marchadier, Catherine Vidal, Martine Cohen-Solal, Hervé Petite, and Moussa Hamadouche. "Oestrogen deficiency modulates particle-induced osteolysis." Arthritis Research & Therapy 13, no. 3 (2011): R100. http://dx.doi.org/10.1186/ar3381.

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13

West, Christine P. "GnRH analogues in the treatment of fibroids." Reproductive Medicine Review 2, no. 3 (October 1993): 181–97. http://dx.doi.org/10.1017/s0962279900000703.

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Uterine fibroids are estimated to affect up to 25% of women of reproductive age and are a common cause of morbidity, being associated with menstrual dysfunction, iron deficiency anaemia, pregnancy wastage and subfertility. Their pathogenesis remains unknown but their association with ovarian function and oestrogen production is undisputed and supported by their occurrence only after puberty and the shrinkage observed after the menopause. This oestrogen dependency has recently been exploited therapeutically through investigation of the use of agents that induce a hypo-oestrogenic state, the gonadotrophin-releasing hormone (GnRH) or luteinizing hormone-releasing hormone (LHRH) analogues.
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14

Findlay, J. K., K. Britt, J. B. Kerr, L. O'Donnell, M. E. Jones, A. E. Drummond, and E. R. Simpson. "The road to ovulation: the role of oestrogens." Reproduction, Fertility and Development 13, no. 8 (2001): 543. http://dx.doi.org/10.1071/rd01071.

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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.
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15

Shin, Jae I. "Fowler's syndrome—progesterone deficiency or oestrogen excess?" Nature Reviews Urology 11, no. 10 (August 26, 2014): 553. http://dx.doi.org/10.1038/nrurol.2013.277-c1.

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16

Ho, Pak-Chung, Grace W. K. Tang, and John W. M. Lawton. "Lymphocyte subsets in patients with oestrogen deficiency." Journal of Reproductive Immunology 20, no. 1 (May 1991): 85–91. http://dx.doi.org/10.1016/0165-0378(91)90025-l.

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17

Hall, Wendy L., Gerald Rimbach, and Christine M. Williams. "Isoflavones and endothelial function." Nutrition Research Reviews 18, no. 1 (June 2005): 130–44. http://dx.doi.org/10.1079/nrr2005101.

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AbstractDietary isoflavones are thought to be cardioprotective due to their structural similarity to oestrogen. Oestrogen is believed to have beneficial effects on endothelial function and may be one of the mechanisms by which premenopausal women are protected against CVD. Decreased NO production and endothelial NO synthase activity, and increased endothelin-1 concentrations, impaired lipoprotein metabolism and increased circulating inflammatory factors result from oestrogen deficiency. Oestrogen acts by binding to oestrogen receptors α and β. Isoflavones have been shown to bind with greater affinity to the latter. Oestrogen replacement therapy is no longer thought to be a safe treatment for prevention of CVD; isoflavones are a possible alternative. Limited evidence from human intervention studies suggests that isoflavones may improve endothelial function, but the available data are not conclusive. Animal studies provide stronger support for a role of isoflavones in the vasculature, with increased vasodilation and endothelial NO synthase activity demonstrated. Cellular mechanisms underlying the effects of isoflavones on endothelial cell function are not yet clear. Possible oestrogen receptor-mediated pathways include modulation of gene transcription, and also non-genomic oestrogen receptor-mediated signalling pathways. Putative non-oestrogenic pathways include inhibition of reactive oxygen species production and up regulation of the protein kinase A pathway (increasing NO bioavailability). Further research is needed to unravel effects of isoflavones on intracellular regulation of the endothelial function. Moreover, there is an urgent need for adequately powered, robustly designed human intervention studies in order to clarify the present equivocal findings.
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18

Lean, J. M., J. W. M. Chow, and T. J. Chambers. "The rate of cancellous bone formation falls immediately after ovariectomy in the rat." Journal of Endocrinology 142, no. 1 (July 1994): 119–25. http://dx.doi.org/10.1677/joe.0.1420119.

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Abstract We have recently found that administration of oestradiol-17β (OE2) to rats stimulates trabecular bone formation. It is not known, however, whether oestrogen has a similar action on bone formation rate under physiological circumstances. Oestrogen is known to suppress bone resorption, and oestrogen-deficient states in the rat, as in humans, are associated with an increase in bone resorption that entrains an increase in bone formation. To see if the latter masks a relative reduction in bone formation, due to oestrogen deficiency, we measured bone formation very early after ovariectomy, before the resorption-induced increase in bone formation becomes established. To do this, rats were administered fluorochrome labels before and after ovariectomy, spaced at weekly intervals in the first, and 3-day intervals in the second experiment. In both experiments there was a decrease in indices of bone formation in the labelling interval immediately following ovariectomy such that, using the shorter fluorochrome intervals, the mineral apposition rate fell to 69%, the double-labelled surface to 45%, and the bone formation rate to 36% of sham-ovariectomized levels. The reduction was not sustained in the subsequent label intervals, presumably masked by the increase in bone formation attributable to increased resorption. These results suggest that if bone formation is assessed before this resorption-entrained increase in bone formation occurs, oestrogen deficiency is associated with a reduction in dynamic indices of bone formation. Thus, these experiments suggest that oestrogen stimulates bone formation under physiological circumstances, and that the osteopaenia that follows oestrogen deficiency may be attributable not only to an increase in bone resorption, but also to a relative deficiency in bone formation. Journal of Endocrinology (1994) 142, 119–125
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19

Tobias, J. H., and T. J. Chambers. "Transient reduction in trabecular bone formation after discontinuation of administration of oestradiol-17β to ovariectomized rats." Journal of Endocrinology 137, no. 3 (June 1993): 497–503. http://dx.doi.org/10.1677/joe.0.1370497.

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ABSTRACT While the osteopenia associated with oestrogen deficiency is thought to arise from a relative defect in bone formation with respect to resorption, oestrogen administration itself leads to a decrease, rather than an increase, in bone formation. This decrease in bone formation, which arises from oestrogen's inhibitory effect on bone turnover, presumably masks any underlying tendency of oestrogen treatment towards stimulation of bone formation. To investigate this further, we have examined the early effect of discontinuing the administration of oestradiol-17β (OE2; 40 μg/kg on bone formation indices in ovariectomized 13-week-old rats, before the turnover-induced increase in formation occurs. Histomorphometric indices were assessed at the proximal tibial metaphysis 0, 7, 10, 13 and 16 days following discontinuation of OE2 treatment. Measurements of body weight, uterine weight and longitudinal growth rate confirmed that there were rapid effects of OE2 deficiency on these parameters. We could detect no significant increase in bone resorption, as measured by osteoclast surface and number, until 16 days after ending treatment with OE2; this was coincidental with a reduction in bone volume. Shorter periods of OE2 deficiency were associated with a marked decrease in bone formation, as assessed by dynamic histomorphometric indices. This inhibition of bone formation was largely due to a reduction in double fluorochrome-labelled trabecular surfaces, which were decreased by approximately 70%. We conclude that ending OE2 administration in ovariectomized rats caused a striking decrease in trabecular bone formation, if such indices are assessed prior to the subsequent turnover-induced increase in formation. This suggests that oestrogen treatment in ovariectomized rats is associated with a stimulatory effect on bone formation, in addition to its recognized anti-resorptive action. Journal of Endocrinology (1993) 137, 497–503
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20

Coxam, Véronique. "Prevention of osteopaenia by phyto-oestrogens: animal studies." British Journal of Nutrition 89, S1 (June 2003): S75—S85. http://dx.doi.org/10.1079/bjn2002798.

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Osteoporosis has become a major public health problem. Because the biggest culprit in the process of bone loss is oestrogen deficiency, hormone replacement therapy remains the mainstay for prevention, but prophylaxis by this means is limited. Phyto-oestrogens deserve special mention because emerging data support the suggestion that these weakly oestrogenic compounds, present in plants, may prevent bone loss associated with the menopause and thus represent a potential alternative therapy for a range of hormone-dependent conditions, including postmenopausal symptoms. A substantial body of work in animal models in the past few years has provided convincing data for significant improvements in bone mass and other endpoints following feeding with soya. Thus, phyto-oestrogens appear to have potential promise for maintaining or modestly improving bone mass of human subjects when consumed at optimal dosages. However, we must appreciate the limits of the information reached before extrapolating to man and we need to gather more data before health professionals can actively advocate the increased consumption of soya. Indeed, it will be important further to characterise the physiological effects of phytooestrogens and their margins of safety.
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21

Compston, JE. "Hormone replacement therapy for osteoporosis: clinical and pathophysiological aspects." Reproductive Medicine Review 3, no. 3 (October 1994): 209–24. http://dx.doi.org/10.1017/s0962279900000880.

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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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22

Santos, Isabel, and Steve Clissold. "Urogenital disorders associated with oestrogen deficiency: the role of promestriene as topical oestrogen therapy." Gynecological Endocrinology 26, no. 9 (April 14, 2010): 644–51. http://dx.doi.org/10.3109/09513591003767948.

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23

Cotter, Alice A., Christopher Jewell, and Kevin D. Cashman. "The effect of oestrogen and dietary phyto-oestrogens on transepithelial calcium transport in human intestinal-like Caco-2 cells." British Journal of Nutrition 89, no. 6 (June 2003): 755–65. http://dx.doi.org/10.1079/bjn2003848.

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Recently, dietary phyto-oestrogens (PO) have been suggested as possible alternatives to oestrogen therapy (hormone replacement therapy) as a means of preventing bone loss associated with ovarian hormone deficiency. While PO, which exhibit oestrogen-like activity, act directly on bone cells, their protective effect on bone may be partly due to their ability to enhance Ca absorption. Therefore, the aim of the present study was to investigate the effect of 17β-oestradiol and two commonly consumed soyabean PO (genistein and daidzein) on Ca absorption in the human Caco-2 intestinal-like cell model. Caco-2 cells were seeded onto permeable filter supports and allowed to differentiate into monolayers. On day 21, the Caco-2 monolayers (n 8–18 per treatment), grown in oestrogen-replete or -deplete media, were then exposed to 10 nM-17β-oestradiol, 1 nM-1,25-dihydroxycholecalciferol, or 50 μM-genistein or -daidzein for 24 h. After exposure, transepithelial and transcellular transport of 45Ca and fluorescein transport (a marker of paracellular diffusion) were measured. As expected, 1,25-dihydroxycholecalciferol stimulated Ca absorption in Caco-2 cells, by up-regulating transcellular transport, whereas 17β-oestradiol had no effect on Ca absorption. Unexpectedly, both PO decreased Ca absorption (by about 17–19 % compared with control, P<0·05), by reducing transcellular Ca transport in Caco-2 cells grown in oestrogen-replete media. This inhibitory effect disappeared when monolayers were grown in oestrogen-deplete media. In conclusion, PO at high luminal concentrations either had no effect or reduced Ca absorption in Caco-2 cells, dependent on oestrogen status. The effect of lower concentrations of these compounds needs to be investigated.
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24

Banks, Emily. "From Dogs’ Testicles to Mares’ Urine: The Origins and Contemporary use of Hormonal Therapy for the Menopause." Feminist Review 72, no. 1 (September 2002): 2–25. http://dx.doi.org/10.1057/palgrave.fr.9400059.

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Contemporary hormonal therapy for the menopause has its conceptual origins in the ancient tradition of organotherapy. The popular but pharmacologically inactive precursors of hormonal therapy were developed as part of a resurgence of interest in organotherapy in the 19th century, which coincided with increasing medicalization of the menopause and the view that the ovaries were responsible for the ‘feminine’ identity and wellbeing of women. The subsequent chemical identification of oestrogens allowed the development of pharmacologically active hormonal therapy for the menopause, which was probably first used clinically in the late 1920s. Around this time, emphasis shifted from the ovaries to oestrogen as being responsible for femininity and health, with the menopause and ageing increasingly defined as oestrogen deficiency diseases. Hormonal therapy for the menopause was first used predominantly for women who had a premature menopause. In the 1960s, universal prescription was increasingly promoted as a way of preventing diseases of later life and the perceived ‘defeminization’ of women by menopause. Scientific evidence regarding the risks and benefits of hormonal therapy for the menopause has been accruing over the last 70 years; its interpretation has been affected by background beliefs regarding the effects of oestrogen and the menopause on women.
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25

Coxam, Véronique. "Phyto-oestrogens and bone health." Proceedings of the Nutrition Society 67, no. 2 (April 15, 2008): 184–95. http://dx.doi.org/10.1017/s0029665108007027.

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As oestrogen deficiency is the main cause in the pathogenesis of osteoporosis hormone-replacement therapy remains the mainstay for prevention. However, prophylaxis by hormone-replacement therapy is limited. Phyto-oestrogens, which are weakly-oestrogenic compounds present in plants, deserve particular mention because emerging data support the suggestion that they may prevent bone loss associated with the menopause. In the past few years extensive research using animal models has provided convincing data to indicate a significant improvement in bone mass or other end points following feeding with soyabean. Moreover, observational studies relate the lower incidence of osteoporosis among women in the Eastern world to a diet rich in phyto-oestrogens. However, it is not valid to extrapolate to the Western situation. The varied clinical trials that have been published suggest that isoflavones reduce bone loss in women in the early period post menopause, but a definitive result requires more investigations of the effect of phyto-oestrogens on bone health that have substantial sample size and are of long duration. In addition, the clinical efficacy of soya foods in preventing osteopenia depends on their intestinal metabolism. Thus, phyto-oestrogens are a source for putative innovative dietary health intervention for post-menopausal women. However, more data are necessary, particularly in relation to their effect on the risk of fracture.
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26

Di Naro, Edoardo, Matteo Loverro, Ilaria Converti, Maria Teresa Loverro, Elisabetta Ferrara, and Biagio Rapone. "The Effect of Menopause Hypoestrogenism on Osteogenic Differentiation of Periodontal Ligament Cells (PDLC) and Stem Cells (PDLCs): A Systematic Review." Healthcare 9, no. 5 (May 12, 2021): 572. http://dx.doi.org/10.3390/healthcare9050572.

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(1) Background: Menopause is a physiological condition typified by drastic hormonal changes, and the effects of this transition have long-term significant clinical implications on the general health, including symptoms or physical changes. In menopausal women, the periodontium can be affected directly or through neural mechanism by oestrogen (E2) deficiency. The majority of the biological effects of E2 are modulated via both oestrogen receptor-α (ERα) and oestrogen receptor- β (ERβ). There is evidence that hypoestrogenism has a substantial impact on the aetiology, manifestation and severity of periodontitis, via the regulation of the expression of osteoprogesterin and RANKL in human periodontal ligament cells through ERβ. However, the mechanistic understanding of oestrogen in periodontal status has been partially clarified. The aim of this paper was to synopsize the recent scientific evidence concerning the link between the menopause and periodontitis, through the investigation of physio-pathological impact of the oestrogen deficiency on osteogenic differentiation of PDLSCs and PDLSC, as well as the dynamic change of ERα and ERβ. (2) Methods: Search was conducted for significant studies by exploring electronic PubMed and EMBASE databases, and it was independently performed by two researchers. All studies on the impact of oestrogen level on alveolar bone resorption were searched from 2005 to July 2020. Data selection was in concordance with PRISMA guidelines. (3) Results: Eight studies met the criteria and were included in this systematic review. All studies reported that oestrogen deficiency impairs the osteogenic and osteoblastic differentiation of PDL cells and oestrogen affects the bone formation capacity of cells. Seven studies were conducted on animal samples, divided into two groups: the OVX animals and animals who received the sham operation. (4) Conclusions: There is a multitude of data available showing the influence of menopause on periodontal status. However, the evidence of this line to investigation needs more research and could help explain the physiological linkage between menopause state and periodontal disease.
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27

Goulding, A., and E. Gold. "Norethindrone acetate only partially protects the skeleton of rats treated with the LHRH agonist buserelin from oestrogen-deficiency osteopaenia." Journal of Endocrinology 137, no. 1 (April 1993): 27–33. http://dx.doi.org/10.1677/joe.0.1370027.

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ABSTRACT In women with endometriosis there is concern that therapeutic use of LH-releasing hormone (LHRH) analogues, to lower ovarian oestrogen production and control endometrial hyperplasia, leads to unwanted oestrogen-deficiency bone loss. We have developed an animal model of this LHRH-mediated oestrogen-deficiency bone loss in the rat, using buserelin. The aim was to use this model to determine whether the progestogen, norethindrone acetate, could counter oestrogen-deficiency bone loss associated with prolonged treatment with the LHRH agonist buserelin. Four groups of animals which had their bones labelled with 45Ca were studied for 4 weeks: group A, control; group B, buserelin treated; group C, norethindrone acetate treated; group D, norethindrone acetate + buserelin treated. Buserelin was given daily (19·2 pmol/kg body wt); norethindrone was given orally three times / week (1·47 μmol/kg body wt). Bone resorption was monitored by measuring the urinary excretion of hydroxyproline and 45Ca and bone 45Ca content. Buserelin-treated rats developed similarly depressed plasma oestradiol-17β values in the presence and absence of progestogen, and both groups given buserelin had significantly smaller uteri than controls or rats given norethindrone without buserelin. However, norethindrone did not prevent buserelin-mediated increases in bone resorption. At the end of the study total body calcium values (mean ± s.d.) in the four groups were (mg) respectively; 2594 ± 123; 2260 ± 92 (P < 0·001 compared with controls); 2616 ± 221; 2415 ± 130 (P < 0·02 compared with controls). Rats given norethindrone and buserelin in combination had higher values (P < 0·02) than animals given buserelin alone, but significantly less total body calcium than controls (P < 0·02). We conclude that progestogen confers partial, but not complete, protection of the skeleton of buserelin-treated rats from oestrogen-deficiency bone loss. Journal of Endocrinology (1993) 137, 27–33
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28

Beardsworth, S. A., and D. W. Purdie. "Selective Oestrogen Receptor Modulators." British Menopause Society Journal 4, no. 1 (March 1998): 30–32. http://dx.doi.org/10.1177/136218079800400109.

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Postmenopausal oestrogen deficiency causes a wide spectrum of adverse consequences that may be prevented or reversed by hormone replacement therapy (HRT). However, acceptance of HRT and then long term continuation is poor. Many reasons are given for this poor acceptance but the two most important factors are the return of withdrawal bleeding and the fear of breast cancer. Thus an ideal therapeutic agent should produce the beneficial effects of oestrogen in non-reproductive tissue such as bone, without proliferative effects on breast and uterine tissue. Compounds that possess tissue specific oestrogen agonist and antagonist properties are described as selective oestrogen receptor modulators, or SERMs. A number of SERMs, including raloxifene and idoxifene, are currently undergoing phase III clinical trials with encouraging results. Their imminent use should provide a great advance in the management of the menopause.
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29

O'Loughlin, Peter D., and Howard A. Morris. "Oestrogen deficiency impairs intestinal calcium absorption in the rat." Journal of Physiology 511, no. 1 (August 1998): 313–22. http://dx.doi.org/10.1111/j.1469-7793.1998.313bi.x.

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30

ROSANO, G. M. C., P. COLLINS, J. C. KASKI, D. C. LINDSAY, P. M. SARREL, and P. A. POOLE-WILSON. "Syndrome X in women is associated with oestrogen deficiency." European Heart Journal 16, no. 5 (May 1995): 610–14. http://dx.doi.org/10.1093/oxfordjournals.eurheartj.a060963.

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31

Tobias, J. H., and T. J. Chambers. "Symptoms of oestrogen deficiency in women with oestradiol implants." BMJ 299, no. 6703 (September 30, 1989): 854. http://dx.doi.org/10.1136/bmj.299.6703.854-b.

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32

Wardle, P., and R. Fox. "Symptoms of oestrogen deficiency in women with oestradiol implants." BMJ 299, no. 6707 (October 28, 1989): 1102. http://dx.doi.org/10.1136/bmj.299.6707.1102.

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33

Studd, J., A. Henderson, T. Garnett, N. Watson, and M. Savvas. "Symptoms of oestrogen deficiency in women with oestradiol implants." BMJ 299, no. 6712 (December 2, 1989): 1400–1401. http://dx.doi.org/10.1136/bmj.299.6712.1400-b.

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34

Torricelli, P., F. Veronesi, S. Pagani, N. Maffulli, S. Masiero, A. Frizziero, and M. Fini. "In vitro tenocyte metabolism in aging and oestrogen deficiency." AGE 35, no. 6 (December 29, 2012): 2125–36. http://dx.doi.org/10.1007/s11357-012-9500-0.

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35

Simpson, Evan, and Richard J. Santen. "Celebrating 75 years of oestradiol." Journal of Molecular Endocrinology 55, no. 3 (October 5, 2015): T1—T20. http://dx.doi.org/10.1530/jme-15-0128.

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Oestrogens exert important effects on the reproductive as well as many other organ systems in both men and women. The history of the discovery of oestrogens, the mechanisms of their synthesis, and their therapeutic applications are very important components of the fabric of endocrinology. These aspects provide the rationale for highlighting several key components of this story. Two investigators, Edward Doisy and Alfred Butenandt, purified and crystalized oestrone nearly simultaneously in 1929, and Doisy later discovered oestriol and oestradiol. Butenandt won the Nobel Prize for this work and Doisy's had to await his purification of vitamin K. Early investigators quickly recognized that oestrogens must be synthesized from androgens and later investigators called this process aromatization. The aromatase enzyme was then characterized, its mechanism determined, and its structure identified after successful crystallization. With the development of knock-out methodology, the precise effects of oestrogen in males and females were defined and clinical syndromes of deficiency and excess described. Their discovery ultimately led to the development of oral contraceptives, treatment of menopausal symptoms, therapies for breast cancer, and induction of fertility, among others. The history of the use of oestrogens for postmenopausal women to relieve symptoms has been characterized by cyclic periods of enthusiasm and concern. The individuals involved in these studies, the innovative thinking required, and the detailed understanding made possible by evolving biologic and molecular techniques provide many lessons for current endocrinologists.
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36

Kawamoto, S., S. Ejiri, E. Nagaoka, and H. Ozawa. "Effects of oestrogen deficiency on osteoclastogenesis in the rat periodontium." Archives of Oral Biology 47, no. 1 (January 2002): 67–73. http://dx.doi.org/10.1016/s0003-9969(01)00086-3.

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37

Frizziero, A., F. Vittadini, G. Gasparre, and S. Masiero. "Impact of oestrogen deficiency and aging on tendon: concise review." Muscle Ligaments and Tendons Journal 04, no. 03 (January 2019): 324. http://dx.doi.org/10.32098/mltj.03.2014.11.

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38

Yang, J., SM Pham, and DL Crabbe. "Effects of oestrogen deficiency on rat mandibular and tibial microarchitecture." Dentomaxillofacial Radiology 32, no. 4 (July 2003): 247–51. http://dx.doi.org/10.1259/dmfr/12560890.

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39

Marsden, Jo. "Treatment of oestrogen deficiency in women with previous breast cancer." British Menopause Society Journal 6, no. 2_suppl (September 2000): 18–19. http://dx.doi.org/10.1258/136218000322579164.

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40

Kaski, J. C. "Cardiac syndrome X in women: the role of oestrogen deficiency." Heart 92, suppl_3 (May 1, 2006): iii5—iii9. http://dx.doi.org/10.1136/hrt.2005.070318.

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41

Cowell, CT, HJ Woodhead, AF Kemp, JN Briody, and R. Howman-Giles. "Skeletal changes associated with oestrogen deficiency in a young male." Bone 27, no. 4 (October 2000): 43. http://dx.doi.org/10.1016/s8756-3282(00)80151-9.

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42

Balestrieri, Antonio, Marco Faustini-Fustini, Vincenzo Rochira, and Cesare Carani. "Clinical implications and management of oestrogen deficiency in the male." Clinical Endocrinology 54, no. 4 (April 2001): 431–32. http://dx.doi.org/10.1046/j.1365-2265.2001.01227.x.

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43

Brasil, S. C., R. M. M. Santos, A. Fernandes, F. R. F. Alves, F. R. Pires, J. F. Siqueira, and L. Armada. "Influence of oestrogen deficiency on the development of apical periodontitis." International Endodontic Journal 50, no. 2 (February 17, 2016): 161–66. http://dx.doi.org/10.1111/iej.12612.

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44

de Lignières, B., and E. A. MacGregor. "Risks and Benefits of Hormone Replacement Therapy." Cephalalgia 20, no. 3 (April 2000): 164–69. http://dx.doi.org/10.1046/j.1468-2982.2000.00037.x.

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Menopause, the permanent cessation of menstruation, is due to ovarian failure, which may lead to oestrogen deficiency diseases, particularly osteoporosis, cardiovascular disease and cerebrovascular disease. Mortality and morbidity caused by these conditions can be modified by using hormone replacement therapy, but the benefits of this therapy must be weighed against the increased risk of breast cancer and the symptomatic side-effects the treatment may cause. The combination of transdermal oestrogen and natural progesterone offers the most favourable risk-to-benefit profile.
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45

Bunce, G. E., and Mahmood Vessal. "Effect of zinc and/or pyridoxine deficiency upon oestrogen retention and oestrogen receptor distribution in the rat uterus." Journal of Steroid Biochemistry 26, no. 3 (March 1987): 303–8. http://dx.doi.org/10.1016/0022-4731(87)90093-8.

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46

Schupf, Nicole. "Genetic and host factors for dementia in Down's syndrome." British Journal of Psychiatry 180, no. 5 (May 2002): 405–10. http://dx.doi.org/10.1192/bjp.180.5.405.

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BackgroundThe high risk for dementia in adults with Down's syndrome has been attributed to triplication and overexpression of the gene for amyloid precursor protein (APP). But the wide variation in age at onset must be due to other risk factors.AimsTo identify factors which influence age at onset of dementia in Down's syndrome.MethodStudies of factors which influence formation of beta-amyloid (Aβ) were reviewed, including atypical karyotypes, susceptibility genotypes, gender and oestrogen deficiency, and individual differences in Aβ peptide levels.ResultsThe apolipoprotein E $4 allele, oestrogen deficiency and high levels of Aβl-42 peptide are associated with earlier onset of dementia, while atypical karyotypes and the apolipoprotein E $2 allele are associated with reduced mortality and reduced risk of dementia.ConclusionsFactors which influence Aβ levels, rather than overexpression of APP, may account for the differences in age at onset of dementia in Down's syndrome.
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47

Hoyland, Judith A., Charlotte Baris, Lindsay Wood, Pauline Baird, Peter L. Selby, Anthony J. Freemont, and Isobel P. Braidman. "Effect of ovarian steroid deficiency on oestrogen receptor ? expression in bone." Journal of Pathology 188, no. 3 (July 1999): 294–303. http://dx.doi.org/10.1002/(sici)1096-9896(199907)188:3<294::aid-path361>3.0.co;2-y.

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48

Soelaiman, Ima Nirwana, Wang Ming, Roshayati Abu Bakar, Nursyahrina Atiqah Hashnan, Hanif Mohd Ali, Norazlina Mohamed, Norliza Muhammad, and Ahmad Nazrun Shuid. "Palm Tocotrienol Supplementation Enhanced Bone Formation in Oestrogen-Deficient Rats." International Journal of Endocrinology 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/532862.

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Postmenopausal osteoporosis is the commonest cause of osteoporosis. It is associated with increased free radical activity induced by the oestrogen-deficient state. Therefore, supplementation with palm-oil-derived tocotrienols, a potent antioxidant, should be able to prevent this bone loss. Our earlier studies have shown that tocotrienol was able to prevent and even reverse osteoporosis due to various factors, including oestrogen deficiency. In this study we compared the effects of supplementation with palm tocotrienol mixture or calcium on bone biomarkers and bone formation rate in ovariectomised (oestrogen-deficient) female rats. Our results showed that palm tocotrienols significantly increased bone formation in oestrogen-deficient rats, seen by increased double-labeled surface (dLS/Bs), reduced single-labeled surface (sLS/BS), increased mineralizing surface (MS/BS), increased mineral apposition rate (MAR), and an overall increase in bone formation rate (BFR/BS). These effects were not seen in the group supplemented with calcium. However, no significant changes were seen in the serum levels of the bone biomarkers, osteocalcin, and cross-linked C-telopeptide of type I collagen, CTX. In conclusion, palm tocotrienol is more effective than calcium in preventing oestrogen-deficient bone loss. Further studies are needed to determine the potential of tocotrienol as an antiosteoporotic agent.
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49

Rachon, D., J. Mysliwska, K. Suchecka-Rachon, J. Wieckiewicz, and A. Mysliwski. "Effects of oestrogen deprivation on interleukin-6 production by peripheral blood mononuclear cells of postmenopausal women." Journal of Endocrinology 172, no. 2 (February 1, 2002): 387–95. http://dx.doi.org/10.1677/joe.0.1720387.

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Various hormones can influence the expression of interleukin-6 (IL-6) and oestrogens are the most extensively studied. There is, however, controversy about the nature of the IL-6 secreted by human cells and its regulation by 17beta-oestradiol. The aim of this work was to clarify whether oestrogen deprivation after menopause may contribute to an enhanced IL-6 production by peripheral blood mononuclear cells (PBMC) in postmenopausal women. Twenty-two healthy postmenopausal women, age range 45-63 years, with clinical symptoms of oestrogen deficiency were enrolled in the study. The control group consisted of 16 healthy young women, age range 22-31 years, with regular menses and who were not taking oral contraceptives. Levels of IL-6 in the sera and PBMC culture supernatants were measured by the biological B9 cell-proliferation assay and expression of the IL-6 gene in non-stimulated PBMC was detected by RT-PCR. The effect of 17beta-oestradiol on spontaneous IL-6 production by the PBMC of postmenopausal women was also studied in vitro and in vivo. Seventeen out of the twenty-two postmenopausal women were given hormonal replacement therapy of 50 microg 17beta-oestradiol/day transdermally and the spontaneous production of IL-6 by the PBMC was analysed after 6 and 12 months of treatment. The postmenopausal women had significantly higher serum levels of IL-6 than the young controls. The spontaneous production of IL-6 by non-stimulated PBMC into the culture supernatants was also significantly higher in the postmenopausal women compared with the young. We also found that IL-6 gene expression was present in the non-stimulated PBMC isolated directly from the venous blood of the majority of the postmenopausal women. Women with IL-6 gene expression in the non-stimulated PBMC had significantly lower serum levels of 17beta-oestradiol compared with those where the IL-6 gene was not expressed in the PBMC. Our in vitro experiments showed that 17beta-oestradiol at concentrations of 10(-9) M and 10(-10) M decreased spontaneous IL-6 production by the PBMC of postmenopausal women. In vivo treatment with 17beta-oestradiol transdermally also significantly decreased spontaneous IL-6 production by the PBMC of postmenopausal women after 12 months of the therapy. Our results indicate that oestrogen deprivation after menopause may enhance IL-6 production by the PBMC of postmenopausal women. We suspect that the late complications of oestrogen deficiency, such as osteoporosis, coronary heart disease and Alzheimer's disease, may be mediated by an exaggerated production of IL-6 - a cytokine which seems to play a pivotal role in the pathogenesis of these age-related diseases.
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50

Fiad, Tarek M., Sean K. Cunningham, and T. Joseph McKenna. "Role of progesterone deficiency in the development of luteinizing hormone and androgen abnormalities in polycystic ovary syndrome." European Journal of Endocrinology 135, no. 3 (September 1996): 335–39. http://dx.doi.org/10.1530/eje.0.1350335.

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Fiad TM, Cunningham SK, McKenna TJ. Role of progesterone deficiency in the development of luteinizing hormone and androgen abnormalities in polycystic ovary syndrome. Eur J Endocrinol 1996;135:335–9. ISSN 0804–4643 The aetiology of polycystic ovary syndrome (PCOS) is unknown. It is uniquely characterized by oligomenorrhoea or amenorrhoea associated with normal or high oestrogen levels. This prospective clinical study was designed to examine the possible role of the lack of cyclical exposure to progesterone in the development of gonadotrophin and androgen abnormalities in PCOS. Gonadotrophin, androgen and oestrogen levels were measured in 15 PCOS patients and 10 normal subjects untreated and following treatment with the progestogen medroxyprogesterone acetate (MPA). When compared to control subjects, PCOS patients had significantly higher luteinizing hormone (LH) pulse height, pulse amplitude, integrated LH levels, LH response to gonadotrophin-releasing hormone (GnRH) and LH/FSH ratio; LH pulse frequency was similar in the two groups. In addition, the testosterone/sex hormone binding globulin ratio (T/SHBG), androstenedione and oestrone concentrations in the plasma were significantly higher in PCOS than in control subjects. When PCOS patients were treated with MPA for 5 days, there were significant decreases (p < 0.02–0.001) to values no longer different from normal: from 8.7 ± 1.2 to 5.6 ± 0.8 IU/l for integrated LH levels (untreated and MPA-treated PCOS); from 31.2 ±3.5 to 12.9 ±1.5 IU/l for LH response to GnRH; from 2.4 ± 0.26 to 1.3 ± 0.2 for LH/FSH ratio; and from 10.4 ± 0.63 to 8.5 ± for androstenedione. Significant decreases (p < 0.05–0.005) to values that still remained significantly higher than in normal subjects occurred for: LH pulse height, 11.05 ± 1.3 to 6.88 ± 0.79 IU/l (untreated and MPA-treated PCOS); LH pulse amplitude, 2.8 ± 0.5 to 1.8 ± 0.2 IU/l; total testosterone, 2.5 ± 0.2 to 2.0± 0.2 nmol/l; T/SHBG ratio, 14.1 ± 1.7 to 11 ± 1.5; and oestrone, 265 ± 24 to 208 ± 29 pmol/l. These results are consistent with the concept that ovulation failure and progesterone deficiency play a facilitatory role in the development of the hypothalamic-pituitary abnormality giving rise to disordered LH secretion in PCOS. TJ McKenna. Department of Investigative Endocrinology. St Vincent's Hospital, Elm Park. Dublin 4, Ireland
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