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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

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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 hydro

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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 gon

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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&lsquor; (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

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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 a

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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, b

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19

Tobias, J. H., та T. J. Chambers. "Transient reduction in trabecular bone formation after discontinuation of administration of oestradiol-17β to ovariectomized rats". Journal of Endocrinology 137, № 3 (червень 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 forma

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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 i

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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.

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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 proba

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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 wit

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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

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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 thei

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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 oe

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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

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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, oestrog

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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 ovariectomi

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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 c

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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, a

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