The growing number of middleaged and older people includes a concomitant continuous increase in the number

The growing number of middleaged and older people includes a concomitant continuous increase in the number of women who live most of their lives in a state hypoestrogenic. More and more women can expect to live another 79 years and experiencing the consequences of loss of gonadal hormones. br Although the time spent in menopause (currently up to one third of the life cycle) has increased with the phenomenon of increased longevity, the actual age of menopause around 5051 years has not changed since antiquity. The women of ancient Greece experienced menopause at the same age as modern women with the transition to menopause symptom usually starts at around 45.547.5 years.1, 2 factors that lower the age of menopause are few and physiological are smoking, 2 hysterectomy, carrier of Fragile X, autoimmune disorders, and living at high altitude. br menopause results for the loss of ovarian sensitivity to gonadotropin stimulation, which is directly related to follicular decline and dysfunction. The oocytes from ovaries undergo atresia throughout a womans life cycle, and both the quantity and quality of follicles undergo a critical decline of approximately 2025 years after menarche. Thus, the variable menstrual cycle length during perimenopause may be due to anovulation or irregular maturation of the follicles. Hormonal fluctuations can not be responsible of any irregular bleeding during this period, therefore, pelvic pathology (eg, uterine fibroids, uterine polyps, endometrial hyperplasia, endometrial cancer), which becomes more frequent during this time, they must be excluded by endometrial sampling, such as endometrial biopsy (EMB) or dilatation and curettage (DC). br During the fifth decade of life, many women are lulled into a false sense of security, thinking that they are infertile because they are so close to menopause. Although declines in fertility, pregnancy can still occur, as evidenced by a relatively high rate of unwanted pregnancies in women aged 4044 years. In fact, the number of unwanted pregnancies in this age group has increased over the last decade, 3, which highlights the need for continuous contraceptive practice in heterosexual couples. br A shorter duration of the menstrual cycle is the most common change in menstrual cyclicity that occurs during the perimenopausal period in women who have no pelvic pathology and who remain ovulatory.4 the follicular phase of the menstrual cycle is shortened due to the decreased number of functional follicles. Because these follicles, which are stimulated by follicle stimulating hormone (FSH) in the first part of the menstrual cycle have been reduced in number, less recruitment of oocytes is produced and the follicular phase is shortened accordingly. However, once ovulation occurs, the luteal phase remains fairly constant, at 14 days. br Over time, as the follicles of aging become more resistant to gonadotropin stimulation, movement of FSH and luteinizing hormone (LH) levels increase. High levels of FSH and LH lead to stimulation of the ovarian stroma, resulting in increased levels of estrone and decreased levels of estradiol. Also falling inhibin levels during this time due to the negative feedback of elevated FSH levels.5 With the onset of menopause and the loss of function of the follicles, the most significant change in hormonal profile is the dramatic decrease circulating levels of estrogen. Without a follicular source, the highest proportion of postmenopausal estrogen secretion is derived from the ovarian stroma and adrenal androstenedione that is aromatized to estrone in the peripheral circulation. Testosterone levels also decrease with menopause, 6, but this decrease is not as marked as the decline in the 17estradiol.7 br With the cessation of ovulation, estrogen production by aromatization of androgens in the stroma Ovarian and extragonadal production sites continue, without opposition, the production of progesterone by the corpus luteum. Perimenopausal and menopausal women are therefore often exposed to unopposed estrogen for long periods, which can lead to endometrial hyperplasia, a precursor to endometrial cancer. Estradiol levels decrease significantly due to loss of follicular production with menopause and menopause, but estrone, androstenedione that is aromatized from sources nonfollicular still occurs and is the main source of circulating estrogen in postmenopausal women . br Androgen aromatization to estrogens can occur in adipose tissue, muscle, liver, bone, bone marrow, fibroblasts, and hair roots.6 Because most of the conversion of androgens to estrogens occurs in adipose tissue, is often considered Women who are obese, have more circulating estrogen should have fewer complaints of vasomotor symptoms. However, this is not always the case, and vasomotor symptoms of menopause can be as frequent and severe in overweight women and in lean women. br The clinical indication that menopause has occurred is the measure of an elevated FSH level. The FSH level increases more than the level of LH due to reduced renal clearance of FSH compared with LH. A little high or borderline levels of FSH in perimenopausal women menopause can not be a reliable indicator of menopause due to the wide range of FSH and LH levels in response to increased gonadotropinreleasing hormone (GnRH) the sensitivity of the hypothalamus and increased to GnRH. Measurement of FSH and LH levels again in the perimenopausal patient after 23 months is helpful to establish whether women are progressing through menopause. Women with elevated, but not postmenopausal FSH levels are still at risk of pregnancy and contraception should still be used until the levels of FSH remain in the postmenopausal range. br Excellent resources for patient education, visit eMedicine Women's Health Center and Bone Health Center. Also, see the eMedicine's patient education menopause, female sexual problems, and hormone replacement and osteoporosis. br Throughout the time that the physiological changes in response to gonadotropins and their secretions are produced, with resulting wide variation in hormone levels, women often experience several symptoms that are collectively termed the climacteric syndrome. Typical climacteric symptoms include hot flashes or flushes, insomnia, weight gain and bloating, mood swings, irregular menses, mastodynia, and headache. As noted, the length of time during which menopause occurs is very variable, symptoms may begin during perimenopause and continue for 510 years after menopause. br irregular ovarian function and considerable fluctuation in estrogen, not estrogen deficiency causes climacteric symptoms during menopause, so hormone fluctuations stop using oral contraceptives (OCs) and hormone therapy (HT) relieves climacteric symptoms. Ovarian function and menstruation therefore generally does not resume if the woman has experienced a year of amenorrhea. The cessation of menstruation in women of appropriate age is still the best confirmation of the loss of follicular function. As advanced years postmenopause, with a consequent loss of ovarian response to gonadotropins, associated symptoms of menopause are also reduced. br The effects of gonadal hormone depletion may be evident on pelvic exam, with changes seen in perimenopause and in some women. The reproductive organs of women of reproductive age are different in appearance from those of a woman who was the menopause. With the loss of estrogen, the vaginal lining becomes red due to thinning of the epithelial layer and increased visibility of small blood vessels in the area. Later, as subsequent atrophy of the vaginal epithelium, the surface becomes pale due to a reduced number of capillaries. A decrease in urine pH to a change in the bacterial flora can cause itching and malodorous discharge. Rugation also decreases, and the vaginal wall becomes soft. These changes often result in dyspareunia insertion and, for many women ultimately lead to sexual abstinence if not treated. br Within the pelvis, the uterus becomes smaller. Fibroids, if any, are less symptomatic, sometimes decline to the point where it can not be felt on pelvic exam. Endometriosis and adenomyosis are also relieved with the onset of menopause, and many patients with pelvic pain finally achieve permanent pain relief. br The ovary of menopause and decreases in size and not palpable during gynecological examinations. A palpable ovary in orders for a pelvic exam a full assessment of all menopausal or postmenopausal women. br For older women, a general loss of pelvic tone also occurs, and this may manifest as organ prolapse or urinary reproductive tract (see Uterine prolapse and prolapse. Vaginal Pressure, pressure lower back, or bulge in the vaginal opening is common in women with prolapse. On examination, cystocele prolapse, rectocele, and uterine cancer are obvious, as causes of these symptoms. br Atrophic cystitis, when present, can simulate a urinary tract infection. Report Women's symptoms of urinary frequency, urgency and incontinence. But women are more prone to urinary tract infection during this time because of atrophic cystitis, and a growing urine should be obtained in all symptomatic women. br In addition to alterations in the pelvic organs, significant changes occur throughout the body. The skin loses elasticity, bone mineral density (BMD) decreases, and the dense breast tissue, is replaced by fat tissue, making mammographic evaluation easier. br The most common reason a woman presents at menopause is due to the symptoms of hot flashes. flashes, or flushes, which are unpredictable at the start, and sometimes occur for many years, occur in about 75% of women who are perimenopausal or postmenopausal. Hot flashes often cause embarrassment and discomfort, and sleep disturbances and emotional lability, especially if they are intense and occur frequently. Vasomotor episodes usually last a few minutes. episodes vary in frequency from every hour to every few days. br A woman who is dumped to the extent that it is important sleep disorders may also complain of cognitive or affective disorders from sleep deprivation . The vasomotor color is described as a feeling of warmth or heat that starts in the umbilical area and moves upward toward the head, followed by the sweat of the head and upper body. Other cardiovascular or neurologic symptoms (eg , palpitations, dizziness, lightheadedness, vertigo) may also occur with or without flushing, making the episode more difficult to classify as simply a symptom of the climacteric. Because of the wide range of symptoms, symptomatic women who have risk factors for a condition that menopause should be assessed thoroughly. br Although osteoporosis is one of the most important conditions in older women, the condition is often not taken seriously by menopausal women. With appropriate intervention, the Osteopenia is a largely preventable consequence of menopause. Osteoporosis is defined as bone mineral density (BMD) equal to or greater than 2.5 standard deviations (SDs) below the peak bone mass or T score. The Osteopenia is a 1.02.49 BMD SD below the T score. br In 2001, Grady and Cummings conducted a metaanalysis of 22 trials with data on a total of 8800 women. They found a 27% reduction in risk nonvertebral fractures in older women who received hormone therapy. For hip and wrist fractures, risk reduction was 40%, increasing to 55% in women under 60 years.8 The data from the Women # 39; s Health Initiative (WHI) also showed decreased bone fractures in women with hormone therapy. Since hormone therapy is primarily indicated for the relief of vasomotor symptoms, hormones are no longer firstline therapy for osteoporosis. br In onset of menopause, BMD is quickly lost due to bone resorption, detached from the bone formation is accelerated, while the training according to the rate of menopause. Trabecular bone is affected more than cortical bone, and bone loss is therefore more commonly seen in spinal coxial, and radial sites. normal bone loss associated with aging is different from the accelerated bone loss observed after menopause. The only bone loss A few years after the onset of menopause can be as high as 20% of the bones for life loss.8 br The overall effect of postmenopausal bone loss is the reduction of bone strength, leading to an increased risk fracture. The youngest women in the cessation of ovarian function, loss of bone mass is likely to be severe. Similarly, the lower bone mass womans to enter menopause, the most serious of osteoporosis will be. The severity of osteoporosis is also related to race, being worse in whites than in Asians, and less severe in darkskinned women. Other risk factors are smoking and slim. Osteoclasts are been shown to have estrogen receptors, and these are hypotheses to be the mechanism by which estrogen replacement protects against osteoporosis. br Bone densitometry is the factor most accurate clinical prediction of osteoporosis. If bone mass is less than 1 standard deviation below the average of the measured specific bones, then the individual is in a much higher risk of fracture. Other risk factors, such as low serum estrogen levels, female sex, low serum androgens, smoking, physical inactivity, low body weight, and little exposure to sunlight are risk factors for osteopenia and osteoporosis. Bone densitometry testing is recommended for all postmenopausal women. Neither age of initial detection of BMD or optimal frequency of detection was determined. br As noted above, estrogen therapy (ET) is considered a promising treatment for osteoporosis, but indications of hormone therapy have changed, other medications commonly used to treat osteoporosis . Preparations of oral and transdermal estrogen have been approved for the prevention of osteoporosis in postmenopausal women who are considered at risk. Postmenopausal women and elderly should be treated quickly and on a long term unless therapy is contraindicated estrogen. br With the loss of ovarian function is a universal phenomenon and not all women can or will use hormone therapy, other treatments have been developed. These include raloxifene, calcitonin and bisphosphonates. Raloxifene is a modulator selective estrogen receptor (SERMs), and acts directly on estrogen receptors in the bone to reduce bone resorption, thus reducing risk9 vertebral fractures and increased BMD. No effect on hip fracture risk has br documented.9 Calcitonin is a peptide hormone that acts by inhibiting osteoclasts, which are involved in bone resorption activity. A decrease in the rate of vertebral fractures has been demonstrated with this therapy, and a small increase in BMD in older women. Serum calcium should be monitored in patients taking this medicine. br Bisphosphonates are the most useful drug treatment and work as antiresorptive. They have shown a beneficial effect on the incidence of vertebral and hip fractures and to cause a more significant increase in BMD of raloxifene calcitonin.10, 11 Two widely used and effective bisphosphonates are alendronate and risedronate. Vertebral Efficacy with Risedronate Therapy (VERT) study was conducted in 110 centers and included 2458 postmenopausal women had vertebral fractures. Risedronate was administered at a dose of 5 mg for 36 months and showed a statistically significant reduction in relative risk (RR) of new vertebral fractures (RR = 0.59, 95% confidence interval [CI], 1858%). The cumulative incidence of nonvertebral fractures was also reduced.11 br Both alendronate and risedronate was first introduced with a daily dose for the treatment of osteoporosis. Patients can now prescribe a weekly dose alendronate and risedronate, which increases their tolerance and reduces side effects. A new bisphosphonate, ibandronate, has recently been approved for monthly use. The main side effects of bisphosphonates remain gastrointestinal upset and reflux. Patients with significant GERD should avoid the use of bisphosphonates unless approved by a gastroenterologist. Supplementation with 10001500 mg of calcium per day remains a pillar of prevention therapy, as vitamin D and regular weight exercise support. excess salt, animal protein, alcohol and caffeine offset these benefits. br coronary artery disease (CAD) is the leading cause of morbidity and mortality in men and postmenopausal women. Menopause increases the risk even more for women, independent of age. Before menopause, the risk of CAD for women lags behind men at risk for about 10 years. After menopause, women come to have similar risks of CAD as men of the same age. As a result, the death rate from CAD in women is increasing. The Framingham study was critical to show the relationship between menopause and increased cardiovascular mortality rate.12 br Women # 39; s Health Initiative (WHI) was a randomized controlled trial that addressed the question of whether postmenopausal women who take hormone therapy or estrogen therapy for prevention of CAD.13, 14 more than 27,000 women participated in the WHI. The study found that hormone therapy and estrogen therapy are not indicated for the prevention of CAD. The analysis of the WHI emerging data show that the immediate use of hormone therapy / estrogen therapy in the perimenopause and time may reduce the risk of CAD. The WHI clearly demonstrates that women more than 9 years post menopause should not start hormone therapy or estrogen therapy for prevention of CAD. At this time, hormone therapy / estrogen therapy is indicated primarily to relieve vasomotor symptoms. br In starting hormone therapy or estrogen therapy in the immediate periphery or in the postmenopausal time is believed to be beneficial because significant atherosclerotic changes have not happened yet. After 9 years have passed since menopause , arterial damage seems to have begun. studies are ongoing to test these theories in humans and primate models. Studies hormones and arterial plaques in ovariectomized monkeys promising in this area.15, 16 new trials support the protective effects of estrogen when used in a few years of menopause has come from the subanalysis by Manson et al in 2007 which showed that coronary artery calcification was lower in women placed on oral conjugated equine estrogens br placebo.17 those benefit of estrogen on cardiovascular mortality rates is due to many factors. One mechanism that appears to be effects of estrogen on lipid metabolism, including reducing lowdensity lipoprotein (LDL) and increased high density lipoprotein (HDL). Studies have suggested that the best predictors of CAD in men and women are different18 and triglycerides, HDL and lipoprotein (a) may be more significant in women.19 br Women with elevated lipoprotein (a) levels should be treated more aggressively, and therapy should be considered include estrogen therapy and a statin. A positive relationship between estrogen therapy and cardiovascular risk reduction in primary has been shown in several studies, and risk reduction in women taking estrogen therapy may be similar to reducing the risk of those receiving specific lipids to reduce therapy.20 However, taking into account data from WHI or hormone therapy or estrogen therapy for CAD should be given at this time. The main indication for hormone therapy / estrogen therapy is symptomatic relief of vasomotor symptoms. br The Heart and Estrogen / progestin Replacement (HERS) Study, 21, 7, 22 a study of 2763 postmenopausal women with known CAD, compared the effect of continuous combined hormone therapy compared to placebo for an average of 4.2 years. Without reducing rates of CAD charitable events was initially observed in the hormone therapy group. In fact, the first rate of adverse events was higher in the treatment arm than in the placebo group, offsetting the reduction in the risk later in the therapy group hormone. A 11% reduction in LDL and a 10% increase in HDL levels were evident in the treatment group. These observations together suggest that the protective effects of estrogen on cardiovascular morbidity resulting from the mechanisms of many and not only the reduction of lipids, and that estrogen alone is not adequate therapy for secondary prevention of CAD. br The Postmenopausal Estrogen / Progestin Interventions (PEPI) Trial, which included 875 healthy postmenopausal women, compared with various CAD risk factors as predictors of outcomes in women receiving different regimens of hormones by the participants randomized to receive placebo or 1 of 5 regimens of estrogen / progestin therapy.23 All groups treatment showed an overall improvement in levels of HDL and LDL compared with the placebo group. The improvement in the level of HDL was better in the group receiving unopposed estrogen than in the other treatment groups, however, people using unopposed estrogen also had the highest rate of endometrial hyperplasia. br The Nurses Health Study showed a reduction of approximately 11% of primary cardiovascular disease risk in postmenopausal women using HRT compared with women who had never used hormone therapy, regardless of the duration of use.24 The risk reduction did not appear to be dose dependent. However, these data have been eclipsed by the WHI. br The greatest beneficial effect of estrogen seems to be on endothelial function. The women undergoing angioplasty appear to be protected against restenosis by estrogen therapy.25 early atherosclerosis progression in postmenopausal women who smoked, as measured by carotid intimal thickness with time was greater than in women who smoked and were on estrogen therapy.26 studies in monkeys have shown that the coronary vasculature has a favorable response to conjugate equine estrogens.27, 28 These results are being investigated by other studies in humans, the breakdown of age groups in the WHI data, and in animal studies.29, 16, 27 br Estrogen therapy is known to benefit postmenopausal women in a multitude of ways, mainly through the relief of vasomotor symptoms associated with time postmenopausal . Estrogen is also beneficial for the prevention and treatment of osteoporosis. There is much controversy over the use of estrogen and breast cancer. Some studies show an increased risk of breast cancer with estrogen use in postmenopausal women, while others show a decrease. Estrogens possible link to cancer is also suggested by the fact that the risk of breast cancer is higher in women with an earlier age of menarche and the later age of menopause. With age early in pregnancy, however, and there is a cessation of menstruation hormonal changes, reduction in risk. The role of estrogen in breast cancer development is still being studied. br In Women # 39; s Health Initiative (WHI), the incidence of breast cancer increased in the estrogen / progestin versus placebo arm of the study (38 vs. 30 per 10,000 people; hazard ratio [HR] = 1.26]). However, the incidence of cancer decreased breast estrogen alone versus placebo arm of the study (26 vs 33 per 10,000 personyears [HR = 0.77]) .13, 14 The role of estrogen remains puzzling in the development of breast cancer. In the Today, no woman with a strong family or personal history of breast cancer should be given hormone therapy or estrogen therapy. br The data indicate a slightly higher RR with the use of estrogen in approximately 1.11.330, 31, but not all evidence supports this finding.32 The risk appears to be related to duration of use, longerterm users to be more affected.33 br The data suggest that the sequential addition of progestin to the regimen increases the RR of developing cancer later breast cancer beyond the risk of estrogen alone, although he has suggested that continuous combined hormone therapy using much smaller doses of progestin attenuates this most risk.34 previous studies evaluating the risk of breast cancer and estrogen therapy were carried out at a time when the progestin in hormone therapy is administered cyclically. br In particular, women with a history of use of hormone therapy are more localized tumors and improved survival rates. That is, the women receiving hormone therapy who are diagnosed with breast cancer are found to have more favorable stop when diagnosis31, including smaller tumor size, lymph node negative, and more welldifferentiated tumor histology.35, 36, 37, 38, 39, 40, 41, 42, 43 br A beneficial effect on mortality rates of breast cancer has been demonstrated in postmenopausal women who received hormone therapy compared with controls with no history of hormone therapy use.30 study results do not agree on whether this is due to early detection or for purposes of selftherapy on breast tissue. The general belief is that any increase in risk is small and that each patient should be evaluated as a candidate for estrogen therapy or hormone therapy on an individual basis, taking into account the overall balance of risks and benefits. An essential tenet in the management of menopause is that each individual is unique and that treatment should be adapted accordingly. The main indication for hormone therapy and estrogen therapy at this time is the relief of vasomotor symptoms. br The association between estrogen and memory function is an interesting area of research. Normal aging itself causes a decrease in certain cognitive abilities, and lack of estrogen can contribute to this process. If this is the case, estrogen therapy in postmenopausal women may be able to preserve this function and delay or even prevent the decline in certain cognitive functions . One difficulty inherent in this field are the limitations of objective tests of cognitive functions like memory. In the past, estrogen therapy has been associated with better performance on memory tests in postmenopausal women than in controles postmenop�usicas que no recib�an estr�genos therapy.44, 45 El efecto del estr�geno es una de frenar el declive de la funci�n de la memoria preservada. Datos de la WHI no muestran una mejor�a en la funci�n cognitiva en las mujeres que tomaron ya sea estr�geno o la terapia hormonal therapy.13, 14 de br Actualmente, los datos sugieren que las mujeres tienen una mayor incidencia de la enfermedad de Alzheimer que los hombres, incluso teniendo en cuenta la mayor esperanza de vida de las mujeres, debido a la enfermedad de Alzheimer es principalmente una relacionada con la edad condition.46 En estudios anteriores, la terapia de estr�geno parece reducir la relaci�n riesgo de desarrollar enfermedad de Alzheimer y / o retrasar su onset.47, 48 estr�geno no se ha demostrado que muestran una mejora en la funci�n cognitiva en pacientes con enfermedad de Alzheimer, es decir, que no puede revertir el deterioro cognitivo anterior y por lo tanto no tiene ninguna funci�n como �nica modalidad de tratamiento en la enfermedad de Alzheimer. De datos de WHI est� de acuerdo con esta opini�n . br La perimenopausia es con frecuencia un tiempo de s�ntomas depresivos asociados con efectos hormonales directos a trav�s de variaciones en los niveles y cambios en las circunstancias de la vida y secundaria a los efectos tales como el estr�genorelacionados con las alteraciones del sue�o y los s�ntomas vasomotores. Sin embargo, la depresi�n mayor se asocia con el sexo femenino en todas las edades, y la demostraci�n objetiva de un grupo de casos alrededor de la menopausia ha sido dif�cil, aunque esto parece ser cierto anecd�tica. br Independientemente de si se cumplen los criterios para un diagn�stico definitivo de la depresi�n mayor, los s�ntomas depresivos debe considerarse siempre en el contexto del nivel de funcionamiento; cualquier consideraci�n deterioro �rdenes de intervenci�n. br En todos, pero muy pocos casos, distinguir la etiolog�a de los s�ntomas como la depresi�n primaria frente a la menopausia no suele ser posible. El tratamiento de los s�ntomas depresivos con los estr�genos en la perimenopausia, el periodo de posparto, de 49 a�os y el s�ndrome premenstrual es com�n, con el consiguiente mejoramiento observado en el funcionamiento y estado de �nimo , tanto subjetiva como objetiva, en muchos casos cl�nicos. La depresi�n cl�nica, sin embargo, garantiza el tratamiento con antidepresivos, con estr�geno mostraron beneficios como terapia adyuvante en este escenario. A corto plazo el uso de estr�genos durante la �poca de la fluctuaci�n de estr�genos parece ser de alguna benefit.50 br Microcelulares los efectos del estr�geno en el SNC a�n no han sido claramente definidos, pero puede revelar los procesos complejos por los que el estr�geno tiene un efecto directo en el funcionamiento del SNC. Uno de estos procesos puede llegar a ser una reducci�n en el da�o de los radicales libres por la terapia de estr�geno. br Aumenta la secreci�n de gonadotropinas dram�ticamente despu�s de la menopausia. Los niveles de FSH son m�s altas que los niveles de LH, y ambos aumentan a niveles incluso m�s altos que en el aumento durante el ciclo menstrual. El aumento de FSH precede a la de la LH. La gran variaci�n c�clica de estradiol y estrona observado durante los a�os de la menstruaci�n cesa, y la fluctuaci�n en los niveles es peque�o y sin importancia, con la media que es muy muy inferior. Los niveles de estradiol circulantes tienen gamas muy diferentes antes y despu�s de la menopausia, y estos niveles son obviamente mucho menor en la menopausia. Frotis del epitelio vaginal ofrecer una imagen compuesta de la estimulaci�n de estr�genos end�genos y ex�genos en el tiempo, el m�s estr�geno, mayor es el n�mero de c�lulas superficiales. No hay cambios espec�ficos relacionados con la menopausia se han encontrado en la funci�n tiroidea. br Biopsia del endometrio puede mostrar una serie de apariciones de endometrio, de leve a proliferar atr�fica. No se observan cambios secretores despu�s de la menopausia debido a que no se produce la ovulaci�n, y por lo tanto no se forma el cuerpo l�teo para producir progesterona. La hiperplasia endometrial es un signo de hiperestimulaci�n por los estr�genos de cualquiera de las fuentes end�genas o terapia de reemplazo y puede ser un precursor del c�ncer de endometrio. La hiperplasia endometrial tambi�n puede ser sugerido por ecograf�a (el grosor del endometrio de 5 mm), que es �til para tratar de excluir a la hiperplasia y c�ncer de endometrio en las mujeres posmenop�usicas. br La raz�n principal para tratar los s�ntomas de la fluctuaci�n de niveles de estr�geno antes de la menopausia son reales para proporcionar alivio de los s�ntomas vasomotores, reducir el riesgo de embarazo no deseado, evitar la irregularidad de los ciclos menstruales, y conservar el hueso. br El momento de comenzar la terapia de los pacientes depende de la enfermedad actual o enfermedades, si los hubiere, y la historia m�dica. Si una mujer es perimenop�usicas o postmenop�usicas ayuda a la hora de elegir el tipo m�s adecuado de la terapia . Cada paciente debe tomar una decisi�n despu�s de recibir asesoramiento sobre todos los hechos y una explicaci�n de las opciones. Por ejemplo, la mujer perimenop�usicas pueden iniciar una terapia hormonal, si ella o su c�nyuge ha sido objeto de un procedimiento de esterilizaci�n, mientras que la misma mujer puede necesitar una OCP si todav�a necesita control de la natalidad. Many factors, including personal history, family history, smoking, peer and commercial influences, culture, ethnicity, and economics, also play roles in the final decision, and all must be carefully weighed by the clinician and patient together. br Adverse effects of replacement therapy may include bloating, mastodynia, vaginal bleeding, and headaches. Unexplained adverse effects are often the reason for discontinuation of therapy, and reassuring counseling as well as options and dose combinations should be tried before therapy is stopped. br Hormone therapy can be administered systemically through the oral, transdermal, or topical routes or locally via the vaginal route using cream, ring, or tablet. Topical preparations are used solely to treat vaginal symptoms. br Contraindications to estrogen therapy are undiagnosed vaginal bleeding, severe liver disease, pregnancy, venous thrombosis, and personal history of breast cancer. Welldifferentiated and early endometrial cancer, once treatment for the malignancy is complete, is no longer an absolute contraindication. Progestins alone may relieve symptoms if the patient is unable to tolerate estrogens. br Alternative products, ranging from herbal preparations to dietary supplements that contain various phytoestrogens, are reputed to ease the transition from perimenopause to postmenopause and are widely available. However, these agents have not undergone the same scrutiny in randomized controlled trials as the pharmaceutical products. Overthecounter herbal products and phytoestrogens, including soy, are assumed to act the same as their pharmaceutical counterparts, but the herbal and vitamin industry is currently unregulated by the FDA. In women who cannot (due to a history of breast cancer) or choose not to take estrogen therapy/hormone therapy and suffer from hot flashes or flushes, the SSRIs (in particular, venlaxifine) have been shown to alleviate vasomotor symptoms. br br