Department of Obstetrics and Gynaecology

Maturitas 86 (2016) 53–58

Contents lists available at ScienceDirect

Maturitas

jo u r n al hom ep age: www.elsev ier .com/ locate /matur i tas

eview article

anaging the menopause: An update

elen Robertsa,∗, Martha Hickeyb

Department of Obstetrics and Gynaecology, University of Auckland, Private Bag 92019, Auckland, New Zealand Department of Obstetrics & Gynaecology, University of Melbourne and the Royal Women’s Hospital, Parkville Vic 3052, Australia

r t i c l e i n f o

rticle history: eceived 4 January 2016 eceived in revised form 12 January 2016 ccepted 13 January 2016

eywords:

a b s t r a c t

Vasomotor symptoms (VMS), genito-urinary syndrome of menopause (GSM), sleep disturbance, sexual dysfunction and mood disturbance are common during the menopause transition. The degree of “bother” from symptoms should guide discussions about treatment. Moderate dose estrogen-containing hormone therapy (HT) is currently the most effective treatment for VMS and also improves vaginal dryness. The indication for HT is moderate to severe VMS in women without contraindications. It should not be pre-

enopause ormone therapy

scribed or continued for the treatment of chronic disease. GSM can effectively be treated with vaginal (topical) estrogens. The dose, delivery system and duration of treatment for HT should be individualised to relieve symptoms. For most healthy women aged 50–59 years, the risks of HT are low. Several widely available non-hormonal agents can treat VMS for those who should avoid or do not wish to take estrogen. These include selected antidepressants and gaba-agonists.

© 2016 Elsevier Ireland Ltd. All rights reserved.

ontents

1. What is the menopause? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53 2. What is the duration of menopausal vasomotor symptoms? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54 3. How can vasomotor symptoms be treated? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54 4. What are the risks and benefits of HT? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54 5. For how long should women take HT? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55 6. How should unscheduled bleeding with HT be managed? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55 7. How does menopause affect sleep? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55 8. How should the genitourinary syndrome of menopause be managed? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55 9. What is the advice for menopause in younger women? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 10. What are other alternatives to HT for menopausal symptoms? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 11. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57

Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57 Funding . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57 Provenance and peer review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57

. What is the menopause? period [1]. The menopause transition starts at around 47 years and lasts for 5–8 years on average. Whilst the timing of menopause

The “menopause” is the final menstrual period. The menopause ransition is the time from the onset of menstrual cycle changes r vasomotor symptoms until one year after the final menstrual

∗ Corresponding author at: Department of Obstetrics and Gynaecology, Faculty of edicine and Health Sciences, University of Auckland, Private Bag 92019, Auckland, ew Zealand. Fax: +64 9 303 5969.

E-mail address: h.roberts@auckland.ac.nz (H. Roberts).

ttp://dx.doi.org/10.1016/j.maturitas.2016.01.007 378-5122/© 2016 Elsevier Ireland Ltd. All rights reserved.

is relatively constant, both the nature and severity of symptoms varies substantially between women from different ethnicities and geographical locations for reasons that are poorly understood.

Midlife may be a vulnerable period for a number of physi- cal and psychological conditions. In order to manage menopause

effectively and not overlook conditions which require different management, clinicians need to be aware what symptoms can be attributed to endocrine changes during the menopause tran- sition. These “core” symptoms of menopause include VMS, vaginal

54 H. Roberts, M. Hickey / Maturitas 86 (2016) 53–58

Table 1 Recommendations for HT use (6).

Outcome Recommendation Level of Evidence

Prevention of CVD Do not use I-A Menopausal symptoms Moderate dose HT most effective for VMS therapy I-A

Progestin alone I-A Selected Antidepressants/clonidine/gabapentin I-B

Vaginal dryness Low dose vaginal estrogen. Progestin not required

I-A III-C

Recurrent UTIUrge incontinence Low dose vaginal estrogen I-B II-1A

Table 2 Recommendations for HT use in women with particular conditions (6).

Medical history Recommendation to use for symptom relief Level of Evidencea

Personal history or high risk of VTE

Do not use oral HT I-A consider transdermal III-C

Diabetes Can use HT I-A Breast cancer Uncertainty re risks of HT I-B Surgical menopause Offer HT I-A Premature ovarian insufficiency Offer HT

Recommend use to average age of menopause I-A III-B

a I: Evidence obtained from at least one properly randomized controlled trial. II-1: Evidence from well-designed controlled trials without randomization. III: Opinions of r xpert B g evid o king.

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espected authorities based on clinical experience, descriptive studies or reports of e . There is fair evidence to recommend the clinical preventive action. C: The existin f the clinical preventive action; however, other factors may influence decision-ma

ryness and urinary symptoms (now called “genito-urinary syn- rome of menopause”) [2], sexual dysfunction, mood and sleep isturbance [3]. The recently published NICE menopause guide-

ines advises that women presenting with a reduction in menstrual requency and/or VMS aged >45 years do not need further inves- igation [4]. Women commonly have more than one symptom at

enopause, and clinical evaluation should include discussion of ymptom “bother” to guide treatment.

. What is the duration of menopausal vasomotor ymptoms?

Vasomotor symptoms (VMS); “hot flushes” or “night sweats” re normal during the menopause transition and affect around 0% of women [5].The mechanisms of vasomotor symptoms are oorly understood, but are thought to reflect disturbances of the ypothalamic thermoregulatory system after estrogen exposure hen withdrawal [6]. Recent longitudinal studies indicate that the verage duration of VMS is around 7.4 years and those who start ushing before their final menstrual period may have the most per- istent symptoms [7]. Around 10% have symptoms lasting for as ong as 12 years [8] and symptoms may persist for many decades n some women [9].

. How can vasomotor symptoms be treated?

Treatment of moderate to severe VMS and their potential seque- ae of sleep disturbance, difficulty concentrating and subsequent educed quality of life, remains the primary indication for treat- ent [10]. The key clinical consideration guiding treatment is how

bothersome” symptoms are. This reflects that the frequency and everity of VM and other symptoms, and also psychological and ocial factors vary substantially between women [11].

Women should be provided with information about VMS and hat behavioural and pharmacological treatments are available.

or those who require pharmacological therapies, average dose HT

s the most effective treatment for VMS with reductions in both fre- uency and severity in the order of 75% [12] and HT may improve uality of life in symptomatic women [13]. HT should be avoidedn those with unexplained vaginal bleeding, active liver disease,

committees. A: There is good evidence to recommend the clinical preventive action ence is conflicting and does not allow to make a recommendation for or against use

previous breast cancer, coronary heart disease, stroke, personal history of thromboembolic disease or known high inherited risk. CVD risk factors do not automatically preclude HT but should be taken into account [4]. There is observational evidence that trans- dermal estrogen (≤50 �g) is associated with a lower risk of deep vein thrombosis, stroke, and myocardial infarction compared to oral therapy [10] and may be the preferable delivery system, par- ticularly for women with higher thromboembolic risk (Table 2). A mathematical analysis in the NICE guidelines concluded that the VTE risk with transdermal delivery is no different to controls [4]. Dosing of HT should start low and aim to reduce troublesome symptoms. Minimising estrogen exposure reduces VTE risk [14] and may reduce side-effects such as mastalgia and unscheduled bleeding [15]. Some may wish to avoid higher doses of HT and accept ongoing symptoms, and this should be part of the clini- cal discussion. Younger menopausal women may require higher doses to relieve symptoms, but there is currently little evidence to support this. The inclusion of progestogen appears to increase breast cancer risk, but progestogens are still indicated to prevent endometrial hyperplasia and cancer risk [16]. Low dose HT e.g. 0.3 mg of conjugated equine estrogens, ≤1 mg 17 � estradiol [16] may take up to 6–8 weeks before there is adequate symptom relief [6]. Those in the menopause transition [1] may need to consider contraception. Tibolone, a synthetic steroid with weak estrogenic, progestogenic, and androgenic properties, used at the daily dose of 2.5 mg, reduces VMS but may be less effective than combined HT. Tibolone causes less unscheduled bleeding than combined HT [17]. The tissue selective estrogen complex (combination of 0.45 mg of oral conjugated equine estrogen and 20 mg bazedoxifene (a SERM)) has been approved for the management of moderate to severe VMS in the US and Europe [18]. Comparative efficacy and safety with conventional HT is not yet known.

4. What are the risks and benefits of HT?

Discussion of risk should consider absolute rather than relative

risk. In general, absolute risks are small in healthy women during the menopause transition or within 10 years of menopause [19]. The 13 year cumulative follow up from WHI gives absolute risks for these women currently taking HT and how these change 7–8 years

H. Roberts, M. Hickey / Matu

Table 3 Absolute risks attributable to HT per 10,000 women/year aged 50–59 years during study intervention period [20].

Outcome E + P E

Breast cancer +6 −5 Stroke +5 −1 Pulmonary embolus +6 +3 CHD +5 −11 Hip fracture −3 +3

Table 4 Absolute risks attributable to HT per 10,000 women/year aged 50–59 years during 13 years of cumulative follow up [20].

Outcome E + P E

Breast cancer +9 (SS) −7 (NSS)

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i b T N l m a r

t [ s v t f n s m d p

e w h i d t

D t a

CHD +5 (NSS) −11 (SS) All cause mortality -5(NSS) −12 (NSS)

fter HT is stopped. Unlike combined therapy, there is no increase n breast cancer risk found with estrogen alone [20] (Table 3). After T is stopped, stroke and VTE risk disappear, as does the fracture enefit. There is no difference in all-cause mortality with either ombined or estrogen only therapy. However after discontinuation f combined HT the increased risk of breast cancer persists for 8 ears and 7 years after discontinuation of estrogen only treatment he reduced risk of CHD persists [20] (Table 4). Observational and ase control data indicate that the type of progestin may contribute o breast cancer risk, with testosterone derived products poten- ially conferring greater risk compared to natural (micronized) rogesterone [21]. Systemic progestogen can be minimised using n intrauterine delivery system (which is also contraceptive) but hether this affects breast cancer risks associated with combined T is not known [22].

A meta-analysis of 52 epidemiological studies showed an ncreased risk of ovarian cancer with both estrogen only and com- ined hormone therapy after 5 years of use from age 50 years [23]. here have been various critiques of this paper, however the US ational Institutes of Health has commented that due to present

ower dose HT use and the fact that ovarian cancer is far less com- on than cardiovascular disease and breast cancer, the overall risk

ssessment of hormone therapy is not strongly affected by these esults [24].

There is wide spread consensus that HT should not be used for he prevention of chronic disease including CVD (Table 1 ), diabetes 10] or to prevent cognitive decline [10,25] and that it should not be tarted in women aged >60 years. The Kronos Early Estrogen Pre- ention Study (KEEPS-Cog) [26] and Early versus Late Intervention rial with estradiol (ELITE) [27] compared estrogen with placebo or cognitive function in early menopausal women and showed o difference between estrogen and placebo. The KEEPS trial also howed no changes in cardiovascular risk markers with transder- al HT which offers some reassurance about CV risks with HT, but

oes not support the “timing hypothesis”, that early use of HT may revent later CVD in women [28].

Reduced sexual desire is common with age, but may not be both- rsome [6]. Systemic and topical (vaginal) estrogens reduce pain ith intercourse [29]. A systematic review indicates that HT may ave a small to moderate positive effect on sexual function, but it

s unclear whether this is entirely attributable to improved vaginal ryness [30]. There is insufficient evidence that tibolone is superior o conventional HT to improve sexual function [30].

A systematic review showed that exogenous androgens (as

HEA) may marginally improve sexual function [31] and testos-erone may also help, but the quality of evidence is low and there re no long term safety data [32] (Table 5).

ritas 86 (2016) 53–58 55

5. For how long should women take HT?

Current international guidelines advise consideration of HT in healthy women within 10 years of their final menstrual period with moderate to severe VMS [19] but there is less clarity on when to stop. This decision can be made on an individual basis and in the absence of contraindications some guidelines advise that it can be used for as long as the woman feels the benefits outweigh the risks for her [33]. Balancing the increasing risk of breast can- cer with duration of use (combined HT) and additional concerns about increased cardiovascular and cerebrovascular risk with age has meant that short-term use (under 5 years) may provide the best risk benefit ratio for most women [34]. Whilst overall use of HT has declined in most countries, recommendations about shorter peri- ods of use mean that more women are navigating how and when to stop. Of clinical importance is that stopping HT commonly leads to recurrent VMS [35] and may also trigger new onset VMS [36].There is no consensus about whether stopping “cold turkey” or tapering are preferable to avoid recurrent symptoms [37].

6. How should unscheduled bleeding with HT be managed?

Unscheduled bleeding refers to bleeding between withdrawal bleeding with cyclic HT or any bleeding after the first 6 months with continuous combined HT. Unopposed estrogen should not be used in women who retain their uterus [10]. Unscheduled or heavy bleeding in women over 40 years requires investigation before starting HT [38]. Since HT will not reliably regulate or stop bleed- ing, a low dose combined HT or intrauterine progestogen may be preferable. In postmenopausal women, unscheduled bleeding in the first 6 months of combined continuous HT use is common and does not necessarily need to be investigated [39], provided that Pap smears are up to date. Women should be advised about the high chance of unscheduled bleeding during this time. Unsched- uled bleeding after 6 months or new onset unscheduled bleeding should be investigated [39].

7. How does menopause affect sleep?

Prospective data indicate that new onset sleep disturbance may affect up to one third of women during the MT [40,41]. Common problems include multiple awakenings, difficulty falling asleep and difficulty getting back to sleep. The relationship between VMS and sleep disturbance at menopause is not well defined and sleep prob- lems are not necessarily due to VMS [41]. There is a bidirectional relationship between sleep disturbance and mood disturbance, particularly depressed mood. Clinical evaluation should specifi- cally enquire about depressive or anxiety disorder. Not surprisingly, menopausal symptoms which interrupt sleep may be more trou- blesome than daytime symptoms, and this should be considered when targeting therapy [42].

8. How should the genitourinary syndrome of menopause be managed?

Genitourinary syndrome is a relatively new terminology describing vulvovaginal changes at menopause, as well as urinary symptoms of frequency, urgency, nocturia, dysuria and recurrent urinary tract infections [43]. Vaginal dryness is common after menopause and unlike VMS usually persists and may worsen with time [29]. Vaginal estrogen is effective and whilst systemic absorp-

tion does occur, it does not induce endometrial hyperplasia (level of evidence III-C). Concerns about systemic absorption mean that vaginal estrogens may be avoided in breast cancer patients taking aromatase inhibitors [6]. The relationship between HT and urinary

56 H. Roberts, M. Hickey / Maturitas 86 (2016) 53–58

Table 5 Additional educational resources of therapies for menopausal symptoms.

Patient information

1. Pamphlet: Menopause. Should I take HRT? http://bestpractice.bmj.com/best-practice/pdf/patient-summaries/en-gb/532536.pdf 2. Cochrane Consumer network http://consumers.cochrane.org/healthcare-users-cochrane 3. National Center for Complementary and Alternative Medicine, US National Institutes of Health

Intervention Conclusion Reference

Acupuncture No evidence of significant difference for flushes when acupuncture was compared with sham acupuncture.

S. Dodin, C. Blanchet, I. Marc, E. Ernst, T. Wu, C. Vaillancourt, et al., Acupuncture for menopausal hot flushes. Cochrane Database Syst. Rev. (2013) Issue 7. Art. No: CD007410. Doi: 10.1002/14651858. CD007410.pub2.)

Yoga Does not improve VMS K.M. Newton, S.D. Reed, K.A. Guthrie, K.J. Sherman, C. Booth-LaForce, B. Caan, et al., Efficacy of yoga for vasomotor symptoms: a randomized controlled trial, Menopause (2014) 21, 339–346. Doi: 10.1097/GME.0b013e31829e4baa

Phytoestrogens No flush benefit overall with the exception of products containing a minimum of genistein 30 mg per day

H. Roberts, A. Lethaby, Phytoestrogens for menopausal symptoms: a Cochrane review summary, Maturitas (2014) 78, 79–81

Omega 3 Does not improve VMS L.S. Cohen, H. Joffe, K.A. Guthrie, K.E. Ensrud, M. Freeman, J.S. Carpenter, et al., Efficacy of omega-3 for vasomotor symptoms treatment: a randomized controlled trial, Menopause (2014) 21, 347–354. Doi: 10.1097/GME.0b013e31829e40b8.

Exercise for flushes Exercise is not an effective treatment for vasomotor menopausal symptoms.

A.J. Daley, A. Thomas, A.K. Roalfe, H. Stokes-Lampard, S. Coleman, M. Rees, et al., The effectiveness of exercise as treatment for vasomotor menopausal symptoms: randomised controlled trial, BJOG (2015) 122, 565–575. B. Sternfeld, K.A. Guthrie, K.E. Ensrud, A.Z. LaCroix, J.C. Larson, A.L. Dunn, et al., Efficacy of exercise for menopausal symptoms: a randomized controlled trial, Menopause (2014

i e u ( i q c ( d [ fl t

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devices) for hot flushes after breast cancer [56]. Randomised stud- ies have showed mixed results, but a systematic review found that

ncontinence depends on the delivery route. Systemic HT wors- ns urinary incontinence [6] but vaginal treatment may improve rge incontinence and prevent recurrent urinary tract infections Table 1). Using very low doses for the first few weeks is helpful if rritation occurs and indeed lower doses of vaginal ET, with less fre- uent administration, often yield satisfactory results [10]. Tibolone an also help vaginal dryness [17]. The oral SERM ospemifene Osphena), 60 mg daily, has been shown to relieve vulvo vaginal ryness and is approved in the USA and Europe for this indication 33]. It has minimal endometrial stimulation, though it does cause ushes in some women [44]. There is insufficient evidence to guide he choice of non-hormonal agents for vulvovaginal symptoms.

. What is the advice for menopause in younger women?

The term premature ovarian insufficiency (POI) is now applied o women aged under 40 and “early menopause” describes women nder 45 years. Diagnosis is made by elevated FSH on 2 occa- ions taken 4–6 weeks apart and VMS and/or menstrual cycle hanges [4]. Most premature/early menopause is iatrogenic, and ollows bilateral oophorectomy for benign indications or may fol- ow chemo/radiation [45]. Where possible, women undergoing reatments likely to induce menopause should be provided with dvice and support before treatment [4]. A fertility referral should e considered. Spontaneous POI or early menopause is less common nd may be hereditary, although no specific genes have been iden- ified. Although observational data shows an association with POI nd an increased risk of osteoporosis, fracture and CVD, there may ot be a causal effect and these associations could result from com- on risk factors [46]. The findings from the large WHI observational

tudy, that women with hysterectomy, regardless of oophorec- omy status, have greater CVD risk factors [47], do not support the ypothesis that changes in exposure to endogenous sex hormones r menopausal status influences CVD risk [48]. Women with POI ay have more intense flushes and guidelines support offering HT

o these women (level of evidence I-A). Guidelines also advise HT

se until average age of menopause [33], although there is no ran- omised evidence (level of evidence III-B) [6] (Table 2). It has always een assumed that older women, who had an early menopause, ould be at an increased risk of fracture. However this was not) 21,330–338

found in a recent report from the Study of Osteoporotic Fractures. Women older than 65 years, with a history of early menopause and no HT use, did not sustain more fractures than did the group who had menopause at the average age. Removal of both ovaries at the time of hysterectomy compared with ovarian conservation was similarly found not to increase the subsequent rate of hip fracture [10,49].

10. What are other alternatives to HT for menopausal symptoms?

Non-hormonal treatments for menopausal symptoms gener- ally only address VMS, and other strategies may be needed to address other troublesome menopausal symptoms. Moderate dose HT remains the most effective treatment for vasomotor and vaginal symptoms, although venlafaxine 75 mg CR is equivalent to low dose estradiol (0.5 mg/day) for VMS [50]. Extensive randomised con- trolled trial data supports the efficacy of selected SSRI and SNRI for VMS. Few other preparations have been directly compared to estro- gen in randomised trials, but a systematic review has identified that clonidine, selected SSRI and SRNI and the gaba-agonist gabapentin are superior to placebo for VMS [51]. In general, these products will reduce VMS by around 50–60% compared to 75% with estrogen. The comparative efficacy of non-hormonal treatments is poorly under- stood as there have been few head-to-head studies, but the SSRI escitalopram is a reasonable first choice since it is well tolerated, reduces the frequency, severity and also interference associated with VMS [52], improves quality of life [53], improves sleep and does not cause sexual dysfunction when used for VMS [54]. Cog- nitive behaviour therapy may reduce bother associated with VMS [55]. A systematic review showed no effect for any other interven- tions (including acupuncture, homeopathy, vitamin E, or magnetic

black cohosh may be effective for VMS [51]. The efficacy and safety of “bio-identical” hormone products is unknown, and the quality, purity and constituents of complementary therapies varies sub- stantially [4].

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H. Roberts, M. Hickey /

1. Conclusion

The menopause transition is a normal physiological event and sually does not require medical intervention. For those with roublesome symptoms impacting on function and quality of life, everal options are available. Clinicians and consumers need to now about the stages of menopause, what is (and is not) normal t menopause, behaviours that may improve bone and cardio- ascular health and general health and wellbeing, the available reatment options and their risks and benefits in order to inform hared decision-making [4]. With informed choice, treatment for enopausal symptoms should be commenced in general practice,

ut may require further referral when there are complex medical onditions, symptoms are unresponsive or there are ongoing trou- lesome side-effects [4]. Where treatment is indicated, this should e reviewed within 3 months for efficacy then at least annually and hould be adapted to the changing stages of menopause.

onflict of interest

No conflict of interest from either author.

unding

No funding received to write this article.

rovenance and peer review

Not commissioned; externally peer reviewed.

eferences

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[2] D.J. Portman, M.L. Gass, on behalf of the Vulvovaginal Atrophy Terminology Consensus Conference Panel. Genitourinary syndrome of menopause: New terminology for vulvovaginal atrophy from the International Society for the Study of Women’s Sexual Health and The North American Menopause Society. Maturitas 2014, [Epub ahead of print], S0378-5122 (14) 00242–00244.

[3] Proceedings from the NIH State-of-the-Science Conference on Management of Menopause-Related Symptoms, March 21-23, 2005, Bethesda, Maryland, USA, Am. J. Med. 118 (2005) 1–171.

[4] National Institute for Health and Clinical Excellence. NICE Clinical Guideline Menopause (2015) https://www.nice.org.uk/guidance/ng23/resources/ menopause-diagnosis-and-management-1837330217413.

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