2. Menopause is defined as the permanent cessation of menses. By convention the diagnosis of
menopause is not made until the individual has had 12 months of amenorrhea.
Menopause is not just cessation of menstruation it is “depletion of ovarian follicles” leading to
decrease in ovarian hormones.
12 months of amenorrhea
• Retrospective diagnosis
• Depletion of ovarian follicles
• Diminution of ovarian hormones
• No independent biological marker
4. Induced menopause may occur after:
• Chemotherapy
• Pelvic radiation, or,
• Bilateral oophorectomy
• Menopause is considered premature when it occurs before 40 years of age but is
otherwise normal and not surgical
• Perimenopause is the time between the onset of the climacteric and the year after the last
menses.
Premenopause - entire reproductive span before onset of the menopausal transition
Postmenopause- the span of life after menopause
5. The Menopausal Transition
Menopausal transition is replacing perimenopause and climacteric as the preferred term
to describe the time of physiologic change around the cessation of ovarian function.
This is the stage which precedes menopause, has an average duration of 4 years, with a
range of 0–10 years.
The mean age at which menopause occurs in developed countries is 51 years and may
be increasing.
6. Another Menopause Staging was First
Published by Dr Behram Anklesaria in 1997
Stage I: From the earliest perimenopausal symptom (usually vasomotor instability or menstrual
irregularity) to menstrual cessation (menopause). The stage can last from 3 years to 5 years.
Stage II: “Five years after menopause.” This stage is further subdivided into Stage IIA and Stage IIB.
Stage IIA: “From the cessation of menstruation up to 1 year” (that is up to confirmation at menopause by WHO
definition). The main symptoms of menopause during this stage are vasomotor instability and urethral syndrome.
Stage IIB: From end of stage IIA up to 4 years.
The common issues here are:
• Atrophic symptoms, vaginitis, dyspareunia
• Urinary symptoms
• Weight gain
• Skin and hair changes
• Genital prolapse
• Late psychological symptoms
• Sexual disorders.
Stage III: “From 5 years after menopause up to an indefinite period; probably life time.”
These are divided into the following:
7. Factors Influencing Age of Menopause
Several factors appear to influence the age at which women experience menopausal
symptoms and the final menstrual period
• Menopause occurs approximately 1 year earlier in smokers
• Occurs earlier in nulliparous women
• Menopause may also occur earlier in women who have had ovarian cystectomies or
unilateral oophorectomies
• Ovarian drilling done for polycystic ovarian disease (PCOD)
• When patient get pelvic radiotherapy or chemotherapy
• In Indian women it is earlier so genetics or racial factors may also be contributing
towards age of menopause.
8. PHYSIOLOGY OF MENOPAUSE
In females throughout reproductive life ovarian follicular depletion is occurring by
atresia.
In fact this process starts earlier in foetal life itself.
At 5 months of foetal age-> the primordial follicles->2 million.
At birth, girls have 1 million primordial follicles, approximately 25% of which remain
at puberty.
During the reproductive years, many follicles will begin to develop during each
ovulatory cycle; except dominant follicle all other follicles become atretic.
So only estimated 500–1,000 follicles remain in the ovaries of a woman, 51 years of
age.
Some follicles persist for a few years after the menopause but these are poorly
responsive.
5th month
of foetal
life
birth puberty 51yrs
2 million 1 million 25% 500-1000
9. 10–15 years before menopause-> of the follicular phase of the cycle -the length of the
menstrual cycle starts decreasing.
This decrease in cycle length continues until the onset of the menopausal transition,
when both the average cycle length and the standard deviation of cycle length begin to
increase as follicles are depleted and ovulation occurs less frequently.
Insufficient follicular development -> inadequate oestrogen production.
With little oestrogen available to stimulate the endometrium-> amenorrhoea
Timing of natural menopause is genetically programmed.
Common allelic variants of the oestrogen receptor gene [oestrogen receptor- (ER-α)
and ER-β] contribute to the variability in the timing of menopause.
10.
11. Hormonal changes
A rise in the concentration of FSH is the earliest and most consistent clinically
measurable hormonal change noted in studies of reproductive aging.
An FSH level measured during the early follicular stage of the menstrual cycle that is
greater than two standard deviations above the mean level in women of reproductive
age is a marker of impending menopausal transition
In the premenopause ovarian granulosa cells under the influence of FSH are producing
oestrogens but because of follicular atresia there is first fall of oestradiol and fall of
inhibin B and this leads to increase in level of FSH but there is further decrease in
levels of oestradiol and it is oestrone that becomes main dominant hormone because of
peripheral conversion of testosterone into oestrone
FSH->+ GC-> estrogen -Premenopause there is follicular atresia-> estardiol and
Inhibin B -> FSH and estardiol -> Estrone becomes dominant (P.c T->E)
12. A slow rise in FSH occurs first, followed by a rise in luteinizing hormone (LH) and a decline
in oestradiol and oestrone. ‘
Ageing of adrenal cortex starts from 3rd decade-> gradual decline in Testosterone
Ovaries continue to produce androgens and so at menopause there is not much fall of
testosterone.
Luteinizing hormone levels remain normal initially, but it is also elevated as ovarian steroid
secretion falls and gonadotrophin-releasing hormone (GnRH) increases because of follicular
atresis inhibin B levels are decreased and this causes early selective increase in FSH.
Inhibin A and B, hormones that are involved in directing follicular development suppress
pituitary FSH production. ‘
As anovulation predominates in perimenopause period FSH and LH remain chronically
elevated
There is a 10-20-fold increase in the FSH level and a 3-5 fold increase in the LH level, and
oestradiol levels fall below 50 pg/mL
13. Even in menopause ovarian theca cells are producing androstenedione and testosterone
under influence of increased levels of LH, and they are the source of androgens in
menopause
By aromatisation adipocytes produce oestrone from testosterone and so in menopause
oestrone becomes dominant hormone.’
14. Final Hormonal Changes with Established
Menopause
The most significant findings are the marked reductions in E2 and oestrone (E1) levels.
The serum E2 < E1
peripheral aromatisation of androgens E1
17. EFFECT OF OESTROGEN DEFICIENCY
Brain and Central Nervous System - Oestrogen receptors are abundant in the brain.
Oestrogen is known to have a role in many brain processes, and the absence of
oestrogen can result in physiologic and symptomatic changes.
Oestrogen is important for cerebral blood flow, cerebral glucose administration,
synaptic activity, neuronal growth, the survival of cholinergic neurons, as well as such
complex functions as cognition.
18. Hot Flushes
Hot flushes- are an early and acute symptom of oestrogen deficiency.
They often begin in the perimenopause when oestrogen levels characteristically
fluctuate widely.
Rapid fall in oestrogen level precipitates the symptoms.
Hot flushes typically last from 0.5 years to 5 years after natural menopause but may
persist as long as 15 years.
Night sweats can be more upsetting than daytime flushes because they disrupt sleep.
19. Physiology of Hot Flushes
these episodes result from a hypothalamic response (probably mediated by catecholamines)
induced by a change in oestrogen status.
The flush has been well-characterised physiologically:
heat dissipation occurs through an increase in peripheral temperature (e.g. in the fingers and toes);
a decrease in skin resistance, associated with diaphoresis
and a reduction in core body temperature.
Skin temperature returns to normal usually within 30 minutes.
No significant change in blood pressure is associated with hot flashes
20. Management
Counselling the woman is most important.
Pharmacological preparations:
The gold standard of treatment for menopausal hot flushes is oestrogen therapy.
Tibolone is another drug which is found to be effective in hot flushes.
The various nonpharmacological options for managing hot flushes are as follows:
• Lifestyle modifications: –
– Avoidance of triggering factors like stress, caffeine, alcohol, spicy foods, beverages
– Avoid smoking ,– Reduction of stress, – Weight loss
—practice meditation, yoga, massage, paced breathing
– Exercise—undertake aerobic and weight-bearing exercises, exercise reduces hot flushes in 50% of
cases,. Behavioural interventions – Paced respiration (slow deep abdominal breathing) – Relaxation
training
21. Mood Changes and Cognitive Function
Oestrogen has a positive effect on mood and contributes to a sense of well-being
Migraines -> Oestrogens and progestins affect central serotoninergic and opioid
neurons.
Because the orderly pattern of oestrogen and progesterone secretion is lost as
menopause approaches, perimenopausal women with a history of menstrual migraines
may experience an exacerbation.
Vision- There is an increased incidence of some vision-threatening conditions in
postmenopausal women. idiopathic full-thickness macular degeneration
Collagen -Oestrogen has a positive effect on collagen, which is important for bone and
skin. Both oestrogen and androgen receptors have been identified in skin fibroblasts.
The loss of collagen is more rapid in the first few years after menopause, and 30% of
skin collagen is lost within the first 5 years after menopause.
22. Urogenital Atrophy
It has been reported that as many as one-third of women aged 50 years and older experience urogenital
problems.
Oestrogen deficiency results in :
• Thin and paler vaginal mucosa , Loss of normal rugosities
• The moisture content is low
• The pH increases (usually pH > 5)
• It may exhibit inflammation and small petechiae
• Cytology reveals a loss in superficial cells and an increase of basal and parabasal cells
In reproductive-age women, the vaginal flora is dominated by lactobacilli.
In postmenopausal women, the vagina is gradually repopulated with diverse flora, including
pathogenic organisms commonly found in urinary tract infections (e.g. coliform bacteria), as a result
of the reduced acidity
23. Functional changes which have been noted include the following:
• Elderly women have lower flow rates
• Higher bladder volume at the first sensation to void
• Increasing urinary residue
• Similarly, changes in collagen in the endopelvic fascia and periurethral tissue account for the
hypermobility and reduced urethral closure pressure and may thus explain the prevalence of
stress incontinence.
Dry and atrophied vaginal and urethral epithelium can cause:
• Vaginal discomfort
• Itching
• Dyspareunia, and
• Recurrent vaginitis.
24. Bone Loss (Osteoporosis) and Fracture
Risk
In women, peak bone mass is achieved by the second decade and begins to decrease thereafter after 35 years
of age.
Risk Factor Assessment The most important risk factors for osteoporosis-related fractures are:
• Prior fracture(s) with trivial trauma as an adult,
• Low bone mineral density (BMD) in patients with or without fracture
• Advancing age
• Family history of osteoporosis, fractures in first-degree relatives
• Vitamin D deficiency (very common in India)
• Low calcium intake (< 300 mg per day)
• Tobacco use
• Alcohol intake
• Any condition that increases the risk of falling
25. Postmenopausal osteoporosis is characterised by low bone mass and microarchitectural
deterioration of bone tissue leading to enhanced bone fragility and increased fracture
risk.
According to the World Health Organisation, osteoporosis is defined based on the
following bone density levels:
• Bone mineral density is compared to two norms—healthy young adults (T-score) and age-
matched (Z-score)
A T-score within 1 SD (+1 or –1) of the young adult mean indicates normal bone
density
• A T-score of 1–2.5 SD below the young adult mean (–1 to – 2.5 SD) indicates low bone
mass.
• A T-score of 2.5 SD or more below the young adult mean (> – 2.5 SD) indicates the
presence of osteoporosis.
Oestrogen deficiency is a dominant pathogenic factor in bone loss. This can be noted for
the first time during perimenopause.
26. Three main sites of increased risk of fracture in post menopause women are:
1. Wrist 2. Hip 3. Spine
The most common fractures due to osteoporosis are vertebral fractures, and yet less
than a third of all vertebral fractures are clinically diagnosed
Back Exercises for Kyphosis-. This is most effective when done in an upright, weight-
bearing position.
27. Prevention and Management of Osteoporosis
A management strategy focused on lifestyle approaches may be all that is needed for women who are at low risk
for osteoporotic fracture.
These life style modifications are:
• No smoking
• Calcium 1,200–1,500 mg per day
• Vitamin D 400–600 IU per day
But mainstay is exercise and these have to be weight bearing and resistance exercises, especially for back muscles to
prevent kyphosis, wrist muscles, to prevent fractures of wrist, to strengthen thigh and buttock muscles to prevent
fractures of hip bone
Bisphosphonates: Alendronate, risedronate, and ibandronate are commonly used for both prevention and
treatment of osteoporosis.
For prevention alendronate is available as a daily tablet of 5 mg and a weekly tablet of 35 mg.
For treatment of postmenopausal osteoporosis the doses available are 10 mg tablets daily and 70 mg tablets
weekly.
28. Selective oestrogen receptor modulators (SERMs): SERMs (e.g.raloxifene are indicated
for the prevention and treatment of osteoporosis. 60 mg tab/ day for prevention as well
as treatment.
Calcitonin: The nasal spray used for osteoporosis treatment that inhibits bone resorption
and reduces fracture rates. Calcitonin is available as a subcutaneous injection (about
100 IU per day) and as a nasal spray (about 200 IU per day) for treatment of
postmenopausal osteoporosis.
Parathyroid hormone (PTH e.g. teriparatide: Daily subcutaneous injections are used for
osteoporosis treatment
29. Tibolone is a synthetic steroid with oestrogenic, progestational and androgenic properties.
It is metabolised by local tissue enzymes and therefore provides a unique “tissue specific
approach” to menopause
It treats climacteric symptoms and does not increase mammographic breast densities (although
data on breast cancer occurrence are not yet available).
Tibolone seems to exert osteoprotective effects similar to oestrogen,
The recommended dose is 2.5 mg daily.
It increases libido, reduces hot flushes and so can be prescribed for that effect along with to
prevent osteoporosis.
Osteoprotegerin: This is a new drug and it is a naturally occurring protein and is a negative
regulator of osteoclast formation that has shown promise as a potential treatment for
osteoporosis.
• Zoledronic acid is new drug approved by FDA. A single intravenous infusion of Zoledronic acid 5
mg over 15-minute period once in a year decreases bone turnover and improves bone density and is
effective in reducing hip, vertebral and other fractures
30. Cardiovascular Effects
• Total cholesterol rises at an accelerated rate after menopause due to increase in LDL
• The oxidation of LDL is also enhanced.
• Prostacyclin production decreases
• Endothelium levels increase
31. Present recommendations specific recommendations from several sources currently
include the following:
• Identify and treat all CHD risk factors
• Do not initiate HT for the prevention of CHD (coronary heart disease)
• Do not initiate HT in patients with known CHD
• If CHD develops while on HT, consider other alternatives.
For prevention and to increase cardiorespiratory endurance 30 minutes/day of moderate
aerobic activity is recommended like walking .
32. MENSTRUAL PROBLEMS
The perimenopausal period begins 2–5 years before the final menstrual period and lasts for 1 year
thereafter.
DUB
Oestradiol levels do not gradually wane in the years before menopause but remain slightly elevated
until 6 months to 1 year before follicular growth and development cease.
The greatest concern about DUB is relative oestrogen excess with endometrial hyperplasia and
neoplasia although the usual finding is a non-neoplastic tissue with oestrogenic effects unopposed by
progesterone.
The menstrual cycle becomes irregular and unpredictable with both short and long follicular phases,
defective ovulation and anovulation and highly erratic cycles.
Anovulatory menorrhagia is frequent in this period but age-related and pathology-related changes in
the uterus and ovaries may also be responsible.
Experience and sensitivity is required to distinguish “normal” perimenstrual patterns from pelvic
pathology
33. CANCER SCREENING IN MENOPAUSE
Leading cancers in women are:
• Breast cancer
• Cervical cancer
• Endometrial cancer.
Recommendations for Screening for Breast Cancer Early diagnosis of breast cancer is important.
The 5-year survival rate depends on the stage at the time of diagnosis and ranges from 100% for stage 0–16% for
stage IV.
Other concomitant medical conditions also influence the survival rate.
• All women should be told at age 20 about the benefits and limitations of BSE.
Breast self-examinations should be supplemented with a clinical breast examination by a health professional
every 3 years until age of 40 years.
After age of 40, women should have a clinical breast examination and a mammogram every year.
• In some instances, physicians may recommend beginning screening mammography before age 40 as in instances
of the woman having a strong family history of breast cancer or a lifetime oestrogen/HRT exposure such as
nulliparity, older age at first birth, early menarche, late menopause or obesity.
34. Management of Menopause
So when women come to us in menopausal transition we have to assess her for the high risk factor which would
influence her quality of life later on and these include following:
• If she is over-weight -> lifestyle modification like weight bearing exercises, regular walk and proper diet.
• Take family history of osteoporosis or fragility fractures or other risk factors for osteoporosis.
• History of diabetes, hypertension ,• History of previous fracture
• History of any drug intake ,• Family or past history of chronic heart disease
• Any history of breast cancer in the family
• Do her Pap smear if already not done and then every year till the age of 50 years
• Do TVS if not already done or if dysfunctional bleeding
• There is no need to do FSH or hormonal levels for diagnosis of menopause
• Advise mammography and BSE (breast self-examination) once in month
• Clinical breast examination (CBE) once in a year, • Mammography 1–2 years after 40 years and every year after
the age of 50 years.
35. Lifestyle Modifications
• Avoid smoking
• Avoid alcohol
• Calcium 1,200–1,500 mg per day preferably from dietary sources
• Vitamin D 600 IU per day
• Exercise specially aerobic for cardiorespiratory and general fitness and weight bearing
and resistance training for sarcopaenia and loss of BMD.
36. Exercise can be:
• Aerobic exercises like walking and dancing, cycling, tread mill every day for
cardiorespiratory benefits
• Balance training
• Flexibility and endurance like yoga
• Strength training and resistance training 2–3 times a week
• Meditation like yoga.
37. Women should be informed about the various side effect of HT in the light of various
studies like WHI, HERS, Million Women Study by taking HRT for a long time, i.e.
more than 5 years may lead to more incidence of breast cancer, CHD and DVT and
stroke.
Advantages of Hormone Therapy Women must also be informed about the benefits of
hormone therapy.
38. VARIOUS TYPES OF HORMONAL AND NON-
HORMONAL PHARMACOLOGICAL AGENTS
AVAILABLE
Natural Oestrogens ->Numerous natural oestrogen preparations are available, the
principle products available being estradiol, estrone and oestriol in that order of potency
• Oestradiol is most physiological oestrogen since it is the predominant circulating
oestrogen in the premenopausal reproductive women
• Oestrone is less potent than oestradiol. Both oestradiol and oestrone have been
demonstrated to be cardioprotective and osteoprotective
Oestriol is a less potent natural oestrogen that has not yet been shown to be
cardioprotective and osteoprotective, but has a good local action on genitourinary
structures and also controls vasomotor symptoms.
39. Semisynthetic Oestrogens
Because native steroids are relatively water insoluble, modifications of oestrogens for oral
administration and GI absorption includes conjugated oestrogens (oestrone sulphate, oestradiol valerate
and conjugated equine oestrogen), micronisation (micronised oestradiol).
Oestradiol valerate: It is a natural human source of oestrogen which is chemically synthesised, provides
rapid relief from climacteric symptoms prevents postmenopausal osteoporosis, and cardiovascular
risks. Bioavailability is good.
Only 3% is sufficient to exert effect on target organ.
Micronisation of oestradiol results in good levels of systemic oestrogens, although it is rapidly
metabolised to oestrone and conjugated to oestrone-3-glucoronide in the liver
40. Synthetic Oestrogens
Ethinyl oestradiol, quinestrol, and diethylstilboestrol, although used in contraceptives and other indications
are not used in HRT because of their increased potency and extended half-life.
• Oral and transdermal oestradiol have provided similar benefits in clinical studies.
Oral and nonoral HT regimens appear to have an equal positive impact on relieving symptoms of
oestrogen loss, such as hot flashes, vulvovaginal atrophy, and loss of BMD.
• Combination of CEE 0.625 mg (conjugated equine oestrogen) with MPA 2.5 mg is as effective as CEE 0.3
mg/ MPA 1.5 mg.
• A combined transdermal patch containing norethisterone acetate 0.25 mg per day and 17B oestradiol 50
microgram per day
Transdermal HRT has favourable effect on adverse effect on glucose and insulin levels, in contrast to oral
therapy.
New preparations are also available in the market with oestradiol as oestrogen and this has also been found
to be effective in dosage from 2 mg/day to as low as 0.5 mg/day.
Progestogens are added for endometrial protection
41. Disadvantage of oral route are:
• Increased VTE risk
Adverse lipid changes
Hepatic side effects
Gastrointestinal irritation
• Peaks and troughs in plasma levels are not stable.
42.
43. USE OF PROGESTERONE FOR HRT
Progesterone generation by the ovaries stops at menopause.
Currently, progesterones are viewed as endometrial protective agents.
They are also used as progesterones only pills in perimenopause and control DUB in
anovular cycles.
They have adverse effects on lipid profile and the breast.
The currently available compounds are:
Progesterone analogues –Dydrogesterone, Hydroxyprogesterone Medroxyprogesterone
acetate,
Testosterone analogues- Norethisterone, Norgestrel ,Levonorgestrel IUD
Newer synthetic -Desogestrel ,progesterones, Norgestimate ,Gestodene
Halogenated progesterone -Cyproterone acetate
Antimineralocorticoid -Drospirenone
45. Present Scenario of HT Risks and
Contraindications
• There may be a small increase in breast cancer risk after several years of HT
Progestogens added to the HT regimen largely eliminate any increased risk of
endometrial cancer.
If hysterectomy has been done then only oestrogen can be given
• The risk for venous thromboembolism (VTE) is increased approximately twofold in
current, but not former, users of HT, although the absolute risk is still very low
• Hormone therapy should be given for the shortest period in the smallest dosage possible
for symptomatic relief only.
46. Contraindications to HT
Unexplained vaginal bleeding and pregnancy: These are temporary but absolute
contraindications to HT.
Past history of breast cancer or endometrial cancer: While usually considered
contraindications to HT, short-term use for severe menopausal symptoms may be
considered with proper precautions.
Women with a past history of venous thrombosis
Hypertriglyceridaemia: Oral oestrogens are contraindicated because of the danger of
precipitating pancreatitis.
Chronic liver disease: Oral HT is a relative contraindication.
HT is not contraindicated in these clinical settings
These conditions include: • Endometriosis • Fibrocystic breast changes • Hypertension •
Mastalgia • Migraine headache • Obesity • Tobacco use • Uterine leiomyomata (fibroids)
47. Temporal Implications of HRT Use
Short-term HRT ->2–3 years
Long-term HRT implies use for more than 5 years.
•HRT relayed placement:-> Changes of the HRT types and forms are made over a
period of time,eg-> shifting from the initial use of oestrogen-progestogen therapy to
gonadomimetic use, to raloxifene and finally in some handing over to the nonhormonal
agents or to vaginal oestriol.
• Concomitant multiple hormone therapy: Where simultaneous administration of some
form of HRT takes place along with another HRT form (e.g. oestrogen-progestogen
combined with raloxifene, oestradiol combined with oestriol or another route (e.g. Oral
EPRT with vaginal oestriol).
Concomitant multimodal therapy: When HRT is variably combined with another
therapeutic modality (e.g. HRT with bisphosphonates and calcium, HRT with
antioxidants, micronutrients, multivitamins, and calcium).
50. Guidelines Indian
Menopause
Society, 2013
International
Menopause
Society, 2016
North American
Menopause Society,
2012
Age of
Initiation
• Begins within 10 years of menopause or < 60 years of
age - ‘Window of Opportunity’ (support
safe use for at least 5 years in healthy women
initiating treatment before age 60)
Duration of
use
• Premature menopause: MHT upto natural age of
menopause 3-5 years
• Continuation of therapy should be decided at the
discretion of the well-informed woman and her health
professional
51. GuidelinesIndian
Menopause
Society, 2013
International
Menopause
Society, 2016
North American
Menopause Society,
2012
Monitoring
• Pre-HT work-up (Indian MS)
• Initial follow-up at 3 months (NAMS)
• Annual follow-up – physical, laboratory/imaging (All)
• Discussion on lifestyle strategies to prevent or reduce
chronic disease (All)
• Currently no indication for increased mammographic
or cervical smear screening.
• Annual mammograms should be proposed in case of
high breast density in women using MHT.
52. Guidelines: Osteoporosis
Indian Menopause
Society, 2013
Revised Global Consensus Statement
on Menopausal Hormone Therapy
2016 The International Menopause Society,
The North American Menopause Society, The
Endocrine Society, The European Menopause
and Andropause Society, The Asia Pacific
Menopause Federation, The International
Osteoporosis Foundation and The Federation
of Latin American Menopause Societies.
MHT
, including tibolone, can be initiated in postmeno- pausal
women at risk of fracture or osteoporosis before the age of 60
years or within 10 years after menopause.
Initiation of MHT after the age of 60 years for the indica- tion
of fracture prevention is considered second-line therapy and
requires individually calculated benefit/risk, compared to
other approved drugs. If MHT is elected, the lowest effective
dose should be used.
Osteoporosis
Estrogen-progesterone
therapy or ET may be used
for prevention and treatment
of osteoporosis in the early
postmenopause in
symptomatic women un- less
there is a contraindication.
ET/EPT prevents all
osteoporotic fractures even
in low-risk population,
53. Guidelines: CV Risk
Indian
Menopause
Society, 2013
International
Menopause
Society, 2016
North American
Menopause Society,
2012/ The
Endocrine Society
2015
CVD
• No/lower risk in healthy women <60 years of age or
within 10 years of menopause
54. Guidelines: Breast Cancer Risk
Indian
Menopause
Society,
2013
International Menopause
Society, 2016
North American
Menopause Society,
2012/ The Endocrine
Society 2015
Breast Cancer
Progesterone
(eg,
dydrogesterone)
+ estrogen may
not increase risk
if given for <5
years
•Breast cancer risk should be
evaluated before MHT
prescription.
•Small increase in risk
(incidence of <1.0/ 1000
women/year of use)
•Risk is lower than increased
risks associated with common
lifestyle factors
•MCP or dydrogesterone could
be associated with a lower risk
than synthetic progestogen
NAMS: Risk of events in
younger women is lower
than that for older women
Endocrine Society:
Observational data suggest
that progesterone or
dydrogesterone may be
associated with a lower
risk, but further studies are
required to confirm this
