INTRODUCTION The polycystic ovary syndrome (PCOS) is an important cause of both

menstrual irregularity and androgen excess in women. When fully expressed, the
manifestations include irregular menstrual cycles, hirsutism, obesity, insulin resistance, and
anovulatory infertility.
The treatment of PCOS will be reviewed here. The epidemiology and pathogenesis, diagnostic
criteria, and clinical manifestations of PCOS are described in detail separately.
(See "Epidemiology and pathogenesis of the polycystic ovary syndrome in
adults" and "Diagnosis of polycystic ovary syndrome in adults" and "Clinical manifestations of
polycystic ovary syndrome in adults".)
OVERVIEW OF APPROACH Women with polycystic ovary syndrome (PCOS) have multiple
abnormalities that require attention, including oligomenorrhea, hyperandrogenism, anovulatory
infertility, and metabolic risk factors such as obesity, insulin resistance, dyslipidemia, and
impaired glucose tolerance. Weight loss, which can restore ovulatory cycles and improve
metabolic risk, is the first-line intervention for most women. Our overall approach is similar to
that described by the 2013 Endocrine Society Clinical Guidelines [1].
Goals The overall goals of therapy of women with PCOS include:
Amelioration of hyperandrogenic symptoms (hirsutism, acne, scalp hair loss)
Management of underlying metabolic abnormalities and reduction of risk factors for type
2 diabetes and cardiovascular disease
Prevention of endometrial hyperplasia and carcinoma, which may occur as a result of
chronic anovulation
Contraception for those not pursuing pregnancy, as women with oligomenorrhea ovulate
intermittently and unwanted pregnancy may occur
Ovulation induction for those pursuing pregnancy
Lifestyle changes We suggest diet and exercise for weight reduction as the first step for
overweight and obese women with PCOS. Available evidence suggests that lifestyle
interventions (diet, exercise, and behavioral interventions) are more effective than minimal
treatment for weight loss and for improving insulin resistance and hyperandrogenism [2].
(See 'Weight reduction' below.)
Oral contraceptives and risk assessment Oral contraceptives (OCs) are the mainstay of
pharmacologic therapy for women with PCOS for managing hyperandrogenism and menstrual
dysfunction and for providing contraception. OCs are associated with an increased risk of
venous thromboembolism (VTE) in all users, but particularly in obese women. There have been
concerns that the presence of PCOS per se may represent an additional independent risk factor
for VTE, but available data do not support this concept. (See "Clinical manifestations of
polycystic ovary syndrome in adults", section on 'Venous thromboembolism'.)
Our approach to the use of OCs in women with PCOS is the same as in women without PCOS.
Risk factors for VTE including obesity, patient age, and family history of VTE should be
assessed. We currently suggest using caution if OCs are prescribed to obese women (body
mass index [BMI] 30 kg/m2) over age 40 years, because these women are at particularly high
risk for VTE. Other relative and absolute contraindications to OC use are outlined in the table
(table 1). Alternatives to oral estrogen-progestin contraceptives include cyclic progestin therapy,
continuous progestin therapy (progestin-only OCs [the minipill]), or a progestin-releasing
intrauterine device (IUD). Cyclic progestin therapy can induce regular withdrawal uterine
bleeding and reduce the risk of endometrial hyperplasia. Both continuous progestin therapy (eg,

a progestin-only OC such as norethindrone 0.35 mg/day) and the progestin-releasing IUD

provide contraception and reduce the risk of endometrial hyperplasia. (See"Risks and side
effects associated with estrogen-progestin contraceptives", section on 'Venous thromboembolic
disease' and 'Endometrial protection' below.)
WOMEN NOT PURSUING PREGNANCY
Menstrual dysfunction
Endometrial protection The chronic anovulation seen in polycystic ovary syndrome (PCOS)
is associated with an increased risk of endometrial hyperplasia and possibly endometrial
cancer. (See "Clinical manifestations of polycystic ovary syndrome in adults", section on
'Endometrial cancer risk' and "Endometrial carcinoma: Epidemiology and risk factors", section
on 'Chronic anovulation'.)
We suggest combined estrogen-progestin contraceptives as first-line therapy for menstrual
dysfunction and endometrial protection.
Combined estrogen-progestin contraceptives provide a number of benefits in women with
PCOS, including:
Daily exposure to progestin, which antagonizes the endometrial proliferative effect of
estrogen
Contraception in those not pursuing pregnancy, as women with oligomenorrhea ovulate
intermittently and unwanted pregnancy may occur
Cutaneous benefits for hyperandrogenic symptoms (see 'Androgen excess' below)
OCs affect insulin sensitivity, carbohydrate metabolism, and lipid metabolism; the effects
depend upon the estrogen dose and androgenicity of the progestin. However, there is no
evidence that women with PCOS are at greater risk for either metabolic adverse effects or
cardiovascular complications of OCs. (See 'Metabolic effects of OCs in PCOS' below and "Risks
and side effects associated with estrogen-progestin contraceptives" and "Clinical manifestations
of polycystic ovary syndrome in adults", section on 'Venous thromboembolism'.)
Absence of pregnancy should be documented before OCs are begun.
An approach to starting OCs in women with PCOS is described below (see 'Choice of oral
contraceptive' below). Risks and side effects of OCs (including breakthrough bleeding) are
similar to those for women without PCOS. Breakthrough bleeding and an overview of estrogenprogestin OCs are reviewed in detail separately. (See"Risks and side effects associated with
estrogen-progestin contraceptives" and "Overview of the use of estrogen-progestin
contraceptives".)
For women with PCOS who choose not to or cannot take OCs, alternative treatments for
endometrial protection are intermittent or continuous progestin therapy, or a progestin-releasing
intrauterine device (IUD) [3]. In this setting, we recommend medroxyprogesterone acetate (5 to
10 mg) for 10 to 14 days every one to two months. An alternative, but one that has been less
well studied, is natural micronized progesterone 200 mg (given for the same duration every one
to two months). Patients should be made aware that progestin therapy alone will not reduce the
symptoms of acne or hirsutism, nor will it provide contraception. However, continuous progestin
therapy with norethindrone 0.35 mg daily provides both contraception and endometrial
protection. This is a progestin-only OC that is also referred to as the minipill. An alternative
progestin option that provides both endometrial protection and contraception are the

levonorgestrel-releasing IUDs. (See "Intrauterine contraception (IUD): Overview", section on

'Levonorgestrel-releasing IUDs'.)
Metformin is a potential alternative to restore menstrual cyclicity, as it restores ovulatory menses
in approximately 30 to 50 percent of women with PCOS [4,5]. Its ability to provide endometrial
protection is less well established, and we therefore consider it to be second-line therapy [6,7].
(See "Metformin for treatment of the polycystic ovary syndrome".)
When metformin is used, we suggest monitoring to confirm that ovulatory cycles have been
established. This can be done with luteal phase serum progesterone measurements or
transvaginal ultrasound. (See "Evaluation of the menstrual cycle and timing of ovulation",
section on 'Detection of ovulation' and "Metformin for treatment of the polycystic ovary
syndrome", section on 'Oligomenorrhea'.)
Androgen excess
Hirsutism Our approach to the management of hirsutism is consistent with the 2008
Endocrine Society Clinical Practice Guidelines on Hirsutism, which suggest an estrogenprogestin contraceptive as first-line pharmacologic therapy for most women [8]. In addition, the
2013 Endocrine Society Clinical Practice Guidelines on the Diagnosis and Treatment of
Polycystic Ovary Syndrome also suggest OCs as first-line therapy for menstrual irregularities
and hirsutism [1]. An antiandrogen is then added after six months if the cosmetic response is
suboptimal (see "Treatment of hirsutism" and "Use of combination estrogen-progestin
contraceptives in the treatment of hyperandrogenism and hirsutism"). OCs and an antiandrogen
may sometimes be started simultaneously at the outset, particularly when the cutaneous
manifestations are particularly bothersome to the patient.
For women with hirsutism and contraindications to OCs, we sometimes
use spironolactone alone, but an alternative form of contraception is essential because, if
pregnancy occurs, an antiandrogen such as spironolactone could prevent development of
normal external genitalia in a male fetus. Spironolactone alone does not regularize menstrual
cycles, and in fact, is sometimes associated with menstrual irregularities. Therefore, in women
using spironolactone as monotherapy for hyperandrogenism, progestin therapy is often needed.
(See "Treatment of hirsutism", section on 'Antiandrogen therapy' and 'Endometrial
protection' above.)
Choice of oral contraceptive We typically start with an OC containing 20 mcg of ethinyl
estradiol combined with a progestin with minimal androgenicity (such as norgestimate). Other
progestins with minimal androgenicity or antiandrogenic properties include desogestrel and
drospirenone, but both have been associated with a possible higher risk of venous
thromboembolism (VTE) (table 2). OCs containing one of the original progestins, norethindrone
or norethindrone acetate, are also good options; while they are not as low in androgenicity, they
have not been associated with excess VTE risk. (See "Risks and side effects associated with
estrogen-progestin contraceptives", section on 'Type of progestin'.)
Higher doses of ethinyl estradiol (30 to 35 mcg) are needed in some women for optimal
suppression of ovarian androgens and management of hyperandrogenic symptoms. Although
transdermal or vaginal ring preparations are potential options, they have not been well studied
for the management of hirsutism and there are concerns about an excess risk of VTE with both
regimens. (See "Transdermal contraceptive patch", section on 'Risk of thrombotic
events' and "Contraceptive vaginal ring", section on 'Cardiovascular events'.)

Antiandrogens After six months, if the patient is not satisfied with the clinical response to
OC monotherapy (for hyperandrogenic symptoms), we typically addspironolactone 50 to 100
mg twice daily. (See "Treatment of hirsutism", section on 'Antiandrogen therapy'.)
Other antiandrogens that are effective include finasteride and cyproterone
acetate (cyproterone is available in most countries, but not the United States). Flutamide is also
effective, but we recommend not using it because of its potential hepatotoxicity.
(See "Treatment of hirsutism", section on 'Antiandrogen therapy' and "Overview of the use of
estrogen-progestin contraceptives".)
Other Gonadotropin-releasing hormone (GnRH) agonists are also sometimes used to
suppress ovarian androgen production; add-back estrogen-progestin therapy is necessary to
avoid bone loss and estrogen deficiency symptoms. Although this approach is effective, it is
limited by its complexity and cost. (See "Treatment of hirsutism", section on 'GnRH agonist'.)
Although some clinicians use metformin to treat hirsutism, the Endocrine Society Clinical
Practice Guidelines suggest against its routine use as it is associated with minimal or no benefit
and is less effective than treatment with OCs and/or antiandrogens [8]. (See "Metformin for
treatment of the polycystic ovary syndrome", section on 'Hirsutism'.)
Hirsutism can also be treated by removal of hair by mechanical means such as shaving,
waxing, depilatories, electrolysis, or laser treatment. In addition, Vaniqa
(eflornithine hydrochloride cream 13.9%) is a topical drug that inhibits hair growth. It is not a
depilatory and must be used indefinitely to prevent regrowth. (See "Removal of unwanted
hair" and "Treatment of hirsutism", section on 'Nonpharmacologic methods'.)
Acne and androgenetic alopecia The management of acne and scalp hair loss
(androgenetic alopecia) in women with PCOS are reviewed in detail separately.
(See "Treatment of acne vulgaris", section on 'Hormonal therapy' and "Treatment of
androgenetic alopecia in men".)
Metabolic abnormalities
Obesity Weight loss, which can restore ovulatory cycles and improve metabolic risk, is the
first-line intervention for most women. The approach to obesity management is the same as that
for patients without PCOS, starting with lifestyle changes (diet and exercise) [9], followed by
pharmacotherapy, and when necessary, bariatric surgery [10]. (See 'Weight reduction' below
and "Obesity in adults: Overview of management" and "Short-term medical outcomes following
bariatric surgery", section on 'Polycystic ovary syndrome'.)
Weight reduction We suggest weight loss strategies using calorie restricted diets combined
with exercise for women with PCOS and obesity. Although there are no large randomized trials
of exercise-specific interventions, a systematic review of exercise therapy in PCOS concluded
that there may be modest weight loss, and improvements in ovulation and insulin sensitivity
[11]. (See "Obesity in adults: Role of physical activity and exercise", section on 'Exercise plus
diet' and "Obesity in adults: Dietary therapy".)
Even modest weight loss (5 to 10 percent reduction in body weight) in women with PCOS may
result in restoration of normal ovulatory cycles [12-14] and improved pregnancy rates [15] in
short-term studies. However, the response to weight loss is variable; not all individuals have
restoration of ovulation or menses despite similar weight reduction [9,10,16]. In addition, there
are no randomized trials and no long-term data on reproductive or metabolic outcomes with
weight loss.

Weight loss results in a decrease in serum androgen concentrations, and in some instances,
improvements in hirsutism. However, data demonstrating an improvement in hirsutism are
limited [2,9].
There is no good evidence that one type of diet is superior to another for women with PCOS.
Low-carbohydrate diets have become very popular for women with PCOS, based upon the
notion that less carbohydrate leads to less hyperinsulinemia and therefore less insulin
resistance. However, a 12-week study of a high protein/lowcarbohydrate diet (30 percent
protein, 40 percent carbohydrate, 30 percent fat) and a low protein/high carbohydrate diet (15
percent protein, 55 percent carbohydrate, 30 percent fat) were equally effective for weight loss,
improvements in menstrual cyclicity, insulin resistance, dyslipidemia, and abdominal fat in one
study of 28 overweight women with PCOS [17]. It is not known if an extremely low carbohydrate
diet would be any more effective for these endpoints. (See "Obesity in adults: Dietary therapy",
section on 'Low-carbohydrate diets'.)
Bariatric surgery Bariatric surgery is another strategy for weight loss in women with PCOS.
In one study of 17 obese women with PCOS with a mean body mass index (BMI) of
50.7 kg/m2, bariatric surgery was associated with a mean weight loss after 12 months of 41 9
kg, restoration of ovulatory cycles, and improvements in insulin resistance, hyperandrogenemia,
and hirsutism scores [10]. (See "Bariatric operations for management of obesity: Indications and
preoperative preparation" and "Short-term medical outcomes following bariatric surgery",
section on 'Polycystic ovary syndrome'.)
Insulin resistance/type 2 diabetes Several drugs, including biguanides (metformin) and
thiazolidinediones (pioglitazone, rosiglitazone), can reduce insulin levels in women with PCOS.
These drugs may also reduce ovarian androgen production (and serum free testosterone
concentrations) and restore normal menstrual cyclicity [18-21]. (See "Metformin for treatment of
the polycystic ovary syndrome" and "Thiazolidinediones in the treatment of diabetes mellitus".)
Although there had been widespread enthusiasm and use of metformin for a number of
indications in PCOS, clinical data no longer support this approach. A detailed discussion of
metformin use in PCOS is found elsewhere. (See "Metformin for treatment of the polycystic
ovary syndrome".)
Strategies recommended by the American Diabetes Association for prevention of type 2
diabetes are discussed separately. The approach in women with PCOS is the same as for
women without PCOS. (See "Prevention of type 2 diabetes mellitus".)
Thiazolidinediones have been less well studied than metformin, but they appear to improve
insulin sensitivity and hyperandrogenemia [18-24]. However, because of limited clinical data,
potential weight gain, and a possible association with cardiovascular adverse events, we do not
recommend the use of thiazolidinediones in women with PCOS who do not have diabetes.
(See "Thiazolidinediones in the treatment of diabetes mellitus".)
Metabolic effects of OCs in PCOS In healthy women, OC use decreases insulin sensitivity,
but in general, this decrease is not clinically significant [25]. It has been assumed that OC use
would also worsen insulin sensitivity in women with PCOS, although data are conflicting, with
studies showing an improvement [26], worsening [27], or no change [28] in insulin sensitivity.
When compared with metformin, OCs may be less beneficial for insulin sensitivity, but better for
androgen suppression and menstrual cycle control [29]. This topic is reviewed separately.
(See "Metformin for treatment of the polycystic ovary syndrome", section on 'Metabolic effects'.)

There are also theoretical concerns that women with PCOS may be at particular risk for
cardiovascular complications with OCs, given their other underlying cardiovascular risk factors.
However, there are no OC risk data specific to women with PCOS. (See "Risks and side effects
associated with estrogen-progestin contraceptives", section on 'Coronary heart disease'.)
The effects of combination OC-metformin therapy are reviewed elsewhere. (See "Metformin for
treatment of the polycystic ovary syndrome", section on 'Metformin plus oral contraceptives'.)
Dyslipidemia The approach to treatment of dyslipidemia in women with PCOS is the same
as for other patients with dyslipidemia. Exercise and weight loss are the first line approach,
followed by pharmacotherapy, if needed. (See "Statins: Actions, side effects, and
administration".)
Statins Statins are effective for dyslipidemia in women with PCOS, but do not appear to
have other clinically important metabolic or endocrine effects. In a meta-analysis of four trials in
244 women randomly assigned to a statin (simvastatin or atorvastatin) or placebo for 6 to 12
months, statin therapy decreased serum low-density lipoprotein (LDL) and triglycerides, but had
no effect on high-density lipoprotein (HDL), fasting insulin, or C-reactive protein. A small
decrease in serum testosterone was observed, but there were no improvements in menstrual
cycle regularity, ovulation, acne, hirsutism, or BMI [30].
Obstructive sleep apnea Sleep apnea, a common disorder in women with PCOS, is an
important determinant of insulin resistance, glucose intolerance, and type 2 diabetes
(see "Clinical manifestations of polycystic ovary syndrome in adults"). In one report of women
with PCOS and obstructive sleep apnea, treatment with continuous positive airway pressure
(CPAP) improved insulin sensitivity and reduced diastolic blood pressure [31].
Nonalcoholic steatohepatitis The prevalence of nonalcoholic steatohepatitis (NASH)
appears to be increased in women with PCOS. Both weight loss andmetformin use appear to
improve metabolic and hepatic function in these women [32,33]. (See "Clinical manifestations of
polycystic ovary syndrome in adults", section on 'Nonalcoholic fatty liver disease'.)
WOMEN PURSUING PREGNANCY
Ovulation induction It is important to complete a basic evaluation of the couple before
initiating therapy in an infertile woman, including a semen analysis of the male. Weight loss
should always be attempted prior to initiating ovulation induction because ovulation can be
restored with a modest amount of weight loss. If unsuccessful, a multistep approach to ovulation
induction is then undertaken (table 3). (See "Ovulation induction with clomiphene
citrate" and "Strategies for improving the efficacy of clomiphene induction of
ovulation" and "Overview of ovulation induction".)
Weight loss In many overweight and obese women with polycystic ovary syndrome (PCOS),
weight loss alone is often associated with a reduction in serum testosterone concentration,
resumption of ovulation, and pregnancy [12,34,35]. As an example, in one series of 18 obese
women with PCOS treated with a hypocaloric diet, mean weight fell from 77 to 57 kg and mean
plasma testosterone concentration fell from 0.75 to 0.39 ng/mL [34]. Moreover, many women
resumed ovulation after the weight loss.
Another study placed 20 women with PCOS and mean body mass index (BMI) of
32 kg/m2, amenorrhea for greater than three months, and increased plasma concentrations of
androstenedione, testosterone, or dehydroepiandrosterone sulfate on a hypocaloric diet (1000
to 1500 kcal/day) [34]. After weight loss ranging from 4.8 to 15.2 kg (mean 9.7 kg), significant

reductions in the concentration of luteinizing hormone (LH) (45 percent decrease), fasting
insulin (40 percent decrease), and testosterone (35 percent decrease) were observed; most of
the women ovulated, and many of the infertile women became pregnant. Similar results were
reported in a small randomized study [35].
Medications
Clomiphene citrate We suggest clomiphene citrate as first-line therapy for ovulation
induction in non-obese women with PCOS (BMI <30 kg/m2) [1]. Approximately 80 percent
of women with PCOS ovulate in response to clomiphene citrate and approximately 50
percent conceive. Clomiphene regimens and success rates are reviewed in detail
elsewhere. (See "Ovulation induction with clomiphene citrate" and "Ovulation induction
with letrozole".)
Letrozole The aromatase inhibitor letrozole is also effective for ovulation induction in
women with PCOS. For obese women with PCOS (BMI 30 kg/m2),letrozole results in
higher cumulative live birth rates than clomiphene citrate. Some experts now suggest
letrozole over clomiphene for ovulation induction in obese PCOS patients, but not in
patients with a BMI <30 kg/m2. Ovulation induction is an off-label use of letrozole. Efficacy
and safety are reviewed in detail separately. (See "Ovulation induction with letrozole".)
Metformin - Metformin is a drug whose major effect is to reduce hepatic glucose output
and thereby lower serum insulin concentrations. Metformin has been used to promote
ovulation either alone or in combination with clomiphene, but clomiphene appears to be
superior for pregnancy rates. Its role in treating infertility is limited [1]. Clinical trial data
supporting this are reviewed elsewhere. (See "Metformin for treatment of the polycystic
ovary syndrome", section on 'Anovulatory infertility'.)
A consensus group has recommended against the routine use of metformin (including
ovulation induction) except in women with glucose intolerance [36]. Metformin therapy for
PCOS and strategies for prevention of type 2 diabetes are discussed in more detail
separately. (See "Metformin for treatment of the polycystic ovary
syndrome" and "Prevention of type 2 diabetes mellitus".)
Gonadotropin therapy - Another method to induce ovulation is administration of
exogenous gonadotropins [37]. A study of 225 women with PCOS treated over a 10-year
period at one center found rates of ovulation and pregnancy of 72 percent and 45 percent,
respectively, after the administration of low-dose gonadotropins [38]. Exogenous
gonadotropin therapy is reviewed in detail elsewhere. Women with PCOS and anovulatory
infertility treated with gonadotropins are at high risk for ovarian hyperstimulation syndrome
(OHSS).
Exogenous gonadotropin regimens are complex and expensive and are best carried out
by experienced clinicians; most clinicians recommend an assessment of fallopian tube
patency before initiating these relatively aggressive therapies. (See "Classification and
treatment of ovarian hyperstimulation syndrome" and"Pathogenesis of ovarian
hyperstimulation syndrome" and "Prevention of ovarian hyperstimulation
syndrome" and "Overview of ovulation induction".)
Other medications
Thiazolidinedione therapy has been investigated for induction of ovulation [6,39-41],
but we do not suggest its use because of concern about its cardiovascular safety.
(See 'Insulin resistance/type 2 diabetes' above and "Thiazolidinediones in the
treatment of diabetes mellitus".)

Although women with PCOS are not likely gonadotropin-releasing hormone (GnRH)
deficient, pulsatile GnRH is moderately effective for ovulation induction. It is currently
available in Europe but not in the United States. In one study of 41 patients
undergoing 114 ovulation induction cycles, 56 percent of women ovulated, and 40
percent of ovulatory patients achieved pregnancy [42]. Ovulatory cycles were
associated with lower BMI and fasting insulin, and higher baseline serum folliclestimulating hormone (FSH) concentrations. Thus, pulsatile GnRH may be a
reasonable option, particularly for lean women with PCOS.
Laparoscopic surgery In the past, wedge resection of the ovaries was a standard treatment
for infertility in women with PCOS. However, this approach has been abandoned, both because
of the efficacy of clomiphene and because of the high incidence of pelvic adhesions seen with
wedge resection. A substitute for wedge resection, laparoscopic ovarian laser electrocautery,
may be effective in some women with PCOS. However, given the other pharmacologic options
for ovulation induction, surgery is not often indicated. The use of laparoscopic surgery for
ovulation induction in PCOS is discussed in detail elsewhere. (See "Laparoscopic surgery for
ovulation induction in polycystic ovary syndrome".)
In vitro fertilization If weight loss, ovulation induction with medications, and/or laparoscopic
ovarian laser electrocautery are unsuccessful, the next step is in vitro fertilization (see "In vitro
fertilization"). Women with PCOS are at increased risk for both multiple gestation and
OHSS. Metformin administration may help to reduce the risk of OHSS in these women.
(See "Metformin for treatment of the polycystic ovary syndrome", section on 'IVF pretreatment'.)
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials,
The Basics and Beyond the Basics. The Basics patient education pieces are written in plain
language, at the 5th to 6th grade reading level, and they answer the four or five key questions a
patient might have about a given condition. These articles are best for patients who want a
general overview and who prefer short, easy-to-read materials. Beyond the Basics patient
education pieces are longer, more sophisticated, and more detailed. These articles are written
at the 10th to 12th grade reading level and are best for patients who want in-depth information
and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a
variety of subjects by searching on patient info and the keyword(s) of interest.)
Basics topics (see "Patient information: Polycystic ovary syndrome (The Basics)")
Beyond the Basics topics (see "Patient information: Polycystic ovary syndrome (PCOS)
(Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS Regardless of the diagnostic criteria used, the
management of polycystic ovary syndrome (PCOS) includes treatment of individual components
of the syndrome (hirsutism, oligomenorrhea, infertility, obesity, and glucose intolerance),
depending upon the patient's goals.
Weight loss, which can restore ovulatory cycles and improve metabolic risk, is the firstline intervention for most women. (See 'Overview of approach' above.)
Oral contraceptives (OCs) are the mainstay of pharmacologic therapy for women with
PCOS for managing hyperandrogenism and menstrual dysfunction and for providing
contraception.

Our approach to the use of OCs in women with PCOS is the same as that for women
without PCOS. Risk factors for venous thromboembolism (VTE) including obesity, patient
age, and family history of VTE should be assessed (table 1).
We suggest caution when prescribing OCs in obese women (body mass index [BMI]
30 kg/m2) over age 40 years because of their greater risk of VTE (Grade 2B). Other
relative and absolute contraindications to OC use are outlined in the table (table 1).
(See 'Oral contraceptives and risk assessment' above.)
For hirsutism or other androgenic symptoms, we suggest an OC as the treatment of
choice (Grade 2B). (See 'Androgen excess' above.)
We typically start with a preparation containing 20 mcg of ethinyl estradiol combined with
a progestin with minimal androgenicity (such as norethindrone, norgestimate, desogestrel,
and drospirenone). Higher doses of ethinyl estradiol are needed in some women for
optimal management of hyperandrogenic symptoms. Concerns about VTE risk with newer
progestins and with drospirenone are reviewed separately. (See "Overview of the use of
estrogen-progestin contraceptives"and "Risks and side effects associated with estrogenprogestin contraceptives", section on 'Type of progestin'.)
If the patient is not satisfied with the clinical response to six months of OC monotherapy
(for hyperandrogenic symptoms), we suggest adding spironolactone(Grade 2B)
(see 'Androgen excess' above). Other options for treating hirsutism are reviewed in detail
elsewhere. (See "Treatment of hirsutism".)
For prevention of endometrial hyperplasia and possibly cancer, we suggest OC therapy
(Grade 2C). (See 'Menstrual dysfunction' above.)
For women with PCOS who choose not to or cannot take OCs, we suggest intermittent
progestin therapy (Grade 2B). (See 'Menstrual dysfunction' above.)
For women with PCOS who desire pregnancy, we first recommend weight loss if the
woman is overweight or obese (Grade 1B). If they are unable to lose weight or modest
weight loss does not restore ovulatory cycles, we suggest initiating ovulation induction
with clomiphene citrate for women with a BMI <30 kg/m2 andletrozole for those with a
BMI 30kg/m2 (Grade 2B) (see 'Ovulation induction' above). This topic is reviewed in
detail separately. (See "Ovulation induction with clomiphene citrate", section on 'Polycystic
ovary syndrome' and "Ovulation induction with letrozole".)