Polycystic ovary syndrome

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Polycystic ovary syndrome is the most common form of chronic anovulation associated with androgen excess. Polycystic ovary syndrome occurs in approximately 5% to 10% of reproductive-age women. The diagnosis of polycystic ovary syndrome is made by excluding other hyper androgenic disorders like non-classic adrenal hyperplasia, androgen-secreting tumors, hyperprolactinemia in women with chronic anovulation and androgen excess. Polycystic ovary syndrome can be diagnosed whenever two of following three criteria are present oligomenorrhea, hirsutism and/or hyperandrogenemia and polycystic ovaries. Prompt investigation and treatment is necessary for patients with excessive vaginal bleeding. The endometrium of the patient with polycystic ovary syndrome must be evaluated by biopsy because of long-term exposure to unopposed estrogen leaves patients at increased risk for endometrial cancer. Polycystic ovary syndrome is also associated with increased metabolic and cardiovascular disorders. Polycystic ovary syndrome is considered to be a heterogeneous disorder with multifactorial causes. Polycystic ovary syndrome risk is significantly increased with a positive family history of chronic anovulation and androgen excess, and this complex disorder may be inherited in a polygenic fashion. Treatment begins with weight loss and metformin, if either or both are indicated, and depending on the patient’s reproductive needs oral contraception supplemented with antiandrogen therapy for patients not wishing to conceive or fertility treatments for patients desiring pregnancy. The prognosis is excellent with treatment. Complications of polycystic ovary syndrome include infertility, irregular uterine bleeding, and increased pregnancy loss

Polycystic ovary syndrome was first described in 1935 by American gynecologists Irving F. Stein, Sr. and Michael L. Leventhal, from whom its original name of Stein–Leventhal syndrome is taken. The earliest published description of polycystic ovary syndrome was in 1721 in Italy. Cyst-related changes to the ovaries were described in 1844.

Polycystic ovary syndrome (PCOS) may be classified into 4 types based on the severity of symptoms into asymptomatic form, mild form, classical form, and metabolic form.

There are several organs involved in the pathogenesis of polycystic ovary syndrome like ovary, adrenal, hypothalamus, pituitary, or insulin-sensitive tissues. The pathophysiology of Polycystic ovary syndrome is not well understood. Insulin resistance leads to compensatory insulin hypersecretion by the pancreas in order to maintain normoglycemia. The resulting hyperinsulinemia promotes ovarian androgen output and may also promote adrenal androgen output.

The underlying event in patients with polycystic ovary syndrome remains unknown, but the hormonal imbalance between LH, FSH and estrogen are mainly responsible for the development of polycystic ovary syndrome. Most studies suggest that more than one factor could play a role in developing polycystic ovary syndrome.

Polycystic ovary syndrome must be differentiated from other causes of irregular or absent menstruation and hirsutism, such as congenital adrenal hyperplasia, cushing’s syndrome, hyperprolactinemia, and other pituitary or adrenal disorders.

Polycystic ovarian syndrome (PCOS) is one of the most common endocrine disorders in reproductive-age women, with a prevalence of 4-12% in the United States. Up to 10% of women are diagnosed with PCOS.

Common risk factors in the development of polycystic ovary syndrome are hyperinsulinemia secondary to insulin resistance, obesity, family history of polycystic ovary syndrome among first-degree relatives, premature adrenarche, fetal androgen exposure, and low birth weight.

There is insufficient evidence to recommend routine screening for polycystic ovary syndrome (PCOS), but according to Royal College of Obstetricians and Gynaecologists (RCOG) thyroid function tests, serum prolactin levels, and a free androgen index are baseline screening tests recommended for women with suspected polycystic ovarian syndrome (PCOS).

If left untreated patients with polycystic ovary syndrome may develop cardiovascular diseases due to elevated cholesterol and increased level of androgens. Increased lengths of time without a menstrual period leads to unopposed exposure of endometrium to estrogen which may be complicated by endometrial cancer. Complications that can develop as a result of polycystic ovary syndrome are insulin resistance/type II diabetes, high blood pressure, dyslipidemia, strokes, miscarriage, and infertility. The prognosis for fertility in patients with polycystic ovary syndrome is good with treatment, unless there are other unknown fertility problems.

Polycystic ovary syndrome was previously defined according to the proceedings of an expert conference sponsored by the National Institutes of Health (NIH) in 1990, which described the disorder as including hyperandrogenism or hyperandrogenemia (or both), oligo-ovulation, and exclusion of known disorders of androgen excess and anovulation. Another expert conference held in Rotterdam in 2003 defined Polycystic ovary syndrome, after the exclusion of related disorders, by the presence of two of the following three features oligo-ovulation or anovulation, clinical or biochemical signs of hyperandrogenism (or both), and polycystic ovaries. In essence, the Rotterdam 2003 criteria expanded the NIH 1990 definition by creating two new phenotypes ovulatory women with polycystic ovaries plus hyperandrogenism and oligo-anovulatory women with polycystic ovaries but without hyperandrogenism.

The significant information that needs to focused in the history of the patient includes menstrual abnormalities, infertility, signs of virilization on physical examination and family history of Polycystic ovary syndrome among first-degree relatives.The most common symptoms of Polycystic ovary syndrome include amenorrhea or oligomenorrhea, abnormal uterine bleeding and androgenization, including hirsutism, acne, oily skin.

Patients with polycystic ovary syndrome usually appear obese. During the physical examination, it is essential to search for and document signs of androgen excess (hirsutism, virilization, or both), insulin resistance (acanthosis nigricans), and the presence of unopposed estrogen action (well-rugated vagina and stretchable, clear cervical mucus) to support the diagnosis of polycystic ovary syndrome

Measurement of the plasma levels of several hormones is helpful in supporting the diagnosis of polycystic ovary syndrome and especially in excluding other disorders. Determining the LH/FSH ratio of 3:1 is virtually diagnostic of polycystic ovary syndrome. However, a normal ratio does not exclude the diagnosis, as LH levels fluctuate widely throughout the course of a day. Other androgens are measured to screen for other virilizing adrenal tumors. Fasting blood glucose is measured to look for diabetes, screening for lipid abnormalities is also employed. Testosterone is measured to exclude a virilizing tumor. Prolactin is measured to exclude a prolactinoma. Thyroid-stimulating hormone (TSH) is measured to rule out hypothyroidism.

There are no electrocardiogram findings associated with polycystic ovary syndrome.

There are no X-ray findings associated with polycystic ovary syndrome.

There are no CT findings associated with polycystic ovary syndrome.

There are no MRI findings associated with polycystic ovary syndrome.

The Rotterdam 2003 criteria include the use of ultrasound as a diagnostic tool in diagnosing polycystic ovary syndrome (PCOS). The typical polycystic-appearing ovary may emerge in a nonspecific fashion on an ultrasound. Multiple (12+) subcapsular follicles ranging from 2 to 9 mm in diameter in a state of arrested development (‘pearl necklace’ appearance) in a single ovary is diagnostic for PCOS on ultrasound.

There are no other imaging findings associated with polycystic ovary syndrome.

Endometrial biopsy is recommended in patients diagnosed with polycystic ovary syndrome because long-term unopposed estrogen stimulation leaves these patients at increased risk for endometrial cancer.

The first step in the management of PCOS is weight loss if the patient is obese, and treatment of type 2 diabetes with metformin. In significantly overweight patients, weight loss alone usually effects a cure and should always be vigorously attempted. Diet and exercise are recommended in all women with PCOS. The next step is the initiation of treatment to break the self-perpetuating anovulatory cycling, either by stimulating ovulation or suppressing androgenic and ovarian activity. The selection of treatment depends on whether the pregnancy is desired. All anti-androgen treatments will take at least 3 months to affect hirsutism. The drug regimen for PCOS depends upon the desire for the fertility of the patient.

Surgery is not considered a first-line therapy for polycystic ovary syndrome (PCOS) and it does not affect insulin resistance or obesity. Surgery is indicated in the treatment of PCOS only in patients desiring pregnancy in whom at least 1 year of conservative therapy has failed.

There is no established method for primary prevention of polycystic ovary syndrome (PCOS).

Secondary preventive measures for polycystic ovary syndrome (PCOS) include lifestyle modifications and use of metformin to prevent diabetes and atherosclerosis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Polycystic ovary syndrome was first described in 1935 by American gynecologists Irving F. Stein, Sr. and Michael L. Leventhal, from whom its original name of Stein–Leventhal syndrome is taken. The earliest published description of polycystic ovary syndrome (PCOS) was in 1721 in Italy. Cyst-related changes to the ovaries were described in 1844.

• In 1721, a description of symptoms resembling PCOS was first published in Italy.^[1]
• In 1844, cyst-related changes to the ovaries were first described.
• In 1935, Irving F. Stein, Sr. and Michael L. Leventhal, American gynecologists, described PCOS for the first time.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Polycystic ovary syndrome (PCOS) may be classified into 4 subtypes based on the severity of symptoms including asymptomatic, mild, classic, and metabolic form.

PCOS may be classified into 4 subtypes based upon severity of symptoms into:^{[1][2] [1]}

• Asymptomatic form: Women with only polycystic ovarian morphology
• Mild form: Polycystic ovarian morphology along with anovulation
• Classical form: Hyperandrogenism along with ovarian dysfunction (anovulation and/or poly cystic ovarian )
• Metabolic form: Combination of mild and classical forms with presence of obesity and/or insulin resistance (abdominal obesity, insulin resistance, increased waist-hip ratio)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

There are several organ systems involved in the pathogenesis of polycystic ovary syndrome like ovary, adrenal, hypothalamus, pituitary, or insulin-sensitive tissues. The pathophysiology of Polycystic ovary syndrome is not well understood. Insulin resistance leads to compensatory insulin hypersecretion by the pancreas in order to maintain normoglycemia. The resulting hyperinsulinemia promotes ovarian androgen output and may also promote adrenal androgen output.

The pathophysiology of polycystic ovary syndrome is not well understood. There are several organ systems involved in the pathogenesis of polycystic ovary syndrome like ovary, adrenal, hypothalamus, pituitary, or insulin-sensitive tissues.^[1][2][3]

• Insulin resistance leads to compensatory insulin hypersecretion by the pancreas in order to maintain normoglycemia.
• The resulting hyperinsulinemia promotes ovarian androgen output and may also promote adrenal androgen output.
• High insulin levels also suppress hepatic production of sex hormone binding globulin (SHBG), which exacerbates hyperandrogenemia by increasing the proportion of free circulating androgens.
• Another factor that promotes ovarian androgen output is the fact that women with polycystic ovary syndrome are exposed to high levels of LH for long term.
• This LH excess seems to be a result of an increased frequency of gonadotropin releasing hormone pulses from the hypothalamus.
• The abnormal hormonal milieu also probably contributes to incomplete follicular development which results in polycystic ovarian morphology.

• Polycystic ovaries develop when the ovaries are stimulated to produce excessive amounts of male hormones (androgens), particularly testosterone, either through the release of an excessive luteinizing hormone (LH) by the anterior pituitary gland or through high levels of insulin in blood (hyperinsulinemia) of women whose ovaries are sensitive to this stimulus.
• These follicles get matured but were never released from the ovary because of abnormal hormone levels resulting in the cyst formation and make a string of pearls appearance.

↑ 5α-reductase reductivity

↓ Hβ-HSD1 activity

↑ Cortisol metabolism

↑ ACTH

↑ Adrenal androgens

Normal serum cortisol

PCOS

• Polycystic ovary syndrome may have a genetic predisposition.
• No specific gene has been identified, and it is thought that many genes could contribute to the development of the polycystic ovarian syndrome.
• The genetic component appears to be inherited in an autosomal dominant fashion with high genetic penetrance but variable expressivity in females.

Common conditions associated with polycystic ovary syndrome are:^[4][5]

• Type 2 diabetes
• Endometrial hyperplasia and cancer
• Infertility
• Hypertension
• Gestational diabetes
• Preeclampsia
• Hirsutism
• Acne

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

The underlying defect in patients with polycystic ovary syndrome (PCOS) remains unknown, but a hormonal imbalance between LH/FSH and estrogen is mainly responsible for the development of polycystic ovary syndrome. Most studies suggest that more than one factor could play a role in developing Polycystic ovary syndrome (PCOS).

The underlying defect in patients with polycystic ovary syndrome (PCOS) remains unknown and is thought to be multifactorial, but abnormal gonadotropin dynamics are mainly responsible for the development of polycystic ovary syndrome. It is suggested that more than one factor could play a role in developing PCOS.^[1][2][3]

• Increased gonadotropin-releasing hormone secretion in the pituitary gland results in increased secretion of serum luteinizing hormone (LH) and an elevated LH/follicle-stimulating hormone (FSH) ratio.
• Hypersecretion of LH results in increased ovarian androgen production, leading to arrest of follicular development with follicular atresia which may result in multiple cysts formation in the ovaries, and anovulatory cycles.
• Genes are thought to be another factor. The genetic component appears to be inherited in an autosomal dominant fashion with high genetic penetrance but variable expressivity in females
• The phenotype appears to manifest itself at least partially via heightened androgen levels secreted by ovarian follicle theca cells from women with the allele.
• The exact gene affected has not yet been identified.
• In rare instances, single-gene mutations can give rise to the phenotype of the syndrome.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Polycystic ovary syndrome must be differentiated from other causes of irregular or absent menstruation and hirsutism, such as congenital adrenal hyperplasia, cushing’s syndrome, hyperprolactinemia, and other pituitary or adrenal disorders.

Polycystic ovary syndrome must be differentiated from other causes of irregular or absent menstruation and hirsutism, such as congenital adrenal hyperplasia, cushing’s syndrome, hyperprolactinemia, and other pituitary or adrenal disorders. The table below summarizes the findings that differentiate polycystic ovary syndrome from other conditions that cause irregular or absent menstruation and hirsutism:^[1][2][3][4]

Disease	Differentiating Features
Pregnancy	Pregnancy always should be excluded in a patient with a history of amenorrhea. Features include amenorrhea or oligomenorrhea, abnormal uterine bleeding, nausea/vomiting, cravings, weight gain (although not in the early stages and not if vomiting), polyuria, abdominal cramps and constipation, fatigue, dizziness/lightheadedness, and increased pigmentation (moles, nipples). Uterine enlargement is detectable on abdominal examination at approximately 14 weeks of gestation. Ectopic pregnancy may cause oligomenorrhea, amenorrhea, or abnormal uterine bleeding with abdominal pain and sometimes subtle or absent physical symptoms and signs of pregnancy.
Hypothalamic amenorrhea	Diagnosis of exclusion Seen in athletes, people on crash diets, patients with significant systemic illness, and those experiencing undue stress or anxiety Predisposing features are as follows weight loss, particularly if features of anorexia nervosa are present or the BMI is <19 kg/m2. Recent administration of depot medroxyprogesterone, which may suppress ovarian activity for 6 months to a year. Use of dopamine agonists (eg, antidepressants) and major tranquilizers Hyperthyroidism In patients with weight loss related to anorexia nervosa, fine hair growth (lanugo) may occur all over the body, but it differs from hirsutism in its fineness and wide distribution.
Primary amenorrhea	Causes include reproductive system abnormalities, chromosomal abnormalities, or delayed puberty. If secondary sexual characteristics are present, an anatomic abnormality (eg, imperforate hymen, which is rare) should be considered. If secondary sexual characteristics are absent, a chromosomal abnormality (eg, Turner syndrome ) or delayed puberty should be considered.
Cushing syndrome	Cushing syndrome is due to excessive glucocorticoid secretion from the adrenal glands, either primarily or secondary to stimulation from pituitary or ectopic hormones; can also be caused by exogenous steroid use. Features include hypertension, weight gain (central distribution), acne, and abdominal striae. Patients may have hyponatremia and elevated plasma cortisol levels on dexamethasone suppression testing.
Hyperprolactinemia	Mild hyperprolactinemia may occur as part of PCOS-related hormonal dysfunction. Other causes include stress, lactation, and use of dopamine antagonists. A prolactinoma of the pituitary gland is an uncommon cause and should be suspected if prolactin levels are very high (>200 ng/mL). Physical examination findings are usually normal. As in patients with PCOS, hyperprolactinemia may be associated with mild galactorrhea, oligomenorrhea, or amenorrhea. However, galactorrhea can occur with nipple stimulation and/or stress when prolactin levels are within normal ranges. A large prolactinoma may cause headaches and visual field disturbance due to pressure on the optic chiasm resulting in classically a gradually increasing bi-temporal hemianopsia
Ovarian or adrenal tumor	Benign ovarian tumors and ovarian cancer are rare causes of excessive androgen secretion; adrenocortical tumors also can increase the production of sex hormones Abdominal swelling or mass, abdominal pain due to fluid leakage or torsion, dyspareunia, abdominal ascites, and features of metastatic disease may be present Features of androgenization include hirsutism, weight gain, oligomenorrhea or amenorrhea, acne, clitoral hypertrophy, deepening of the voice, and high serum androgen (eg, testosterone, other androgens) levels In patients with an androgen-secreting tumor, serum testosterone is not suppressed by dexamethasone
Congenital adrenal hyperplasia	Congenital adrenal hyperplasia is a rare genetic condition resulting from 21-hydroxylase deficiency The late-onset form presents at or around menarche Patients have features of androgenization and subfertility Affects approximately 1% of hirsute patients More common in Ashkenazi Jews (19%), inhabitants of the former Yugoslavia (12%), and Italians (6%) Associated with high levels of 17-hydroxyprogesterone A short adrenocorticotropic hormone stimulation test with measurement of serum17-hydroxyprogesterone confirms the diagnostic assays of a variety of androgenic hormones help define other rare adrenal enzyme deficiencies, which present similarly to 21-hydroxylase deficiency
Anabolic steroid abuse	Anabolic steroids are synthetic hormones that imitate the actions of testosterone by increasing muscle bulk and strength Should be considered if the patient is a serious sportswoman or bodybuilder Features include virilization (including acne and hirsutism), often increased muscle bulk in male pattern, oligomenorrhea or amenorrhea, clitoromegaly, gastritis, hepatomegaly, alopecia, and aggression Altered liver function test results are seen
Hirsutism	Hirsutism is excessive facial and body hair, usually coarse and in a male pattern of distribution Approximately 10% of women report unwanted facial hair There is often a family history and typically some Mediterranean or Middle Eastern ancestry May also result from use of certain medications, both androgens, and others including danazol, glucocorticoids, cyclosporine, and phenytoin Menstrual history is normal When the cause is genetic, the excessive hair, especially on the face (upper lip), is present throughout adulthood, and there is no virilization When secondary to medications, the excessive hair is of new onset, and other features of virilization, such as acne and deepened voice, may be present

Polycystic ovarian syndrome must be differentiated from diseases that cause virilization and hirsutism in female:^[5][6][7]

Disease name	Steroid status	Other laboratory	Important clinical findings
Non-classic type of 21-hydroxylase deficiency	Increased: 17-hydroxyprogesterone Exaggerated Androstenedione, DHEA, and 17-hydroxyprogesterone in response to ACTH	Low testosterone levels	No symptoms in infancy and male Virilization in females
11-β hydroxylase deficiency	Increased: DOC 11-Deoxy-Cortisol Decreased: Cortisol Corticosterone Aldosterone	Low testosterone levels	Hypertension and hypokalemia Virilization
3 beta-hydroxysteroid dehydrogenase deficiency	Increased: DHEA 17-hydroxypregnenolone Pregnenolone Decreased: Cortisol Aldosterone	Low testosterone levels	Salt-wasting adrenal crisis in infancy Mild virilization of genetically female infants Undervirilization of genetically male infants, making it the only form of CAH which can cause ambiguous genitalia in both genetic sexes.
Polycystic ovary syndrome	High DHEAS and androstenedione levels	Low testosterone levels	Polycystic ovaries in sonography Obesity PCOS is the most common cause of hirsutism in women No evidence another diagnosis
Adrenal tumors	Variable levels depends on tumor type	Low testosterone level	Older age Rapidly progressive symptoms
Ovarian virilizing tumor	Variable levels depends on tumor type	Testosterone is high	Older age Rapidly progressive symptoms
Cushing’s syndrome	Increase cortisol & metabolites Variable other steroids	Variable mineralocorticoid excess	Cushingoid appearance
Hyperprolactinemia	Normal levels of most of steroids	Increased prolactin	Infertility, galactorrhea

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Polycystic ovarian syndrome (PCOS) is one of the most common endocrine disorders in reproductive-age women, with a prevalence of 4-12% in the United States. Up to 10% of women are diagnosed with PCOS.

• Approximately 5% to 10% of women of reproductive age are affected.^[1][2]
• Prevalence among first-degree relatives of patients with PCOS is 25% to 50%, suggesting a strong inheritance of the syndrome; there is evidence for possible X-linked dominant transmission.

Polycystic ovary syndrome can appear anytime from menarche until menopause but generally, is seen around menarche and is diagnosed then or in early adulthood.^[3]

Polycystic ovary syndrome occurs in approximately 1 in 10 women.

There is no racial predilection for polycystic ovary syndrome.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Common risk factors in the development of Polycystic ovary syndrome are hyperinsulinemia secondary to insulin resistance, obesity, family history of PCOS among first-degree relatives, premature adrenarche, fetal androgen exposure, and low birth weight.

Common risk factors in the development of Polycystic ovary syndrome are:

• Hyperinsulinemia secondary to insulin resistance; associated with type 2 diabetes mellitus^[1][2][3]
• Obesity
• Family history of PCOS among first-degree relatives
• Premature adrenarche
• Fetal androgen exposure^[2]
• Low birth weight

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

There is insufficient evidence to recommend routine screening for polycystic ovary syndrome (PCOS), but according to Royal College of Obstetricians and Gynaecologists (RCOG) thyroid function tests, serum prolactin levels, and a free androgen index are baseline screening tests recommended for women with suspected polycystic ovarian syndrome (PCOS).

There is insufficient evidence to recommend routine screening for polycystic ovary syndrome (PCOS), but the Royal College of Obstetricians and Gynaecologists (RCOG) recommends the following baseline screening tests for women with suspected polycystic ovarian syndrome (PCOS): ^[1][2]

• Thyroid function tests
• Serum prolactin levels
• Free androgen index

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

If left untreated patients with PCOS may develop cardiovascular diseases due to elevated cholesterol and increased levels of androgens. Increased lengths of time without a menstrual period leads to unopposed exposure of endometrium to estrogen can result in uterine cancer. Complications that can develop as a result of polycystic ovary syndrome are insulin resistance/type II diabetes, high blood pressure, dyslipidemia, strokes, miscarriage, and infertility. The prognosis for fertility in patients with polycystic ovary syndrome is good with treatment, unless there are other unknown fertility problems.

If left untreated patients with PCOS may progress to cardiovascular diseases due to elevated cholesterol and increased levels of androgens. Increased lengths of time without a menstrual period leads to unopposed exposure of endometrium to estrogen which may result in uterine cancer.^[1][2]

Complications that can develop as a result of polycystic ovary syndrome are:^[3][4]

• Endometrial hyperplasia and endometrial cancer
• Insulin resistance/Type II diabetes
• High blood pressure
• Dyslipidemia
• Cardiovascular disease
• Strokes
• Miscarriage
• Infertility

• The prognosis for fertility in patients with polycystic ovary syndrome is good with treatment, unless there are other unknown fertility problems.^[5]
• Regular follow-up is recommended to avoid ovarian hyperstimulation, multiple pregnancies, and endometrial hyperplasia.
• Patients should be counseled regarding the long-term risk of diabetes, hypertension, and endometrial hyperplasia, including the importance of maintaining a BMI <25 kg/m2 and control of other risk factors for type 2 diabetes.

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