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Polycystic Ovary Syndrome (PCOS)

Polycystic Ovary Syndrome (PCOS)

Clinical Focus

Polycystic Ovary Syndrome (PCOS)

    

Contents

Clinical Background

Table 1: Criteria That Characterize PCOS

Individuals Suitable for Testing

Test Availability and Selection

Test Selection and Interpretation

Figure: Laboratory Testing in the Differential Diagnosis of Polycystic Ovary Syndrome (PCOS) and Assessment of Comorbidities

Table 2: Disorders Similar to PCOS and Potentially Distinguishing Symptoms

Appendix

Appendix Table 1: Laboratory Tests for Differential Diagnosis of PCOS and Assessment of PCOS Criteria

Appendix Table 2: Laboratory Tests for Common Comorbidities in Patients With PCOS

References
 

Clinical Background [return to contents]

Polycystic ovary syndrome (PCOS) is a common endocrine disorder that affects about 1 in 15 women of reproductive age.1 The exact cause is unknown but is thought to involve complex genetic and environmental interactions. Insulin resistance, accompanied by compensating hyperinsulinemia, is believed to play a key role in PCOS pathophysiology by increasing androgen production.

No single criterion or test is used to diagnose PCOS, because the syndrome is complex.

The commonly used Rotterdam 2003 criteria define PCOS as the presence of at least 2 of the following 3 criteria, after excluding disorders with similar symptoms: clinical hyperandrogenism, ovulatory dysfunction, polycystic ovaries (Table 1).2 Because there are many such disorders, diagnosis of PCOS is challenging. Furthermore, PCOS exhibits diversity in presentation ranging from phenotypes exhibiting all 3 criteria (Table 1) to mild phenotypes (normal androgens with oligomenorrhea and polycystic ovaries).3 Consequently, diverse diagnostic approaches for PCOS are used in clinical practice,4 which can delay diagnosis. More than one-third of women with PCOS spend >2 years seeking a diagnosis and see ≥3 healthcare professionals.5

Table 1. Criteria That Characterize PCOS

Criteria

Symptoms

Clinical hyperandrogenism

  • Hirsutism (excess facial or body hair)
  • Acne
  • Alopecia ranging from vertex, crown, and diffuse pattern to bitemporal and frontal hairline loss

Ovulatory dysfunction (oligo- or anovulation)

  • Amenorrhea (absence of menstruation)
  • Oligomenorrhea (>35 days between cycles)

Polycystic ovaries

  • ≥12 follicles, 2-9 mm in diameter
  • Increased ovarian volume (>10 mL) in either or both ovaries

Diagnosis of PCOS is especially challenging in adolescent girls and perimenopausal and menopausal women. For adolescents, many symptoms of PCOS are typical for their reproductive maturation during puberty (eg, anovulation and polycystic ovary morphology). Consequently, Endocrine Society guidelines suggest that hyperandrogenism and persistent oligomenorrhea are essential for diagnosis of PCOS in adolescent girls.6 For perimenopausal and menopausal women, no diagnostic criteria for PCOS currently exist. A presumptive diagnosis is suggested based on a well-documented long-term history of hyperandrogenism and oligomenorrhea during the reproductive years.6

Women with PCOS should be assessed for serious comorbidities. They are at greater risk for abnormal uterine bleeding, endometrial cancer, infertility, and pregnancy complications. Compared to the general population, women with PCOS are 4 times more likely to develop type 2 diabetes mellitus, and metabolic syndrome is twice as common.7 In addition, about half of all women with PCOS are obese.7 Women with PCOS who exhibit oligomenorrhea and hyperandrogenism (severe phenotypes) are especially at risk for these comorbidities.3

This Clinical Focus provides information on tests available for the differential diagnosis of PCOS and the identification of common comorbidities. This material is provided for educational purposes only and is not intended as medical advice. A physician's test selection and interpretation, diagnosis, and patient management decisions should be based on their education, clinical expertise and assessment of the patient.

Individuals Suitable for Testing [return to contents]

  • Women of reproductive age with ≥2 of the following criteria: hyperandrogenism, ovulatory dysfunction, and polycystic ovaries

  • Adolescent girls with hyperandrogenism and persistent oligomenorrhea

  • Perimenopausal and menopausal women with a well-documented long-term history of hyperandrogenism and oligomenorrhea

Test Availability and Selection [return to contents]

PCOS is primarily a diagnosis of exclusion, and Quest Diagnostics offers tests and panels for differential diagnosis of PCOS. In addition, Quest offers other tests and panels that may help assess the presence of any of the 3 PCOS criteria and identify common comorbidities (Appendix Tables 1 and 2).

Test Selection and Interpretation [return to contents]

Differential Diagnosis: Diagnoses to Exclude

Conditions that share many symptoms with PCOS, which should be excluded before making a diagnosis, include nonclassic congenital adrenal hyperplasia (CAH), thyroid disease, Cushing syndrome, and hyperprolactinemia.6 Laboratory testing for the differential diagnosis of these disorders is discussed below and in the Figure.

Figure. Laboratory Testing in the Differential Diagnosis of Polycystic Ovary Syndrome (PCOS) and Assessment of Comorbidities

Nonclassic CAH

Nonclassic CAH is often confused with PCOS because of the overlap in symptoms, such as hyperandrogenemia, oligo/amenorrhea, and polycystic ovarian morphology. Unlike PCOS, the disease is almost exclusively caused by genetic defects in the steroidogenic enzyme 21-hydroxylase. Nonclassic CAH is distinguished from PCOS by increased levels of 17-hydroxyprogesterone (17-OHP) caused by partially diminished 21-hydroxylase activity.

Guidelines recommend testing 17-OHP when distinguishing PCOS from nonclassic CAH.6,8,9 High values (≥1,000 ng/dL for 17-OHP for the early follicular phase) indicate 21-hydroxylase deficiency and thus nonclassic CAH.6 Values <200 ng/dL exclude nonclassic CAH, and for values 200 to 1,000 ng/dL, further testing by cosyntropin stimulation is suggested: increased 17-OHP in response to stimulation (>1,000 ng/dL) indicates 21-hydroxylase deficiency and nonclassic CAH rather than PCOS.6

Thyroid disease

Thyroid disease may lead to menstrual disorders similar to those of PCOS and can be distinguished by measuring serum thyroid-stimulating hormone (TSH). The pituitary gland produces more TSH when blood levels of thyroid hormones T3 and T4 are low (hypothyroidism) and less when they are high (hyperthyroidism). TSH values above the upper limit of normal (>4.5 mIU/L) suggest hypothyroidism whereas values below the lower limit of normal (usually <0.1 mIU/L) suggest hyperthyroidism.6

Falsely elevated or depressed TSH values may occur in samples from patients who have received mouse monoclonal antibody preparations during diagnosis or therapy, or those who are exposed to mice.10 Such patients may have developed human anti-mouse antibodies (HAMA) that interfere with accurate analysis. Testing samples from these patients involves pre-treatment to inhibit possible interference.

Hyperprolactinemia

Hyperprolactinemia can present with amenorrhea and hirsutism, often with galactorrhea. It is distinguished from PCOS by higher levels of serum prolactin.6 About 14% of young women (21 to 30 years) with amenorrhea have hyperprolactinemia.11 In women with amenorrhea and galactorrhea, prevalence estimates for hyperprolactinemia are as high as 70%.12

In rare cases, elevated prolactin test results are due to macroprolactin, which is usually an inactive form of a prolactin bound to an IgG. While most women with macroprolactinemia are asymptomatic, a minority may experience menstrual disorders (17%- 39%), infertility (29%- 35%), and galactorrhea (33%- 46%).13,14 One possible reason for the variability is that antibodies may bind epitopes that do not fully inactivate prolactin.13 Macroprolactin is distinguished from prolactin by a polyethylene-glycol precipitation test.

Finally, in extremely rare cases, elevated prolactin levels may be caused by a noncancerous tumor called a prolactinoma, leading to anovulation and hyperandrogenic symptoms such as acne and hirsutism.8

Differential Diagnosis: Diagnoses to Consider

The Endocrine Society recommends a more extensive diagnostic work-up to exclude several disorders in select women with amenorrhea and more severe phenotypes.6 These disorders are discussed below and in the Figure. Symptoms that potentially distinguish these disorders from PCOS are listed in Table 2 and may be used to direct testing.7

Table 2. Disorders Similar to PCOS and Potentially Distinguishing Symptoms7

Disorder

Potentially Distinguishing Symptoms

Virilizing tumors

Severe virilization with rapid onset

Cushing syndrome

Skin thinning, muscle weakness, hypertension

Acromegaly

Enlargement of hands, feet, and face

Hypothalamic amenorrhea

Low body weight, eating disorder, or excessive exercise

Primary ovarian insufficiency

Hot flashes, mood swings, vaginal dryness

Tumors

Adrenal-virilizing tumors may be accompanied by large elevations in androgens: total testosterone levels >150 ng/dL and dehydroepiandrosterone (DHEA) sulfate levels >700 µg/dL.8,15,16 However, American College of Obstetricians and Gynecologists (ACOG) guidelines indicate that there are no specific cutoff levels that define the presence of a tumor versus PCOS.8 The Endocrine Society suggests that marked elevations of serum testosterone and DHEA sulfate should prompt ultrasound imaging of ovaries and magnetic resonance imaging of adrenal glands to assist in differential diagnosis (Figure).6

Cushing syndrome

Cushing syndrome has several symptoms that overlap with PCOS, including acne, hirsutism, and anovulation. Differential diagnosis involves measuring urinary free cortisol (24-hour urinary collection or after a dexamethasone suppression test) or late-night salivary cortisol.6 Cortisol results for these tests are elevated in women with Cushing syndrome compared with women with PCOS who have normal cortisol values.

Acromegaly

Acromegaly, like PCOS, has symptoms of oligomenorrhea and hirsutism. However, it is readily distinguished from PCOS by elevated serum insulin-like growth factor-1 (IGF-I).

Conditions that cause amenorrhea

Conditions characterized by amenorrhea include hyperprolactinemia and hypothyroidism, as well as pregnancy, hypothalamic amenorrhea, and primary ovarian insufficiency.

Pregnancy is distinguished from PCOS by the presence of human chorionic gonadotropin (hCG). As described for TSH, sample pretreatment to remove HAMA may be required for detection of hCG in some patients.

Hypothalamic amenorrhea, including functional hypothalamic amenorrhea, and primary ovarian insufficiency, are distinguished from PCOS by low serum levels of estradiol (postmenopausal levels are typically ≤0.38 pg/mL [free]; ≤10 pg/mL [total]). Serum luteinizing hormone (LH) and follicle stimulating hormone (FSH) measurements are also useful in distinguishing these disorders. In PCOS, serum FSH levels are normal and LH levels are normal or slightly elevated; in hypothalamic amenorrhea, these markers are low to low-normal (luteal phase FSH <1.5 mIU/mL; LH <0.5 mIU/mL). In primary ovarian insufficiency, FSH levels are elevated (postmenopausal levels are typically 23 to 116.3 mIU/mL).

Diagnosis

Laboratory testing can help with diagnosis of PCOS by providing biochemical evidence of hyperandrogenism, assessing ovulatory function, and detecting polycystic ovaries (Appendix Table 1).

Hyperandrogenism

Elevated testosterone levels provide biochemical evidence for hyperandrogenism associated with PCOS. Free testosterone is more commonly elevated than total testosterone, which reflects all forms of testosterone: free, bioavailable, and bound to proteins such as sex hormone-binding globulin (SHBG) and albumin. For diagnosis, the American Association of Clinical Endocrinologists and the Androgen Excess and PCOS Society (AACE/AES) Guide to Best Practices recommend measuring free testosterone levels using free dialysis techniques combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS).9 Measuring free testosterone is preferred over measuring total testosterone because it is more sensitive for hyperandrogenism.9 In addition, LC-MS/MS assays are more accurate than traditional radioimmunoassays.9

Decreased SHBG levels cause elevated free testosterone levels more often than elevated total testosterone levels in hyperandrogenemic women. ACOG guidelines (reaffirmed 2015) suggest measuring SHBG, in addition to free and total testosterone, for evaluating patients with suspected PCOS.8 However, neither AACE/AES nor the Endocrine Society make any specific recommendations regarding SHBG.6,9

Measuring levels of other androgens, including DHEA, DHEA sulfate, 11β-hydroxyandrostenedione, and androstenedione, may also help diagnose PCOS. Elevated levels of these markers are consistent with hyperandrogenemia.17 However, AACE/AES concluded that measuring these markers provides incremental value because relatively few additional patients would be diagnosed.6 In addition, 11β-hydroxyandrostenedione and androstenedione are elevated in women with 21-hydroxylase deficiency, which may limit the discriminatory value of these biomarkers.17

Ovulatory dysfunction

Laboratory testing is useful for monitoring oligo- or anovulation by measuring midluteal progesterone (luteal phase reference range 3.0 to 31.4 ng/mL), especially when bleeding intervals appear to suggest regular ovulation.6

Polycystic ovaries

Laboratory testing can help detect polycystic ovaries when no accurate ovarian ultrasound is available. The approach involves measuring anti-Müllerian hormone; a proposed diagnostic threshold for polycystic ovarian morphology is ≥4.5 ng/mL.9 In addition, baseline values of anti-Müllerian hormone may predict the likelihood of women with PCOS achieving a live birth, as well as identify those less likely to ovulate and conceive on clomiphene therapy.18 Although anti-Müllerian hormone is a promising marker, AACE/AES concluded that more studies are necessary before recommending routine testing for PCOS.18

PCOS Comorbidities

Laboratory tests that help assess common PCOS comorbidities are listed in Appendix Table 2.

Endocrine Society guidelines recommend screening women with PCOS for6:

  • cardiovascular risk factors such as dyslipidemia and metabolic syndrome
  • impaired glucose tolerance every 2 to 5 years

Cardiovascular disease

Most women with PCOS have dyslipidemia, which manifests as decreased high-density lipoprotein-cholesterol (HDL-C) levels and elevated triglycerides. Although obesity is prevalent in women with PCOS, dyslipidemia occurs regardless of BMI.6 The Endocrine Society considers women with PCOS "at risk" of cardiovascular disease if they have high low-density lipoprotein-cholesterol (LDL-C) and non-HDL-C, among other risk factors, such as obesity, cigarette smoking, hypertension, subclinical vascular disease, family history of premature cardiovascular disease, and impaired glucose tolerance. They are considered "high risk" if they have metabolic syndrome, overt vascular or renal disease, obstructive sleep apnea, or type 2 diabetes mellitus.

Impaired glucose tolerance/type 2 diabetes mellitus

For testing impaired glucose tolerance, the guidelines recommend measuring fasting and 2-hour blood glucose levels using a 75-g oral glucose load.6,19 Fasting plasma glucose levels of 100 to 125 mg/dL (or 140 to 199 mg/dL in 2-h specimens) indicate increased risk for diabetes. Diabetes is diagnosed if the fasting glucose is ≥126 mg/dL or if the 2-hour specimen is ≥200 mg/dL.

For patients unwilling or unable to take the oral glucose tolerance test, hemoglobin A1c (HbA1c) can be measured; levels 5.7% to 6.4% indicate increased risk of diabetes, whereas levels of ≥6.5% are consistent with diabetes mellitus.6,19

Other morbidities

Women with PCOS and metabolic risk factors or insulin resistance may be at risk of liver disorders, including nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Endocrine Society guidelines suggest being aware of the possibility of these disorders, but they do not recommend routine screening.6 If NAFLD or NASH is identified, the extent of liver fibrosis may be assessed using the liver fibrosis score.20 A score >0.676 has 67% sensitivity and 97% specificity to identify the presence of advanced fibrosis.20

In addition, ACOG guidelines suggest considering monitoring fasting insulin levels in certain women with PCOS, including younger women, those undergoing ovulation induction, and those with signs of insulin resistance (eg, hypertension, central obesity, and acanthosis nigricans [dark patches of thick, velvety skin on the back of the neck, armpits, and groin]).8 ACOG suggests that routine testing of insulin levels, however, has little utility in other women with PCOS.8

Appendix. Tests for Diagnosis of PCOS and Common Comorbidities [return to contents]

Appendix Tables 1 and 2 are provided for informational purposes only and are not intended as medical advice. A physician's test selection and interpretation, diagnosis, and patient-management decisions should be based on his/her education, clinical expertise, and assessment of the patient.

Appendix Table 1. Laboratory Tests for Differential Diagnosis of PCOS and Assessment of PCOS Criteria

Test Code

Test Name

Clinical Use

Differential Diagnosis:

Nonclassic CAH

 

17180a

17-Hydroxyprogesterone, LC/MS/MS

Diagnose nonclassic CAH

 

17682(X)

17-Hydroxyprogesterone Response to ACTH Stimulation

Diagnose nonclassic CAH

 

90426 a,b

Steroid Panel, PCOS/CAH Differentiation
Includes 11-deoxycortisol (30543), 17-hydroxyprogesterone (17180), androstenedione (17182), DHEA (19894), and total and free testosterone (36170).

Diagnose nonclassic CAH

Thyroid disease

 

899

TSH

Diagnose hyper- or hypothyroidism

 

19537

TSH with HAMA Treatment

Diagnose hyper- or hypothyroidism in the presence of human anti-mouse antibodies (HAMA)

Hyperprolactinemia

 

746

Prolactin

Diagnose hyperprolactinemia

 

16122

Prolactin, Total and Monomeric

Diagnose macroprolactinemia

Tumors

 

402a

DHEA Sulfate, Immunoassay

Diagnose virilizing tumors

 

15983

Testosterone, Total, LC/MS/MS

Diagnose virilizing tumors

Cushing syndrome

 

14534a

Cortisol, Free, 24-Hour Urine

Diagnose Cushing syndrome

 

19897a

Cortisol, LC/MS/MS, Saliva

Diagnose Cushing syndrome

 

93020a

Cortisol, LC/MS/MS, Saliva, 2 Samples

Diagnose Cushing syndrome

 

18921a

Cortisol, LC/MS/MS, Saliva, 4 Samples

Diagnose Cushing syndrome

 

6921

Dexamethasone Suppression Test (DST), 1 Specimen

Diagnose Cushing syndrome

Acromegaly

 

16293a

IGF-I, LC/MS

Diagnose acromegaly

Amenorrhea caused by hypothalamic amenorrhea or primary ovarian insufficiency or pregnancy

 

36169a

Estradiol, Free, LC/MS/MS

Diagnose hypothalamic amenorrhea or primary ovarian insufficiency

 

7137

FSH and LH

Diagnose hypothalamic amenorrhea or primary ovarian insufficiency

 

470

FSH (Follicle Stimulating Hormone)

Diagnose primary ovarian insufficiency

 

8396

hCG, Total, Quantitative

Diagnose pregnancy

 

19720

hCG, Total, with HAMA Treatment

Diagnose pregnancy in the presence of human anti-mouse antibodies (HAMA)

PCOS Criteria:

Hyperandrogenism

 

402a

DHEA Sulfate, Immunoassay

Diagnose hyperandrogenism

 

30740

Sex Hormone Binding Globulin (SHBG)

Diagnose hyperandrogenism

 

90424 a,b

Steroid Panel, Polycystic Ovary Syndrome (PCOS)
Includes androstenedione (17182), DHEA (19894), and total and free testosterone (36170).

Diagnose hyperandrogenism

 

14966

Testosterone, Free, Bioavailable and Total, LC/MS/MS

Diagnose hyperandrogenism

 

36170

Testosterone, Free (Dialysis) and Total, LC/MS/MS

Diagnose hyperandrogenism

 

15983

Testosterone, Total, LC/MS/MS

Diagnose hyperandrogenism

Ovulatory dysfunction

 

17183a

Progesterone, LC/MS/MS

Assess ovulation during the midluteal phase (days 21 to 22)

Polycystic ovaries

 

16842(X)a

Anti-Müllerian Hormone AssessR™

Diagnose polycystic ovaries

ACTH, adrenocorticotropic hormone; DHEA, dehydroepiandrosterone; CAH, congenital adrenal hyperplasia; FSH, follicle stimulating hormone; HAMA, human antimouse antibody; hCG, human chorionic gonadotropin; IGF-I, insulin-like growth factor 1; LC/MS, liquid chromatography-(high resolution) mass spectrometry; LC/MS/MS, liquid chromatography-tandem mass spectrometry; LH, luteinizing hormone; PCOS, polycystic ovary syndrome; SHBG, sex hormone binding globulin; TSH, thyroid-stimulating hormone

a

This test was developed and its analytical performance characteristics have been determined by Quest Diagnostics. It has not been cleared or approved by the U.S. Food and Drug Administration. This assay has been validated pursuant to the CLIA regulations and is used for clinical purposes.

b

Panel components may be ordered separately.

Appendix Table 2. Laboratory Tests for Common Comorbidities in Patients With PCOS

Test Code

Test Name

Clinical Use

483(X)

Glucose

Diagnose diabetes based on fasting glucose

35181

Glucose Tolerance Test, 2 Specimens (75g)
Includes fasting and 2-hour specimens.

Diagnose diabetes based on fasting and 2-hour (post 75g glucose loading) specimens (2-hour OGTT)

496

Hemoglobin A1c

Diagnose diabetes if patient is unable or unwilling to take an OGTT

91083a

Insulin, B-chain, LC/MS/MS

Diagnose hyperinsulinemia associated with PCOS

7600b

Lipid Panel
Includes total cholesterol (334), triglycerides (896), HDL cholesterol (608), calculated LDL cholesterol, cholesterol/HDL ratio, and non-HDL cholesterol.

Diagnose dyslipidemia

14852(X)b,c

Lipid Panel with Reflex to Direct LDL
Same as 7600 plus direct LDL (8293) if triglyceride is >400 mg/dL.

Diagnose dyslipidemia

91398b

Metabolic Syndrome and Glucose Control Including Insulin
Includes glucose (483[X]); insulin (91083); total (334), HDL (608), and LDL (calculated) cholesterol; triglycerides (896); cholesterol/HDL ratio (calculated); and non-HDL (calculated).

Diagnose metabolic syndrome and diabetes

91979b

NAFLD Fibrosis Score
Includes albumin (223), AST (822), ALT (823), glucose (483[X]); platelet count (723), and AST/ALT ratio (calculated).

Identify liver fibrosis in women with PCOS and NAFLD or NASH

ALT, alanine aminotransferase; AST, aspartate aminotransferase; HbA1c, hemoglobin A1c; HDL, high-density lipoprotein; LC/MS/MS, liquid chromatography-tandem mass spectrometry; LDL, low-density lipoprotein; NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis; OGTT, oral glucose tolerance test; PCOS, polycystic ovary syndrome

a

This test was developed and its analytical performance characteristics have been determined by Quest Diagnostics. It has not been cleared or approved by the U.S. Food and Drug Administration. This assay has been validated pursuant to the CLIA regulations and is used for clinical purposes.

b

Panel components may be ordered separately.

c

Reflex tests are performed at an additional charge and are associated with an additional CPT code.

References [return to contents]

  1. Azziz R, Woods KS, Reyna R, et al. The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab. 2004;89:2745-2749.

  2. The Rotterdam ESHRE/ASRM-sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod. 2004;19:41-47.

  3. Clark NM, Podolski AJ, Brooks ED, et al. Prevalence of polycystic ovary syndrome phenotypes using updated criteria for polycystic ovarian morphology: an assessment of over 100 consecutive women self-reporting features of polycystic ovary syndrome. Reprod Sci. 2014;21:1034-1043.

  4. Bonny AE, Appelbaum H, Connor EL, et al. Clinical variability in approaches to polycystic ovary syndrome. J Pediatr Adolesc Gynecol. 2012;25:259-261.

  5. Gibson-Helm M, Teede H, Dunaif A, et al. Delayed diagnosis and a lack of information associated with dissatisfaction in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2017;102:604-612.

  6. Legro RS, Arslanian SA, Ehrmann DA, et al. Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2013;98:4565-4592.

  7. Williams T, Mortada R, Porter S. Diagnosis and treatment of polycystic ovary syndrome. Am Fam Physician. 2016;94:106-113.

  8. ACOG Committee on Practice Bulletins–Gynecology. ACOG Practice Bulletin No. 108: Polycystic ovary syndrome. Obstet Gynecol. 2009;114:936-949.

  9. Goodman NF, Cobin RH, Futterweit W, et al. American Association of Clinical Endocrinologists, American College of Endocrinology, and Androgen Excess and PCOS Society disease state clinical review: guide to the best practices in the evaluation and treatment of polycystic ovary syndrome–Part 1. Endocr Pract. 2015;21:1291-1300.

  10. Tate J, Ward G. Interferences in immunoassay. Clin Biochem Rev. 2004;25:105-120.

  11. Lee DY, Oh YK, Yoon BK, et al. Prevalence of hyperprolactinemia in adolescents and young women with menstruation-related problems. Am J Obstet Gynecol. 2012;206:213 e211-215.

  12. Serri O, Chik CL, Ur E, et al. Diagnosis and management of hyperprolactinemia. CMAJ. 2003;169:575-581.

  13. Vaishya R, Gupta R, Arora S. Macroprolactin; a frequent cause of misdiagnosed hyperprolactinemia in clinical practice. J Reprod Infertil. 2010;11:161-167.

  14. Vallette-Kasic S, Morange-Ramos I, Selim A, et al. Macroprolactinemia revisited: a study on 106 patients. J Clin Endocrinol Metab. 2002;87:581-588.

  15. Azziz R, Carmina E, Dewailly D, et al. The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril. 2009;91:456-488.

  16. Barnes RB, Ehrmann DA, Rosenfield RL. Hyperandrogenism, hirsutism, and polycystic ovary syndrome. In: Jameson JL, De Groot LJ, eds. Endocrinology. Vol II. 6th ed. Philadelphia, PA: Saunders; 2010:2386-2406.

  17. O'Reilly MW, Kempegowda P, Jenkinson C, et al. 11-Oxygenated C19 steroids are the predominant androgens in polycystic ovary syndrome. J Clin Endocrinol Metab. 2017;102:840-848.

  18. Goodman NF, Cobin RH, Futterweit W, et al. American Association of Clinical Endocrinologists, American College of Endocrinology, and Androgen Excess and PCOS Society disease state clinical review: guide to the best practices in the evaluation and treatment of polycystic ovary syndrome–Part 2. Endocr Pract. 2015;21:1415-1426.

  19. American Diabetes Association. Standards of medical care in diabetes—2017. Diabetes Care. 2017;40(suppl 1):S1-S120.

  20. Chalasani N, Younossi Z, Lavine JE, et al. The diagnosis and management of nonalcoholic fatty liver disease: practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2018;67:328-357.
     

 

Content reviewed 04/2018

 
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