Diagnosis of pcos

polycystic ovarian disease is common condition in women of reproductive age group.

1. DIAGNOSIS OF PCOS BY DR. K.SRAVANI, 2 nd yr PG(OBGY), NRIIMS.

2. NATIONAL INSTITIUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT (NICHD-1990) H yperandrogenemia / Clinical signs of hyperandrogenism . Menstrual dysfunction Exclusion of other androgenic disorders

3. ROTTERDAM CRITERIA (2003) 2 out of 3 Polycystic appearing ovary (USG) ,ovarian volume > 10 mL³ and/or more than 12 follicles measuring between 2 - 9 mm in size in at least one ovary. Clinical and/or biochemical signs of H yperandrogenis m. Oligoanovulation

4. Androgen Excess and PCOS Society (AE-PCOS) in 2006 Hyperandrogenism ( hirsutism and/or hyperandrogenemia ), Ovarian dysfunction ( oligoanovulation or PCO) Exclusion of other androgen excess or related disorders.

5. Overall prevalence of PCOS among different populations ( for the three different diagnostic criteria) similar . (NIH 6%, Rotterdam and AE-PCOS 10%). 2006

6. Diagnosis of Polycystic Ovary Syndrome: PCOS is not a specific endocrine disease but a syndrome. A collection of signs and symptoms and that no one sign, symptom, or test is diagnostic. The individual biochemical, clinical, and radiologic components of the commonly utilized diagnostic criteria.

7. Hyperandrogenemia : Circulating levels of total and/or free testosterone above the normal range is the usual basis for diagnosis of hyperandrogenemia . Other androgens that may be elevated in women with PCOS include androstenedione , DHEA, and DHEA-S . The serum DHEA-S concentration is the traditional marker for adrenal androgen excess, it is relatively high and remain stable across the day and cycle.

8. Measuring, total testosterone concentration, usually is Unnecessary. In most cases, clinical evidence of hirsutism provides ample evidence of hyperandrogenism The AEPCOS Society - an elevated serum DHEA-S level as sufficient evidence of Hyperandrogenism . But not considered when diagnosing PCOS per the Rotterdam criteria.

9. Laboratory features Elevated total testosterone Most values in PCOS 70-150 ng/dl (if >200 ng/dl, consider ovarian or adrenal tumor ) Free testosterone more sensitive . Free androgen index > 4.5 (FAI= total testosterone x 100 /SHBG). Considered a better indicator. DHEA-S Most normal or slightly high in PCOS If >800 mcg/dl, consider adrenal tumor

10. Clinical H yperandrogenism Clinical manifestations of hyperandrogenism include hirsutism , acne, and androgenic alopecia, all of which relate to the effects of androgens on the pilosebaceous unit.

11. Hirsutism is the growth of terminal hairs on the face or body in a male pattern and a distressing symptom of PCOS . HIRSUTISM

12. Ferriman Gallwey score Extent of terminal (coarse pigmented) hair growth at each of the following 11 hormonally sensitive sites Upper lip Sideburn area Chin Jaw & Neck Upper back Lower back Chest Upper abdomen Lower abdomen Upper arms Thighs Score of 6 or above used to define clinical hyperandrogenemia

13. Modifie d Ferriman Gallwey score

14. Modified Ferriman Gallwey score 9 areas Score 1-4 0-absence of terminal hair 4-extensive terminal hair growth >8 - hirsutism Standard for assessing the severity of hirsutism in clinical settings. Patients asked for the method & frequency of hair removal (shaving, plucking, waxing), which also provides a clinically relevant measure for assessing the response to treatment.

15. Androgenic Alopecia Androgenic alopecia (also called androgenetic alopecia and female pattern hair loss), describing scalp hair loss in women. The normal hair cycle, the growth (ANAGEN) phase lasts 2–3 years, 90% of the scalp hair. In chronic androgen excess, hair follicles shrink in the anagen phase, leading to less scalp coverage & alopecia. Rotterdam criteria for PCOS, androgenetic alopecia was noted in 22%.

16. The pattern of hair loss in women with PCOS follows the well-recognized “female hair loss” Phenotype. Wherein hair thinning is most apparent at the caput while the frontal hairline remains well preserved. When more severe, the frontal and bitemporal hair line can be involved.

17. ACNE Acne is the second most common manifestation of hyperandrogenism in women with PCOS. Androgen-mediated stimulation of sebaceous secretions is recognized as mechanism for acne, The prevalence of acne among women with PCOS varies with ethnicity, ranging from 12% to 14% among White women ,being higher in Asian Indians ( 25%)

18. No existing standardized methodology for quantifying severity of acne in women with PCOS. In the clinical setting, quantification of acne severity should take into consideration the number, distribution, and severity of the active lesions as well as residual scars. Pictorial records of the affected areas can allow comparative assessment of response to treatment.

19. OVULATORY AND MENSTRUAL DYSFUNCTION Oligomenorrhea is defined as less than eight menstrual cycles per year. Cyclic menses occurring at normal intervals strongly suggest, but not proof of ovulation . Most common menstrual abnormalities in women with PCOS are oligomenorrhea and amenorrhea. Polymenorrhea (regular cycles ) occurring at intervals <21days) is uncommon, < 2% of the PCOS patients.

20. OVULATORY AND MENSTRUAL DYSFUNCTION Oligo or amenorrhea typically begins in the peripubertal period . Reduction in ovulatory events leads to deficient progesterone secretion . Chronic estrogen stimulation of the endometrium with no progesterone results in intermittent breakthrough bleeding or DUB . Increased risk for endometrial hyperplasia and/or E ndometrial CA .

21. Polycystic Ovaries - USG Criteria by ultrasound Increased ovarian volume (>1 O ml ³ ) AND presence of >12 follicles measuring 2-9 mm in diameter in a single ovary. Polycystic ovaries not specific for PCOS > 20% normal women have incidental polycystic ovaries Many small follicles are displaced peripherally and surround the dense central stroma of a polycystic ovary

22. 1/3rd of regularly menstruating women without PCOS, & even 14% of women using oral contraceptives meet the ultrasonographic criteria for PCO. Normal women with PCO have regular menstrual cycles, exhibit normal serum gonadotropin and ovarian & steroid hormone levels, not infertile . By PCO USG Criteria diagnosis of PCOS uplift by 50%, compared to the criteria earlier recommended by the NICHD AE-PCOS Society has recommended , the minimal number of small follicles should be increased from 12(Rotterdam) to a minimum of 25.

23. Polycystic VS. Multicystic Ovaries Polycystic ovaries Bilateral At least 12 follicles Follicular diameter 2 - 9 mm Stroma increased Multicystic ovaries Bilateral Multiple cysts Cyst diameter usually > 10 mm Stroma not increased

24. OVARIAN ABNORMALITIES Thickened sclerotic cortex Multiple follicles in peripheral location 80% of women with PCOS have classic cysts

25. PEARLY WHITE SMOOTH ENLARGED AND THICK WALLED OVARY ON LAPAROSCOPY L aparoscopy

26. ASSOCIATED MEDICAL CONDITIONS Altered gonadotropin Dyslipidemia Insulin resistance Metabolic syndrome—43% of PCOS patients (2 fold higher than age-matched population) Inflammation Cancer risk

27. Abnormal Gonadotropin Secretion Abnormal patterns of gonadotropin is a common feature of women with PCOS. Altered LH/FSH ratios are more often encountered in the lean than in obese women with PCOS. Increased serum LH , low-normal FSH levels, and increased LH/FSH ratios are typical. LH/FSH ratio Levels vary over menstrual cycle, released in pulsatile fashion, affected by OCPs LH/FSH ratio >2

28. The overall prevalence of insulin resistance among women with PCOS is between30% - 35 % Most women with PCOS and insulin resistance are young and have ample pancreatic B-cell reserve,compensatory hyperinsulinemia , allowing them to maintain normal glucose homeostasis, at least in the fasting state. INSULIN RESISTANCE :

29. H yperinsulinemia Fasting glucose level of 110-125 mg/dL Glucose level of 140-199 mg/dL after 75 gm glucose challenge test Stimulated testing with OGTT may be more sensitive than fasting measurements Fasting glucose/insulin ratio (G/I) . A ratio < 4.5 has in general been shown to be > 90% sensitive

30. Acanthosis nigricans A skin condition with dark velvety patches in body folds and creases. Found in 45-50% of PCOS patients.

31. Dyslipidemia Dyslipidemia is perhaps the most common metabolic abnormality observed in women with PCOS. 70% have elevated lipid level, hyperinsulinemia are associated with decreased high-density lipoprotein (HDL)cholesterol and elevated triglyceride levels. Elevated(LDL) may result from hyperandrogenism or reflect a genetic or dietary influence, seen in both lean and obese women with PCOS, prevalent in the setting of excess adiposity.

32. Inflammation PCOS is a proinflammatory state. Glucose can cause inflammatory response in mononuclear cells . Result is recruitment of macrophages, which produce inflammatory cytokines, a systemic inflammatory response and negatively impacting glucose metabolism. CRP is a marker of chronic inflammation and is correlated with insulin resistance, body weight. Treatment with metformin lowers CRP levels

33. Cancer Risk Chronic anovulation, obesity, and hyperinsulinemia risk for proliferative endometrial pathologies such as endometrial hyperplasia and even endometrial cancer The risk for endometrial cancer may be as high as threefold greater .

34. DIFFERENTIAL DIAGNOSIS Thyroid diseases 2.Hyperprolactinemia 3.Non classical CAH 4.Ovarian and Adrenal Androgen secreting tumours. 5.Cushings syndrome 6.Idiopathic hirsutism 7.Severe insulin resistance syndromes.

35. Laboratory evaluation in suspected PCOS: Tests for ruling out common conditions that can mimic PCOS: Serum thyroid-stimulating hormone (TSH) Serum prolactin Serum 17-hydroxyprogesterone (especially in women with pre- or perimenarcheal onset of hirsutism, a family history of CAH) 24-hour urine-free cortisol if suspecting Cushing syndrome

36. Tests that quantify presence, severity, and source of hyperandrogenemia : Serum total and free testosterone (in women with moderate to severe hirsutism and/or acne or alopecia. Serum DHEA-S (to determine adrenal contribution to signs/symptoms of androgen excess)

37. Tests that allow risk assessment: Oral glucose tolerance test (2-hour, 75-g glucose load) with frequent sampling for glucose (also can test insulin levels). Fasting lipid profile Comprehensive metabolic panel Endometrial sampling to rule out endometrial hyperplasia/cancer (In obese women / with history of prolonged periods of oligomenorrhea /amenorrhea i.e , long-term exposure to unopposed estrogen )

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