Evaluation and Treatment of Hirsutism in Premenopausal Women: An Endocrine Society Clinical Practice Guideline

Martin, Kathryn A.; Chang, R. Jeffrey; Ehrmann, David A.; Ibáñez, Lourdes; Løbo, Rogerio A.; Rosenfield, Robert L.; Shapiro, Jerry; Montori, Víctor M.; Swiglo, Brian A.

doi:10.1210/jc.2007-2437

Cited by 376 publications

(279 citation statements)

References 194 publications

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“…Therefore, metformin is not recommended as a first-line treatment for management of menstrual irregularity or clinical hyperandrogenism in PCOS because of the lack of evidence for consistent benefits [37,38,44].…”

Section: Menstrual Irregularity and Clinical Hyperandrogenismmentioning

confidence: 99%

Metformin therapy for the reproductive and metabolic consequences of polycystic ovary syndrome

Sam

Ehrmann

2017

Diabetologia

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Polycystic ovary syndrome (PCOS), the most common hormonal disorder among women of reproductive age, has various metabolic and reproductive consequences. Metformin was originally shown to lower testosterone levels in women with PCOS in the 1990s, an effect presumably related to its insulin sensitising actions. However, the precise mechanisms of metformin action in PCOS remain unclear and there is considerable heterogeneity in the clinical response to this therapy in women with PCOS. Recent evidence indicates that genetic factors may play a significant role in predicting response to metformin therapy in PCOS and future studies are needed to further identify women who are most likely to benefit from this therapy. At present, there is no clear evidence to support broad metformin use in PCOS. Well-designed prospective trials are needed to establish clear benefit for metformin use in the treatment of the reproductive and metabolic consequences associated with PCOS.

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Section: Menstrual Irregularity and Clinical Hyperandrogenismmentioning

confidence: 99%

Metformin therapy for the reproductive and metabolic consequences of polycystic ovary syndrome

Sam

Ehrmann

2017

Diabetologia

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“…34 Hirsutism is considered clinical evidence of hyperandrogenism and equivalent to biochemical evidence of hyperandrogenism in all adult criteria for PCOS ( Table 1) because documentation of hyperandrogenemia can be problematic. 35 However, this criterion is controversial because mild hirsutism is due to ethnic or familial factors rather than hyperandrogenemia half of the time, in contrast to moderate-severe hirsutism, which is usually due to hyperandrogenemia. 36 On the other hand, hyperandrogenemia is variably accompanied by hirsutism: little more than half of hyperandrogenemic PCOS patients are hirsute.…”

Section: Clinical and Biochemical Evidence Of Hyperandrogenism In Adomentioning

confidence: 99%

“…4,35 Sexual hair growth is commonly graded by the FerrimanGallwey score (Fig 3): a total score of 8 to 15 defines mild hirsutism, 16 to 24 moderate hirsutism, in the general US adult population. 35 Hirsutism must be distinguished from hypertrichosis, which is defined as generalized excessive vellus hair growth distributed in a nonsexual pattern, for example, predominantly on forearms or lower legs. This hair growth is not due to androgen excess.…”

Section: Clinical Evidence Of Hyperandrogenismmentioning

confidence: 99%

“…4,42,43 Measurements of total and/or free testosterone are recommended to initiate documentation of hyperandrogenemia. 35,44 Elevated serum free testosterone is the single most sensitive indicator of hyperandrogenemia because the bioactive portion of the serum testosterone is the free fraction. Sex hormone binding globulin (SHBG) serum concentrations govern the fraction of testosterone that is free; they are lowered by obesity and androgen excess itself.…”

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confidence: 99%

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The Diagnosis of Polycystic Ovary Syndrome in Adolescents

2015

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Consensus has recently been reached by international pediatric subspecialty societies that otherwise unexplained persistent hyperandrogenic anovulation using age-and stage-appropriate standards are appropriate diagnostic criteria for polycystic ovary syndrome (PCOS) in adolescents. The purpose of this review is to summarize these recommendations and discuss their basis and implications. Anovulation is indicated by abnormal uterine bleeding, which exists when menstrual cycle length is outside the normal range or bleeding is excessive: cycles outside 19 to 90 days are always abnormal, and most are 21 to 45 days even during the first postmenarcheal year. Continued menstrual abnormality in a hyperandrogenic adolescent for 1 year prognosticates at least 50% risk of persistence. Hyperandrogenism is best indicated by persistent elevation of serum testosterone above adult norms as determined in a reliable reference laboratory. Because hyperandrogenemia documentation can be problematic, moderate-severe hirsutism constitutes clinical evidence of hyperandrogenism. Moderate-severe inflammatory acne vulgaris unresponsive to topical treatment is an indication to test for hyperandrogenemia. Treatment of PCOS is symptom-directed. Cyclic estrogenprogestin oral contraceptives are ordinarily the preferred first-line medical treatment because they reliably improve both the menstrual abnormality and hyperandrogenism. First-line treatment of the comorbidities of obesity and insulin resistance is lifestyle modification with calorie restriction and increased exercise. Metformin in conjunction with behavior modification is indicated for glucose intolerance. Although persistence of hyperandrogenic anovulation for $2 years ensures the distinction of PCOS from physiologic anovulation, early workup is advisable to make a provisional diagnosis so that combined oral contraceptive treatment, which will mask diagnosis by suppressing hyperandrogenemia, is not unnecessarily delayed.Polycystic ovary syndrome (PCOS) is the most common cause of chronic hyperandrogenic anovulation and the single most common cause of infertility in young women. 1 It is also a risk factor for metabolic syndrome-related comorbidities and for impaired wellbeing and mortality. 2 Considerable evidence suggests that PCOS has diverse causes, arising as a complex trait with contributions from both heritable and environmental factors that affect ovarian steroidogenesis. 3,4 Insulinresistant hyperinsulinism, in part related to coexistent obesity, is the most common nonsteroidogenic factor. The complex interactions generally mimic an autosomal dominant trait with variable penetrance: the disorder is correlated in identical twins 5 ; about half of sisters are hyperandrogenic, and half of these also have oligo-amenorrhea and thus PCOS 6,7 ; and polycystic ovaries appear to be inherited as an autosomal dominant trait. 7,8 Three percent to 35% of mothers have PCOS, 9,10 and metabolic syndrome prevalence is high in parents and siblings. 11-13 The syndrome was first described...

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“…Patients with PCOS usually present between the ages of 15-25 years, and their symptoms are slowly progressive with over 1 year usually elapsing from the time the patients first notice the appearance of hair to seeking medical advice (6,7). PCOS is rarely associated with evidence of virilization or severe hyperandrogenaemia (Table 1).…”

Section: Introductionmentioning

confidence: 99%

Investigation of patients with atypical or severe hyperandrogenaemia including androgen-secreting ovarian teratoma

Dennedy

Smith²,

O’Shea³

et al. 2010

European Journal of Endocrinology

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Approximately 7% of women of reproductive age manifest polycystic ovary syndrome (PCOS) and !0.5% have other causes of hyperandrogenism including congenital adrenal hyperplasia (CAH), androgen-secreting tumour of an ovary or an adrenal gland, Cushing's syndrome or hyperthecosis. The presence of features atypical of PCOS should prompt more extensive evaluation than that usually undertaken. Features atypical of PCOS include the onset of symptoms outside the decade of 15-25 years, rapid progression of symptoms, the development of virilization and a serum testosterone concentration in excess of twice the upper limit of the reference range. Ethnic background, family history and specific clinical findings, e.g. Cushingoid appearance, may inform a focused investigation. Otherwise, patients should have measurement of 17-hydroxyprogesterone (17-OHP) under basal conditions ideally in the early morning, and if abnormal, they should have measurement of 17-OHP one hour after the administration of synthetic ACTH, 250 mg i.v., to screen for CAH, which is present in w2% of hyperandrogenic patients. The overnight cortisol suppression test employing 1 mg dexamethasone at midnight is a sensitive test for Cushing's syndrome. Coronal tomographic (CT) scanning of the adrenals and transvaginal ultrasonography of the ovaries are the investigations of choice when screening for tumours in these organs. Less frequently required is catheterization and sampling from both adrenal and ovarian veins, which is a technically demanding procedure with potential complications which may provide definitive diagnostic information not available from other investigations. Illustrative case reports highlight some complexities in the investigation of hyperandrogenic patients presenting with features atypical of PCOS and include only the ninth case report of an androgen-secreting ovarian teratoma.

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Evaluation and Treatment of Hirsutism in Premenopausal Women: An Endocrine Society Clinical Practice Guideline

Cited by 376 publications

References 194 publications

Metformin therapy for the reproductive and metabolic consequences of polycystic ovary syndrome

Metformin therapy for the reproductive and metabolic consequences of polycystic ovary syndrome

The Diagnosis of Polycystic Ovary Syndrome in Adolescents

Investigation of patients with atypical or severe hyperandrogenaemia including androgen-secreting ovarian teratoma

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