Polycystic Ovarian Syndrome (PCOS)

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DESCRIPTION

  • Polycystic ovarian syndrome (PCOS) is a common endocrine disorder with heterogeneous manifestations. It is characterized by hyperandrogenism, insulin resistance, and anovulation, typically presenting as amenorrhea or oligomenorrhea.
  • Clinical characteristics include menstrual dysfunction, infertility, hirsutism, acne, obesity, and metabolic syndrome. The ovaries are often polycystic on imaging, but are not required for diagnosis.
  • The Rotterdam diagnostic criteria include two of the following three: (i) oligo- and/or anovulation; (ii) clinical and/or biochemical signs of hyperandrogenism; (iii) polycystic ovaries on ultrasound.
  • The etiology of PCOS is unknown but presentation and course can be modified by lifestyle factors.
  • System(s) affected: reproductive, endocrine/metabolic, skin/exocrine
  • Synonym(s): Stein-Leventhal syndrome; polycystic ovary disease
ALERT
  • Obesity may amplify PCOS, but it is not diagnostic. 20% of women with PCOS are not obese.
  • Predisposes to and is associated with obesity, hypertension, diabetes, metabolic syndrome, hyperlipidemia, infertility, insulin-resistance syndrome, endometrial hyperplasia, and uterine cancer

EPIDEMIOLOGY

Incidence

Incidence and prevalence are still highly debated due to a wide spectrum of diagnostic features; the National Institutes of Health (NIH) criteria require chronic anovulation and hyperandrogenism.

Prevalence

The prevalence based on NIH criteria is around 5–18% of reproductive age women (1).

ETIOLOGY AND PATHOPHYSIOLOGY

  • Cause(s) are complex, and include genetic and epigenetic susceptibility, hypothalamic and ovarian dysfunction, excess androgen exposure, insulin resistance, and adiposity-related mechanisms (1).
  • Increased GnRH pulsations in the hypothalamus lead to increased production of LH with limited production of FSH.
  • Hyperandrogenism: Ovaries are the main source of excess androgens (75% of circulating testosterone originates in the ovary). Polycystic ovaries have thickened thecal layers and overexpressed LH receptors, which cause excess androgen secretion.
  • Obesity results in compensatory hyperinsulinemia: Women with PCOS have insulin resistance similar to that in type 2 diabetes. Elevated levels of insulin decrease sex hormone–binding globulin (SHBG), increasing bioavailability of testosterone. Insulin may also act directly on adrenal glands, ovaries, and hypothalamus to enhance androgen production.
  • Insulin resistance causes elevated insulin levels and the frequently associated metabolic syndrome or frank diabetes mellitus.

Genetics

Likely a combination of polygenic and environmental factors. Implicated genes include DENND1A and THADA.

RISK FACTORS

See “Commonly Associated Conditions”; cause and effect are difficult to extricate in this disorder.

GENERAL PREVENTION

None known; focus on early diagnosis and treatment to prevent long-term complications.

COMMONLY ASSOCIATED CONDITIONS

Infertility, obesity, obstructive sleep apnea, hypertension, diabetes mellitus, endometrial hyperplasia/carcinoma, fatty liver disease, mood disturbances and depression, hirsutism

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