What is Polycystic ovarian syndrome (PCOS)?
An endocrine condition primarily associated with alterations in testosterone and insulin hormones with known heterogeneous presentations involving a woman’s appearance, fertility, cardio-metabolic risk and mental health.
In 2018, the first international guidelines for PCOS were published.
Diagnosis of PCOS
Diagnosis has been challenging for a number of reasons. The widely accepted Rotterdam criteria holds true for diagnosis. The most important tool in diagnosis involves a detailed clinical history and examination. Biochemical and imaging tests provide supportive evidence for diagnosis.
- Oligo-ovulation or anovulation
- Clinical or biochemical signs of hyperandrogenism
- Polycystic appearing ovaries on ultrasound (PCOM)
Any two of the above three criteria are required for diagnosis after conditions that mimic these symptoms have been excluded (refer to Diagram 1).
1. Oligo-ovulation and anovulation is defined:
First year post menarche, it is common to have irregular menstrual cycles
>1 yr post menarche > 90 days for any cycle
>1- <3 yrs post menarche cycles of <21 to >45 days
> 3 yrs post menarche, <21 or >35 days or <8 cycles a year
Primary amenorrhoea by age 15 or >3 yrs post thelarche
2. Clinical or biochemical signs of hyperandrogenism
Can be objectively quantified using a modified Ferriman Gallway score for the presence of terminal hair (not vellus). Scores of ≥ 4-6 changed from the previous score of 8. Consider racial and ethnic variations.
Acne on its own is not a feature of hyperandrogenism, especially in the adolescent age group. However, severe cystic acne or acne persisting well beyond adolescence with the presence of biochemical evidence of hyperandrogenism can be considered as a criterion.
Assessed by testing for testosterone and SHBG to calculate free androgen index and/or calculated free testosterone in follicular phase.
Androstenedione and DHEAS testing can be done if testosterone levels are normal, and 17 OH progesterone testing if congenital adrenal hyperplasia is suspected.
Other causes of hyperandrogenism include idiopathic hirsutism, classical and non-classical congenital adrenal hyperplasia and obesity related hyperandrogenism. Androgen secreting neoplasia should be suspected in the setting of new and rapidly developing hyperandrogenic symptoms.
3. Ultrasound – Polycystic ovarian morphology (PCOM)
Up to 70% of adolescents meet USG criteria for PCOM as multi-cystic ovaries are common in this age group. Hence USG should not be performed before eight years following menarche.
In adult populations, a transvaginal approach is preferred. More than 20 follicles in either ovary and/ or >10ml ovarian volume is required for the diagnosis.
Caveats to consider:
When the clinical picture is unclear (specially in adolescents), it’s advisable to defer the diagnosis and re-evaluate the patient in a few years. Labelling such a patient as “at risk of PCOS” and deferring the definitive diagnosis for up to eight years post menarche is considered reasonable.
Women with PCOS, as they reach their fourth decade, can develop regular menstrual cycles and notice an improvement in the androgen levels. Similarly, persistence of hyperandrogenic features into menopause is also possible.
Obesity is not part of the diagnostic criteria. It is important to understand that all obese women do not have PCOS and vice versa. Obesity is considered a different entity to PCOS and can lower SHBG and lead to increase FAI contributing menstrual irregularity.
Lean women with PCOS tend to have more hyperandrogenic features whilst obese and overweight individuals are more likely to show signs of insulin resistance.
Even though insulin resistance and raised LH: FSH ratio reflects the underlying pathophysiology in PCOS, these markers are not used as diagnostic criteria due to their non-specificity.
Further reading: https://www.monash.edu/__data/assets/pdf_file/0004/1412644/PCOS_Evidence-Based-Guidelines_20181009.pdf
Questions? Contact the editor.
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