Polycystic Ovary Syndrome (PCOS) is the most common endocrine disorder in women of reproductive age (4–12%). There may be a strong association between Obstructive Sleep Apnoeas (OSA) and the metabolic derangements of PCOS (insulin resistance in particular).
Management of PCOS should consist of appropriate investigations, including assessment of potential OSA, with first line treatments being lifestyle intervention and pharmacological therapies.1
AG, 15 years, was referred for obesity (BMI 35 kg/m2), hypertension, hirsutism, and menstrual irregularity. Normal insulin, glucose and lipid profile, blood pressure, electrocardiography, chest X-ray and lung function, echocardiography. Hormones assay and pelvic ultrasound indicated PCOS. Caloric restriction, exercise program and hormonal treatment were prescribed.
Polysomnography (PSG) was consistent with severe OSA. On observation, tonsils occupied less than 25% of the oropharynx and no indication for tonsillectomy was given. Nasal Continuous Positive Airway Pressure (nCPAP) ventilation (10 cmH2O) was provided. She showed optimal compliance to treatment obtaining significant weight loss, improvement of hyperandrogenism, normalization of pelvic ultrasound and OSA resolution. On day 240 of treatment (BMI 24.7 kg/m2), PSG was normal, nCPAP and hormone treatment were discontinued. On day 540, PSG confirmed the absence of OSA ( Table 1).
|First admission||Day 75||Day 240||Day 540|
|PSG findings||Baseline||nCPAP †||Baseline||nCPAP †||Baseline||Baseline|
|Mean SpO2 (%)||96||97||98||97||96||99|
|Lowest SpO2 (%)||83||88||88||90||94||94|
|SpO2 <90% (%TST)||7.9||0.1||0.1||0.0||0.0||0.0|
|mean tcPCO2 (mmHg)||41||39.7||40.4||41||39.8||38|
OSA are highly prevalent in PCOS, reported in more than 50% PCOS women compared to 19% of controls. Androgen excess, abnormal estrogens and visceral adiposity could be involved.1
De Sousa reported that weight status, hyperandrogenism, insulin resistance and metabolic syndrome do not seem to have significant effects on Respiratory Polysomnographic Variables (RPV) in adolescents with PCOS, suggesting that the pathomechanisms leading to OSA in PCOS patients develop in the later course of the disease. In PCOS adolescents RPV do not differ from healthy controls; however, there seem to be differences concerning sleep architecture.2,3
Adenotonsillectomy represents the first line treatment in the management of paediatric OSA. Non-Invasive Ventilation (NIV) is an additional treatment option for subjects who do not respond to adenotonsillectomy, or in whom it is contraindicated or delayed. No data are reported regarding NIV in adolescent PCOS with OSA. Hoppin et al. described a 15-year-old obese girl with OSA, PCOS and non-alcoholic fatty liver disease who refused NIV was described.4
In conclusion, adolescents with PCOS are also at risk of OSA. In our patient nCPAP, in combination with lifestyle intervention and pharmacological treatment, resulted in the resolution of OSA, normalization of the weight and significant improvement of clinical and biochemical hyperandrogenism.