Poster Presentation ESA-SRB-ANZBMS 2024 in conjunction with ENSA

Obstructive sleep apnoea causing high cortisol: a case report (#639)

Tijana Vlajkovic 1 , Michelle Choe 1
  1. Endocrinology, Te Whatu Ora, Auckland, New Zealand

Pseudo-Cushing’s syndrome is often clinically and biochemically indistinguishable from true Cushing’s syndrome (1). Common causes for pseudo-Cushing’s includes alcohol abuse, neuropsychiatric disorders, chronic kidney disease, obesity, and uncontrolled type 2 diabetes (1). Here, we present a case of pseudo-Cushing’s syndrome secondary to obstructive sleep apnoea (OSA).

 

A 45-year-old male presented with rapid weight gain and deteriorating diabetes and blood pressure control. Initial tests were strongly suggestive of Cushing’s syndrome, showing non-suppressed cortisol with a 1 mg dexamethasone suppression test, and an elevated 24-hour urinary free cortisol. Non-suppressed adrenocorticotropic hormone (ACTH) suggested ACTH-dependent Cushing’s disease. Although pituitary magnetic resonance imaging did not reveal a lesion, serum cortisol suppressed with 8 mg dexamethasone, indicating a likely pituitary rather than ectopic source. Attempted inferior petrosal sinus sampling was unsuccessful due to technical difficulties, leading to hospitalisation for serial serum cortisol measurements. In hospital, the patient was seen by Respiratory due to a history of loud snoring and daytime somnolence as well as frequent desaturations. Commencement of bilevel positive airway pressure (BiPAP) therapy resulted in almost immediate normalisation of serum cortisol measurements, which were previously high and lacked diurnal variation. Similarly, his 24-hour urinary free cortisol and midnight salivary cortisol readings normalised promptly after starting BiPAP.

 

The normalisation of biochemical tests with BiPAP therapy in our patient suggests pseudo-Cushing’s syndrome secondary to OSA. OSA leads to intermittent hypoxemia and sleep fragmentation, which can trigger activation of the hypothalamic-pituitary-adrenal axis (HPA) (2). OSA-related comorbidities, such as obesity and type 2 diabetes, can also stimulate the HPA axis. These hormonal changes are reversible with effective treatment of OSA, highlighting the importance of considering OSA in the differential diagnosis of apparent Cushing’s syndrome (2).

 

Prompt recognition and treatment of OSA can lead to resolution of pseudo-Cushing’s syndrome, thereby avoiding unnecessary investigations and treatments for true Cushing’s syndrome.

  1. Findling JW, Raff H. Recognition of nonneoplastic hypercortisolism in the evaluation of patients with Cushing Syndrome. Journal of the Endocrine Society 2023;7:1-12.
  2. Tamada D, Otsuki M, Kashine S, Hirata, Onodera T, Kitamura T, et al. Obstructive sleep apnea syndrome causes a pseudo-Cushing’s state in Japanese obese patients with type 2 diabetes mellitus. Endocrine Journal 2013;60(12):1289-94.