Poster Presentation ESA-SRB-APEG-NZSE 2022

Cushing’s disease presenting as an embolic stroke in a young patient with patent foramen ovale (#327)

Emma Flaherty 1 , Danish Mahmud 1 2
  1. Department of General Medicine, Armadale Health Service, Mount Nasura, WA, Australia
  2. Curtin Medical School, Curtin University, Perth, WA

Introduction

Cushing’s syndrome has been linked with increased incidence of cardiovascular and venous thromboembolic disease1,2. Here we report a case of a young woman presenting with embolic stroke with previously undiagnosed patent foramen ovale (PFO) and Cushing’s disease.

Case Description

A 35-year-old female presented with stroke-like symptoms including sudden-onset left hemiparesis and visual field loss. Her background medical history included type 2 diabetes mellitus (short duration), hypertension, being overweight (BMI 26) and PCOS. MRI confirmed multi-territory cerebral infarcts and CT Angiogram (Neck/Brain) was unremarkable. Thrombophilia screen and stroke workup, including prolonged Holter monitoring, were also unremarkable apart from a large PFO on echocardiogram.

During her hospital admission, she was noted to have clinical features of Cushing’s syndrome and subsequent outpatient biochemical testing (table 1) indicated ACTH-dependent Cushing’s disease. She was commenced on therapeutic anticoagulation which was changed to dual antiplatelets for three months after the PFO closure with Amplatzer Talisman PFO Occluder.

Pituitary MRI showed microadenoma and Cushing’s disease was confirmed with petrosal sinus sampling, arranged after PFO closure. She was commenced and maintained on metyrapone until trans-sphenoidal resection of pituitary microadenoma six months after cardiac procedure to allow safe discontinuation of antiplatelets.

She had resolution of biochemical and clinical Cushing’s disease after pituitary surgery. She remains on replacement hydrocortisone 18 months later with good neurological recovery and no further cardiovascular, venous or metabolic complications.

Discussion and Learning Points

Our case highlights the importance of considering Cushing’s syndrome as a cause of acquired thrombophilia in younger patients with cardiovascular disease. The pathogenesis involves both over-activation of coagulation cascade (resulting in low APTT) and reduced fibrinolytic activity1. Our patient had previous diagnoses of PCOS, Type 2 Diabetes Mellitus and hypertension, which in retrospect were all likely related to pathological hypercortisolism and went into remission following pituitary surgery.

 

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  1. van der Pas, R., Leebeek, F., Hofland, L., de Herder, W. and Feelders, R., 2013. Hypercoagulability in Cushing's syndrome: prevalence, pathogenesis and treatment. Clinical Endocrinology, 78(4), pp.481-488.
  2. Stuijver, D., van Zaane, B., Feelders, R., Debeij, J., Cannegieter, S., Hermus, A., van den Berg, G., Pereira, A., de Herder, W., Wagenmakers, M., Kerstens, M., Zelissen, P., Fliers, E., Schaper, N., Drent, M., Dekkers, O. and Gerdes, V., 2011. Incidence of Venous Thromboembolism in Patients with Cushing's Syndrome: A Multicenter Cohort Study. The Journal of Clinical Endocrinology & Metabolism, 96(11), pp.3525-3532.