Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2018) 56 P4 | DOI: 10.1530/endoabs.56.P4

Endocrinology Department, Farhat Hached University Hospital, Sousse, Tunisia.


Introduction: Differentiation between mild Cushing’s syndrome (CS) and Pseudo-Cushing syndrome (PCS) can be extremely difficult. A Pseudo-Cushing state can be defined as a part or all of the clinical features that resemble a true CS with some evidence of hypercotisolism but the resolution of the underlying primitive state results in the disappearance of this Cushing state-like. The aim of this work was to describe the diagnostic difficulties of 24 cases of PCS.

Patients and methods: A descriptive study of 24 women referred to the endocrinology department for suspicion of CS.

Results: The mean age of the patients was 33.3 years old. Nine patients were followed for hypertension, 7 for type 2 diabetes and 2 for depression. On examination, the average body mass index was 41.43 kg/m2. The average waist circumference was 118.5 cm. With respect to CS elements, 83.33% of patients had truncal obesity, 29.16% had facial erythrosis, 16.66% had buffalo hump, 16.66% had hirsutism, 8.33% had acne, 16.66% had purple stretch marks and 16.66% has intertrigo. No patient had muscular atrophy or bruising. In the biology, the fasting glucose level was 1.41 g/L on average, the mean triglyceride level was 1.25 g/L and the mean HDL-cholesterol level was 0.44 g/L. About one third of these patients had a metabolic syndrome. The overnight dexamethasone suppression test was negative in 50% of our patients whereas the standard 2-day dexamethasone suppression test was positive in all our patients which allowed us to retain rather the diagnosis of a PCS. Abdominopelvic ultrasound showed hepatic steatosis in seven patients and ovarian dystrophy in one patient. Bone densitometry was requested in two patients with a normal bone profile for age.

Discussion and conclusion: Pseudo-Cushing states share many of the characteristics of CS, including overproduction of cortisol. The hypercotisolism of PCS is caused by the increased activity of the CRH neuron which stimulates the production and release of ACTH. Despite the fact that some symptoms are more specific to CS than PCS, the diagnosis depends always on laboratory results.

Volume 56

20th European Congress of Endocrinology

Barcelona, Spain
19 May 2018 - 22 May 2018

European Society of Endocrinology 

Browse other volumes

Article tools

My recent searches

No recent searches.