Endocrine Abstracts

JOINT1377

Introduction: The diagnosis of Cushing’s syndrome (CS) can be challenging for endocrinologists due to its multifaceted presentation. Accurate differentiation between non-neoplastic hypercortisolism (NNH) states, formerly known as Pseudo-Cushing’s syndrome (PCS), and true CS is crucial, as their treatment approaches and outcomes vary significantly.

Case Report: A 37-year-old female patient with a medical history of hypertension, Iron-deficiency anemia, and depression. Family history revealed a background of familial hypertension. The patient was admitted for the exploration of a 14mm hypodense left adrenal mass, with radiological features suggestive of adenoma. Clinical examination revealed grade II obesity (body mass index 38 kg/m²) with an android phenotype, along with a moon face, supraclavicular and dorsocervical fat pads, and a buffalo hump. However, no other overt clinical features of Cushing syndrome were noted such as facial plethora, purple striae marks, or proximal myopathy. Blood pressure was well-controlled with calcium channel blockers. The patient had undergone investigations for secondary hypertension, excluding renal parenchymal disease, renal artery stenosis, coarctation of the aorta, obstructive sleep apnea, thyroid dysfunction and hyperparathyroidism. Laboratory studies were conducted to assess for adrenal hyperfunction. The aldosterone-to-renin ratio (ARR) and catecholamine excess were negative. However, midnight cortisol and urinary-free cortisol tests were elevated. An oral overnight 1mg dexamethasone suppression test (DST) was performed, which revealed appropriate suppression of serum cortisol to 10ng/ml, thus excluding the diagnosis of endogenous hypercortisolism.

Conclusion: Non-neoplastic hypercortisolism (NNH) states refers to various conditions responsible for mild-to-moderate hypercortisolism, resulting from overactivation of the hypothalamic-pituitary-adrenal axis. The main conditions implicated in NNH comprise: neuropsychiatric disorder, alcohol abuse, insulin-resistant obesity, polycystic ovary syndrome, and end-stage kidney disease. We concluded that the cortisol abnormalities in our patient were due to NNH state, caused by obesity and depression. The concomitant presence of a non-functioning adrenal adenoma further complicated the diagnosis in this case.