Excess glucocorticoid amounts cause Cushing’s symptoms (CS) and could be because

Excess glucocorticoid amounts cause Cushing’s symptoms (CS) and could be because of pituitary adrenal or ectopic tumours. need for comprehensive diagnostic workup in patients with CS. An ACTH-secreting phaeochromocytoma should be checked for in patients with an adrenal mass and elevated ACTH levels. Background Cushing’s syndrome (CS) is caused by excess glucocorticoid levels 1 and may be due to corticosteroid treatment pituitary tumour (Cushing’s disease (CD)) cortisol-secreting adrenal tumour or increased production of an adrenocorticotropic hormone (ACTH) by an extrapituitary (ectopic) tumour.1 2 While CD accounts for 70% of CS cases about 10% of patients with CS have an ectopic ACTH-secreting tumour.3 The incidence of CD in Denmark is 1.2-1.7/million/12 months and that of CS caused by adrenal tumours is usually 0.6/million/12 months.4 Patients with ectopic ACTH-producing tumours are most often diagnosed by pulmonary carcinoids neuroendocrine carcinoids or occult cancers. In the rare cases where CS is usually caused by an ACTH-producing phaeochromocytoma 5 the patients may present with classical CS and an adrenal mass. High levels of catecholamines and ACTH should give the suspicion of the ACTH-secreting phaeochromocytoma. The treatment achievement of phaeochromocytoma depends upon the patient’s presurgical condition.6 Medical procedures on the phaeochromocytoma can possess severe consequences for the individual.7 Within a case group of 54 autopsies with verified phaeochromocytoma 27 from the sufferers had passed away either because of a hypertensive or hypotensive turmoil during medical procedures for non-adrenal pathologies.8 9 As up to 25% of phaeochromocytomas are due to genetic mutations genetic testing is preferred.10 We present two instances of patients with CS because of an ACTH-producing phaeochromocytoma. Case display Case 1: A 70-year-old girl was admitted towards the crisis ward at a local hospital due to vertigo. The individual had a past history of cardiovascular events and was treated with platelet inhibitors Rabbit Polyclonal to EDG3. statins and β-blockers. The individual had smoked for approximately 54 pack-years and there is no grouped genealogy of endocrine disease. At presentation the individual was medically dehydrated and got clinical symptoms of CS using a moon encounter a buffalo hump subcutaneous haematomas truncal weight problems and hirsutism but no MLN2480 abdominal striae. She had hypokalaemia and neutrophilia. Intravenous rehydration using a potassium health supplement was initiated. The individual needed 90?mmol of potassium to keep electrolyte homeostasis daily. Due to suspected CS she was used in the Section of MLN2480 Endocrinology at Odense College or university Hospital for even more diagnostic workup. Case 2: A 67-year-old girl was described MLN2480 our endocrinology outpatient center because of uncontrolled high blood circulation pressure. The individual was acquiring four antihypertensive medications and 20?mmol potassium products daily. She got osteoporosis with compression fractures of Th12 L3 and L4 and there is no genealogy of endocrine illnesses. At display she got scientific symptoms of CS including a reddish moon face violet/purple abdominal striae and hirsutism. She had a normal neutrophil count and normal potassium levels. Investigations Laboratory findings are summarised in table 1. Table?1 Summary of laboratory results Case 1: Twenty-four hour urinary cortisol levels were elevated and a 1?mg dexamethasone suppression test showed incomplete suppression of cortisol. ACTH levels were elevated. MRI of the pituitary gland was normal. The patient reported abdominal pain and a CT scan of the stomach showed bilateral adrenal adenomas. The largest adenoma was located in the right adrenal gland MLN2480 and measured 30×18?mm. The adenoma in the left adrenal gland measured 17×12?mm. Both adenomas experienced high HU-scores of 100. Night-urinary catecholamines and plasma metanephrines were elevated. A fluorine-18-L-dihydroxyphenylalanine (18F-DOPA) positron emission tomography (PET) CT showed a significant pathological uptake of 18F-DOPA in the larger adrenal adenoma (physique 1). The 18F-DOPA PET-CT also revealed a pulmonary infiltration without 18F-DOPA uptake but it was highly positive on a subsequent fluorodeoxyglucose (FDG) PET-CT. Bronchoalveolar lavage and endoscopic bronchial ultrasound recognized the pulmonary lesion as an aspergilloma. Physique?1.