Ectopic ACTH production by a bronchial carcinoid tumour responsive to desmopressin in vivo and in vitro

• Published in: Clinical endocrinology (Oxford) Vol. 47; no. 5; pp. 623 - 627
• Main Authors: Arlt, W., Dahia, P.L.M., Callies, F., Nordmeyer, J.P., Allolio, B., Grossman, A.B., Reincke, M.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.11.1997; Blackwell
• Subjects: ACTH Syndrome, Ectopic - etiology; ACTH Syndrome, Ectopic - metabolism; ACTH Syndrome, Ectopic - physiopathology; Adrenocorticotropic Hormone - metabolism; Biological and medical sciences; Bronchial Neoplasms - complications; Bronchial Neoplasms - metabolism; Bronchial Neoplasms - physiopathology; Carcinoid Tumor - complications; Carcinoid Tumor - metabolism; Carcinoid Tumor - physiopathology; Corticotropin-Releasing Hormone; Deamino Arginine Vasopressin; Female; Humans; Medical sciences; Middle Aged; Pneumology; Polymerase Chain Reaction; Receptors, Vasopressin - genetics; Renal Agents; RNA, Messenger - analysis; Tumor Cells, Cultured; Tumors of the respiratory system and mediastinum; Endocrinopathy; Adrenal cortex diseases; Peptide hormone; ACTH; Hyperadrenocorticism; Carcinoid tumor; Bronchopulmonary; Secretory tumor; Neurohypophyseal hormone; Adrenal gland diseases; Bronchus disease; Tumor; Adult; Female; Hormonal investigation; Human; Lung disease; Desmopressin; Respiratory disease; Cushing syndrome; Case study; Polymerase chain reaction; Response; Adenohypophyseal hormone; Molecular biology
• ISSN: 0300-0664; 1365-2265
• DOI: 10.1046/j.1365-2265.1997.3091129.x

A desmopressin‐induced ACTH increase has been recently suggested to be specific for pituitary‐dependent Cushing's disease. We present the case of a 47‐year‐old woman with Cushing's syndrome due to ectopic ACTH production by a bronchial carcinoid. While CRH failed to induce an ACTH or cortisol response, intravenous administration of desmopressin led to a 47% increase in serum ACTH and a 42% increase in serum cortisol concentration. After surgical removal of the tumour, the desmopressin response became negative. In vitro, ACTH production by tumour cells obtained at surgery was also stimulated by desmopressin but not by CRH. Additional receptor mRNA expression studies using RT‐PCR revealed expression of both V2 and V3 vasopressin receptor subtypes in the carcinoid tumour at a level comparable to that recently described in pituitary corticotroph adenomas. This case illustrates that ACTH stimulation by desmopressin is not specific for pituitary‐dependent Cushing's syndrome as vasopressin receptor subtypes known to interact with desmopressin may also be found in ectopic tumours producing ACTH.