Article (Scientific journals)
Food-dependent Cushing's syndrome mediated by aberrant adrenal sensitivity to gastric inhibitory polypeptide.
Reznik, Y.; Allali-Zerah, V.; Chayvialle, J. A. et al.
1992In New England Journal of Medicine, 327 (14), p. 981-6
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Keywords :
Adrenal Glands/drug effects/pathology/physiopathology; Adrenocorticotropic Hormone/blood; Adult; Cushing Syndrome/etiology; Dexamethasone/diagnostic use; Eating/physiology; Female; Gastric Inhibitory Polypeptide/pharmacology/physiology; Humans; Hydrocortisone/blood/urine; Hyperplasia; In Vitro Techniques; Middle Aged; Octreotide/pharmacology/therapeutic use
Abstract :
[en] BACKGROUND: Some patients with Cushing's syndrome have nodular adrenal hyperplasia. In most the disease is corticotropin-dependent, but in others it is corticotropin-independent. The cause of the adrenal hyperplasia in the latter patients is not known. METHODS: We studied a 49-year-old woman with Cushing's syndrome and nodular adrenal hyperplasia in whom food stimulated cortisol secretion. Plasma cortisol concentrations were measured in response to the ingestion of mixed meals, glucose, protein, and fat and after the administration of various gastrointestinal and other types of hormones. We also studied the ability of the long-acting somatostatin analogue octreotide to prevent the food-induced increase in plasma cortisol concentrations and to ameliorate the clinical manifestations of Cushing's syndrome in this patient. RESULTS: The patient's fasting plasma cortisol concentrations were subnormal, ranging from 3.0 to 7.5 micrograms per deciliter (83 to 207 nmol per liter), and they increased to as high as 16.5 micrograms per deciliter (455 nmol per liter) after a mixed meal. Her urinary cortisol excretion ranged from 164 to 250 micrograms per day (453 to 690 nmol per day) and could not be suppressed by a large dose of dexamethasone. Plasma corticotropin concentrations were virtually undetectable at all times. The ingestion of glucose, protein, and fat increased plasma cortisol concentrations to 3.6, 2.2, and 4 times the base-line value, respectively; the meal-induced and glucose-induced increases were inhibited by octreotide. The infusion of gastric inhibitory polypeptide (GIP) increased the patient's plasma cortisol concentration to 3.7 times the base-line value, but had no effect in normal subjects. The patient's fasting plasma GIP concentrations were normal both before and after a meal, and there was a close correlation between her plasma cortisol and GIP concentrations. Treatment with octreotide decreased urinary cortisol excretion and ameliorated the clinical manifestations of Cushing's syndrome. CONCLUSIONS: The development of aberrant adrenal sensitivity to GIP can result in food-dependent adrenal hyperplasia and therefore in Cushing's syndrome.
Disciplines :
Endocrinology, metabolism & nutrition
Author, co-author :
Reznik, Y.
Allali-Zerah, V.
Chayvialle, J. A.
Leroyer, R.
Leymarie, P.
Travert, G.
LEBRETHON, Marie-Christine ;  Centre Hospitalier Universitaire de Liège - CHU > Pédiatrie
Budi, I.
Balliere, A. M.
Mahoudeau, J.
Language :
English
Title :
Food-dependent Cushing's syndrome mediated by aberrant adrenal sensitivity to gastric inhibitory polypeptide.
Publication date :
1992
Journal title :
New England Journal of Medicine
ISSN :
0028-4793
eISSN :
1533-4406
Publisher :
Massachusetts Medical Society, United States - Massachusetts
Volume :
327
Issue :
14
Pages :
981-6
Peer reviewed :
Peer Reviewed verified by ORBi
Available on ORBi :
since 16 April 2015

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