title: Management of hyperglycaemia in Cushing's disease: experts' proposals on the use of pasireotide.
abstract: Cushing's disease causes considerable morbidity and mortality, including cardiovascular, metabolic, respiratory and psychiatric complications, bone demineralization and increased susceptibility to infections. Metabolic complications include a high prevalence of impaired glucose tolerance, fasting hyperglycaemia and diabetes. Although pituitary surgery is the gold-standard treatment, other treatment strategies such as radiotherapy and medical therapy to reduce cortisol synthesis may be proposed in the event of recurrence or failure, or when surgery is not an option. Bilateral adrenalectomy can also be considered. One of the medical treatments used in Cushing's disease is the somatostatin analogue pasireotide, which acts on adrenocorticotropic hormone (ACTH) secretion by the pituitary. Its efficacy in reducing urinary free cortisol, plasma cortisol and ACTH, and in improving the clinical signs of the disease has been demonstrated. Its observed adverse effects are similar to the known effects of first-generation somatostatin analogues, although disturbances of carbohydrate metabolism are more frequent and more severe with pasireotide. The aim of the present review was to summarize the epidemiology and pathophysiology of the disturbances of glucose metabolism that arise in Cushing's disease, and to propose recommendations for detecting and monitoring glucose abnormalities and for managing pasireotide-induced hyperglycaemia.
authors.affiliation: Service Endocrinologie, CHU Côte-de-Nacre, 14033 Caen, France. reznik-y@chu-caen.fr
authors.forename: Y
authors.initials: Y
authors.lastname: Reznik
authors.forename: J
authors.initials: J
authors.lastname: Bertherat
authors.forename: F
authors.initials: F
authors.lastname: Borson-Chazot
authors.forename: T
authors.initials: T
authors.lastname: Brue
authors.forename: P
authors.initials: P
authors.lastname: Chanson
authors.forename: C
authors.initials: C
authors.lastname: Cortet-Rudelli
authors.forename: B
authors.initials: B
authors.lastname: Delemer
authors.forename: A
authors.initials: A
authors.lastname: Tabarin
authors.forename: S
authors.initials: S
authors.lastname: Bisot-Locard
authors.forename: B
authors.initials: B
authors.lastname: Vergès
mesh_terms: D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D002986:Clinical Trials as Topic; D004359:Drug Therapy, Combination; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D006943:Hyperglycemia / Q000139:chemically induced* / Q000188:drug therapy / Q000453:epidemiology / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D008687:Metformin / Q000627:therapeutic use; D015337:Multicenter Studies as Topic; D047748:Pituitary ACTH Hypersecretion / Q000097:blood / Q000188:drug therapy* / Q000453:epidemiology / Q000378:metabolism; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism; D010907:Pituitary Hormones / Q000009:adverse effects / Q000627:therapeutic use*; D017410:Practice Guidelines as Topic; D012008:Recurrence; D013004:Somatostatin / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D006442:Glycated Hemoglobin; D006854:Hydrocortisone; D007004:Hypoglycemic Agents; D008687:Metformin; D010907:Pituitary Hormones; D013004:Somatostatin; C517652:hemoglobin A1c protein, human; C517782:pasireotide