New perspectives in the treatment of cushing's syndrome

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Regardless of etiology, all cases of endogenous Cushing's syndrome are due to increased production of cortisol by the adrenal gland. Most are caused by adrenocorticotrophic hormone (ACTH)-secreting pituitary adenomas. Alternatively, the glucocorticoid excess may be due to adrenal neoplasia or t...

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Autor principal: Labeur, M.
Otros Autores: Arzt, E., Stalla, G.K, Péz-Pereda, M.
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 2004
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h 89; kn 62; mdl 12330a; pd 98059; uo 126
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Biblioteca Central Dr. Luis F. Leloir (FCEN) de Universidad de Buenos Aires
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100 1 |a Labeur, M. 
245 1 0 |a New perspectives in the treatment of cushing's syndrome 
260 |c 2004 
270 1 0 |m Páez-Pereda, M.; Max Planck Institute of Psychiatry, Dept. of Endocrinology, Kraepelinstr. 10, 80804 Munich, Germany; email: marcelo@mpipsykl.mpg.de 
506 |2 openaire  |e Política editorial 
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520 3 |a Regardless of etiology, all cases of endogenous Cushing's syndrome are due to increased production of cortisol by the adrenal gland. Most are caused by adrenocorticotrophic hormone (ACTH)-secreting pituitary adenomas. Alternatively, the glucocorticoid excess may be due to adrenal neoplasia or to ectopic ACTH-secreting tumors. Cushing's syndrome is characterized by endocrine and metabolic alterations such as truncal obesity, hypertension, weakness, amenorrhea, hyperglycemia, osteoporosis and depression. Unless treated, the disease is associated with high morbidity, and ultimately, mortality. Depending on the etiology of Cushing's syndrome two different treatment modalities are possible: reduction of pituitary ACTH production or reduction of adrenocortical cortisol secretion. In the absence of efficient drug therapy, transsphenoidal resection of the pituitary adenoma is the primary treatment of choice for the reduction of ACTH secretion. In the last years there was much progress in understanding the molecular mechanisms that control the function of the hypothalamic-pituitary-adrenal axis. Thus, new insights made it possible to identify potential drug targets for the treatment of Cushing's syndrome. The present article reviews different drug targets and therapeutic options including drugs that control the central ACTH regulation, e.g. by modulating signaling pathways and transcriptional regulation of ACTH biosynthesis, corticotrophin releasing hormone (CRH) or glucocorticoid receptor antagonists, inhibitors of glucocorticoid synthesis, ketoconazole, somatostatin and dopamine analogs. Some of these substances might be useful for the treatment of Cushing's syndrome. © 2004 Bentham Science Publishers Ltd.  |l eng 
593 |a Max Planck Institute of Psychiatry, Dept. of Endocrinology, Kraepelinstr. 10, 80804 Munich, Germany 
593 |a Lab. Fisiologia Biologia Molecular, FCEN, Universidad de Buenos Aires, Pabellon 11, 1428 Buenos Aires, Argentina 
690 1 0 |a ACTH 
690 1 0 |a CUSHING'S SYNDROME 
690 1 0 |a GLUCOCORTICOIDS 
690 1 0 |a HPA AXIS 
690 1 0 |a POMC 
690 1 0 |a 1 [N,O BIS(5 ISOQUINOLINESULFONYL) N METHYLTYROSYL] 4 PHENYLPIPERAZINE 
690 1 0 |a 2 (2 AMINO 3 METHOXYPHENYL)CHROMONE 
690 1 0 |a 4 AMINOBUTYRATE AMINOTRANSFERASE INHIBITOR 
690 1 0 |a AMINOGLUTETHIMIDE 
690 1 0 |a BROMOCRIPTINE 
690 1 0 |a CABERGOLINE 
690 1 0 |a CORTICOTROPIN 
690 1 0 |a CORTICOTROPIN RELEASING FACTOR 
690 1 0 |a CORTICOTROPIN RELEASING FACTOR ANTAGONIST 
690 1 0 |a CYPROHEPTADINE 
690 1 0 |a CYTOKINE RECEPTOR 
690 1 0 |a DOPAMINE DERIVATIVE 
690 1 0 |a DOPAMINE RECEPTOR STIMULATING AGENT 
690 1 0 |a GLUCOCORTICOID 
690 1 0 |a GLUCOCORTICOID ANTAGONIST 
690 1 0 |a GLUCOCORTICOID RECEPTOR ANTAGONIST 
690 1 0 |a HORMONE RECEPTOR BLOCKING AGENT 
690 1 0 |a KETOCONAZOLE 
690 1 0 |a METYRAPONE 
690 1 0 |a MITOTANE 
690 1 0 |a N (2 PHENYLCYCLOPENTYL)AZACYCLOTRIDECAN 2 IMINE 
690 1 0 |a N [2 (4 BROMOCINNAMYLAMINO)ETHYL] 5 ISOQUINOLINESULFONAMIDE 
690 1 0 |a OCTREOTIDE 
690 1 0 |a RETINOIC ACID 
690 1 0 |a ROSIGLITAZONE 
690 1 0 |a SEROTONIN ANTAGONIST 
690 1 0 |a SOMATOSTATIN DERIVATIVE 
690 1 0 |a UNINDEXED DRUG 
690 1 0 |a UO 126 
690 1 0 |a VALPROIC ACID 
690 1 0 |a ADRENAL DISEASE 
690 1 0 |a ADRENAL FUNCTION 
690 1 0 |a ALOPECIA 
690 1 0 |a AMENORRHEA 
690 1 0 |a BLOOD CLOTTING DISORDER 
690 1 0 |a CLINICAL TRIAL 
690 1 0 |a CORTICOTROPIN RELEASE 
690 1 0 |a CUSHING SYNDROME 
690 1 0 |a DEPRESSION 
690 1 0 |a DIARRHEA 
690 1 0 |a DIZZINESS 
690 1 0 |a DOSE RESPONSE 
690 1 0 |a DRUG EFFICACY 
690 1 0 |a DRUG ERUPTION 
690 1 0 |a DRUG TARGETING 
690 1 0 |a GASTROINTESTINAL SYMPTOM 
690 1 0 |a GLUCOSE BLOOD LEVEL 
690 1 0 |a HEADACHE 
690 1 0 |a HORMONAL REGULATION 
690 1 0 |a HORMONE SUBSTITUTION 
690 1 0 |a HUMAN 
690 1 0 |a HYDROCORTISONE RELEASE 
690 1 0 |a HYPERGLYCEMIA 
690 1 0 |a HYPERTENSION 
690 1 0 |a HYPOGONADISM 
690 1 0 |a HYPOPHYSIS ADENOMA 
690 1 0 |a HYPOTHALAMUS HYPOPHYSIS ADRENAL SYSTEM 
690 1 0 |a INCREASED APPETITE 
690 1 0 |a LIVER TOXICITY 
690 1 0 |a MOLECULAR BIOLOGY 
690 1 0 |a MORBIDITY 
690 1 0 |a MORTALITY 
690 1 0 |a MUSCLE HYPOTONIA 
690 1 0 |a MUSCLE WEAKNESS 
690 1 0 |a MYALGIA 
690 1 0 |a NAUSEA 
690 1 0 |a NONHUMAN 
690 1 0 |a OBESITY 
690 1 0 |a OSTEOPOROSIS 
690 1 0 |a PATHOGENESIS 
690 1 0 |a PRURITUS 
690 1 0 |a PSYCHOPATHY 
690 1 0 |a REVIEW 
690 1 0 |a SIDE EFFECT 
690 1 0 |a SIGNAL TRANSDUCTION 
690 1 0 |a SOMNOLENCE 
690 1 0 |a TASTE DISORDER 
690 1 0 |a TRANSCRIPTION REGULATION 
690 1 0 |a TRANSSPHENOIDAL HYPOPHYSECTOMY 
690 1 0 |a VOMITING 
690 1 0 |a XEROSTOMIA 
690 1 0 |a ADRENOCORTICOTROPIC HORMONE 
690 1 0 |a ANIMALS 
690 1 0 |a CUSHING SYNDROME 
690 1 0 |a DRUG DELIVERY SYSTEMS 
690 1 0 |a HUMANS 
690 1 0 |a RECEPTORS, CORTICOTROPIN-RELEASING HORMONE 
653 0 0 |a h 89; kn 62; mdl 12330a; pd 98059; uo 126 
700 1 |a Arzt, E. 
700 1 |a Stalla, G.K. 
700 1 |a Péz-Pereda, M. 
773 0 |d 2004  |g v. 4  |h pp. 335-342  |k n. 4  |p Curr. Drug Targets: Immune, Endocr. Metab. Disord.  |x 15680088  |t Current Drug Targets: Immune, Endocrine and Metabolic Disorders 
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