New perspectives in the treatment of cushing's syndrome
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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paper:paper_15680088_v4_n4_p335_Labeur2023-06-08T16:24:08Z New perspectives in the treatment of cushing's syndrome Labeur, Marta Susana Páez Pereda, Marcelo ACTH Cushing's syndrome Glucocorticoids HPA axis POMC 1 [n,o bis(5 isoquinolinesulfonyl) n methyltyrosyl] 4 phenylpiperazine 2 (2 amino 3 methoxyphenyl)chromone 4 aminobutyrate aminotransferase inhibitor aminoglutethimide bromocriptine cabergoline corticotropin corticotropin releasing factor corticotropin releasing factor antagonist cyproheptadine cytokine receptor dopamine derivative dopamine receptor stimulating agent glucocorticoid glucocorticoid antagonist glucocorticoid receptor antagonist hormone receptor blocking agent ketoconazole metyrapone mitotane n (2 phenylcyclopentyl)azacyclotridecan 2 imine n [2 (4 bromocinnamylamino)ethyl] 5 isoquinolinesulfonamide octreotide retinoic acid rosiglitazone serotonin antagonist somatostatin derivative unindexed drug uo 126 valproic acid adrenal disease adrenal function alopecia amenorrhea blood clotting disorder clinical trial corticotropin release Cushing syndrome depression diarrhea dizziness dose response drug efficacy drug eruption drug targeting gastrointestinal symptom glucose blood level headache hormonal regulation hormone substitution human hydrocortisone release hyperglycemia hypertension hypogonadism hypophysis adenoma hypothalamus hypophysis adrenal system increased appetite liver toxicity molecular biology morbidity mortality muscle hypotonia muscle weakness myalgia nausea nonhuman obesity osteoporosis pathogenesis pruritus psychopathy review side effect signal transduction somnolence taste disorder transcription regulation transsphenoidal hypophysectomy vomiting xerostomia Adrenocorticotropic Hormone Animals Cushing Syndrome Drug Delivery Systems Humans Receptors, Corticotropin-Releasing Hormone 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. Fil:Labeur, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Péz-Pereda, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2004 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15680088_v4_n4_p335_Labeur http://hdl.handle.net/20.500.12110/paper_15680088_v4_n4_p335_Labeur |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
topic |
ACTH Cushing's syndrome Glucocorticoids HPA axis POMC 1 [n,o bis(5 isoquinolinesulfonyl) n methyltyrosyl] 4 phenylpiperazine 2 (2 amino 3 methoxyphenyl)chromone 4 aminobutyrate aminotransferase inhibitor aminoglutethimide bromocriptine cabergoline corticotropin corticotropin releasing factor corticotropin releasing factor antagonist cyproheptadine cytokine receptor dopamine derivative dopamine receptor stimulating agent glucocorticoid glucocorticoid antagonist glucocorticoid receptor antagonist hormone receptor blocking agent ketoconazole metyrapone mitotane n (2 phenylcyclopentyl)azacyclotridecan 2 imine n [2 (4 bromocinnamylamino)ethyl] 5 isoquinolinesulfonamide octreotide retinoic acid rosiglitazone serotonin antagonist somatostatin derivative unindexed drug uo 126 valproic acid adrenal disease adrenal function alopecia amenorrhea blood clotting disorder clinical trial corticotropin release Cushing syndrome depression diarrhea dizziness dose response drug efficacy drug eruption drug targeting gastrointestinal symptom glucose blood level headache hormonal regulation hormone substitution human hydrocortisone release hyperglycemia hypertension hypogonadism hypophysis adenoma hypothalamus hypophysis adrenal system increased appetite liver toxicity molecular biology morbidity mortality muscle hypotonia muscle weakness myalgia nausea nonhuman obesity osteoporosis pathogenesis pruritus psychopathy review side effect signal transduction somnolence taste disorder transcription regulation transsphenoidal hypophysectomy vomiting xerostomia Adrenocorticotropic Hormone Animals Cushing Syndrome Drug Delivery Systems Humans Receptors, Corticotropin-Releasing Hormone |
spellingShingle |
ACTH Cushing's syndrome Glucocorticoids HPA axis POMC 1 [n,o bis(5 isoquinolinesulfonyl) n methyltyrosyl] 4 phenylpiperazine 2 (2 amino 3 methoxyphenyl)chromone 4 aminobutyrate aminotransferase inhibitor aminoglutethimide bromocriptine cabergoline corticotropin corticotropin releasing factor corticotropin releasing factor antagonist cyproheptadine cytokine receptor dopamine derivative dopamine receptor stimulating agent glucocorticoid glucocorticoid antagonist glucocorticoid receptor antagonist hormone receptor blocking agent ketoconazole metyrapone mitotane n (2 phenylcyclopentyl)azacyclotridecan 2 imine n [2 (4 bromocinnamylamino)ethyl] 5 isoquinolinesulfonamide octreotide retinoic acid rosiglitazone serotonin antagonist somatostatin derivative unindexed drug uo 126 valproic acid adrenal disease adrenal function alopecia amenorrhea blood clotting disorder clinical trial corticotropin release Cushing syndrome depression diarrhea dizziness dose response drug efficacy drug eruption drug targeting gastrointestinal symptom glucose blood level headache hormonal regulation hormone substitution human hydrocortisone release hyperglycemia hypertension hypogonadism hypophysis adenoma hypothalamus hypophysis adrenal system increased appetite liver toxicity molecular biology morbidity mortality muscle hypotonia muscle weakness myalgia nausea nonhuman obesity osteoporosis pathogenesis pruritus psychopathy review side effect signal transduction somnolence taste disorder transcription regulation transsphenoidal hypophysectomy vomiting xerostomia Adrenocorticotropic Hormone Animals Cushing Syndrome Drug Delivery Systems Humans Receptors, Corticotropin-Releasing Hormone Labeur, Marta Susana Páez Pereda, Marcelo New perspectives in the treatment of cushing's syndrome |
topic_facet |
ACTH Cushing's syndrome Glucocorticoids HPA axis POMC 1 [n,o bis(5 isoquinolinesulfonyl) n methyltyrosyl] 4 phenylpiperazine 2 (2 amino 3 methoxyphenyl)chromone 4 aminobutyrate aminotransferase inhibitor aminoglutethimide bromocriptine cabergoline corticotropin corticotropin releasing factor corticotropin releasing factor antagonist cyproheptadine cytokine receptor dopamine derivative dopamine receptor stimulating agent glucocorticoid glucocorticoid antagonist glucocorticoid receptor antagonist hormone receptor blocking agent ketoconazole metyrapone mitotane n (2 phenylcyclopentyl)azacyclotridecan 2 imine n [2 (4 bromocinnamylamino)ethyl] 5 isoquinolinesulfonamide octreotide retinoic acid rosiglitazone serotonin antagonist somatostatin derivative unindexed drug uo 126 valproic acid adrenal disease adrenal function alopecia amenorrhea blood clotting disorder clinical trial corticotropin release Cushing syndrome depression diarrhea dizziness dose response drug efficacy drug eruption drug targeting gastrointestinal symptom glucose blood level headache hormonal regulation hormone substitution human hydrocortisone release hyperglycemia hypertension hypogonadism hypophysis adenoma hypothalamus hypophysis adrenal system increased appetite liver toxicity molecular biology morbidity mortality muscle hypotonia muscle weakness myalgia nausea nonhuman obesity osteoporosis pathogenesis pruritus psychopathy review side effect signal transduction somnolence taste disorder transcription regulation transsphenoidal hypophysectomy vomiting xerostomia Adrenocorticotropic Hormone Animals Cushing Syndrome Drug Delivery Systems Humans Receptors, Corticotropin-Releasing Hormone |
description |
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. |
author |
Labeur, Marta Susana Páez Pereda, Marcelo |
author_facet |
Labeur, Marta Susana Páez Pereda, Marcelo |
author_sort |
Labeur, Marta Susana |
title |
New perspectives in the treatment of cushing's syndrome |
title_short |
New perspectives in the treatment of cushing's syndrome |
title_full |
New perspectives in the treatment of cushing's syndrome |
title_fullStr |
New perspectives in the treatment of cushing's syndrome |
title_full_unstemmed |
New perspectives in the treatment of cushing's syndrome |
title_sort |
new perspectives in the treatment of cushing's syndrome |
publishDate |
2004 |
url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_15680088_v4_n4_p335_Labeur http://hdl.handle.net/20.500.12110/paper_15680088_v4_n4_p335_Labeur |
work_keys_str_mv |
AT labeurmartasusana newperspectivesinthetreatmentofcushingssyndrome AT paezperedamarcelo newperspectivesinthetreatmentofcushingssyndrome |
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1768543867070578688 |