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...

Descripción completa

Detalles Bibliográficos
Autores principales: Labeur, Marta Susana, Páez Pereda, Marcelo
Publicado: 2004
Materias:
Acceso en línea: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
Aporte de:
id paper:paper_15680088_v4_n4_p335_Labeur
record_format dspace
spelling 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
_version_ 1768543867070578688