Linked Life Data

19041802

Source:http://linkedlifedata.com/resource/pubmed/id/19041802

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-12-1
pubmed:abstractText
Cushing's disease caused by pituitary corticotroph adenoma in dogs is usually treated by medical treatment, and the efficacy of this treatment has been reported. However, controversy remains as to whether reduced negative feedback through the inhibition of cortisol secretion, similar to Nelson's syndrome, may appear as an adverse effect. The purpose of this study was to investigate the effect of reduced negative feedback through the inhibition of cortisol secretion by daily trilostane administration on the pituitary-adrenal axis in clinically normal dogs. Dogs were administered 5mg/kg trilostane twice a day every day for 8 weeks (n=8) or 16 weeks (n=3). After the initiation of trilostane administration, plasma adrenocorticotropic hormone (ACTH) concentrations were increased remarkably. As assessed by magnetic resonance imaging (MRI) during administration, the pituitary became enlarged. After trilostane administration, the cytoplasmic areas of the pituitary corticotrophs were increased and the ratio of pituitary corticotrophs to all cells in the anterior lobe was greater in the trilostane-treated dogs than that in untreated animals. In addition, histological examinations revealed bilateral adrenal cortical hyperplasia. Using real-time PCR quantification, the expression of proopiomelanocortin (POMC) mRNA in the pituitary and ACTH receptor (ACTH-R) mRNA in the adrenal gland was greater in the dogs treated with trilostane than in untreated dogs. These results indicate that reduced negative feedback induced hyperfunction of the pituitary corticotrophs and pituitary enlargement in healthy dogs. These changes suggest that the inhibition of cortisol secretion by trilostane may increase the risk for accelerating the growth of corticotroph adenomas in dogs with Cushing's disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1879-0054
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
36
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
32-44
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:19041802-Adrenal Glands, pubmed-meshheading:19041802-Adrenocorticotropic Hormone, pubmed-meshheading:19041802-Animals, pubmed-meshheading:19041802-Antineoplastic Agents, pubmed-meshheading:19041802-Corticotrophs, pubmed-meshheading:19041802-Dihydrotestosterone, pubmed-meshheading:19041802-Dogs, pubmed-meshheading:19041802-Feedback, Physiological, pubmed-meshheading:19041802-Female, pubmed-meshheading:19041802-Hydrocortisone, pubmed-meshheading:19041802-Hyperplasia, pubmed-meshheading:19041802-Hypothalamus, pubmed-meshheading:19041802-Magnetic Resonance Imaging, pubmed-meshheading:19041802-Male, pubmed-meshheading:19041802-Pituitary Gland, pubmed-meshheading:19041802-Pro-Opiomelanocortin, pubmed-meshheading:19041802-RNA, Messenger, pubmed-meshheading:19041802-Receptors, Corticotropin
pubmed:year
2009
pubmed:articleTitle
Trilostane-induced inhibition of cortisol secretion results in reduced negative feedback at the hypothalamic-pituitary axis.
pubmed:affiliation
Division of Veterinary Surgery, Department of Veterinary Science, Faculty of Veterinary Medicine, Nippon Veterinary and Life Science University, 1-7-1 Kyonan-cho, Musashino-shi, Tokyo 180-8602, Japan.
pubmed:publicationType
Journal Article