This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Determination of the underlying etiology of hypercortisolism is extremely challenging due to the nonspecificity of available tests. Consequently, the treatment currently offered for this highly morbid condition is unsuccessful in 20-25% of subjects. We propose that analysis of the 24 hour secretory profile of salivary cortisol, serum cortisol, and plasma ACTH will provide sensitive markers for the correct diagnosis of the etiology of hypercortisolism. In addition, sleep-disordered breathing (SDB) is common in subjects with Cushing s syndrome. It is unclear whether the SDB results from the associated obesity or whether there is a direct effect of the glucocorticoids on sleep centers. We hypothesize that (1) the use of salivary cortisol 24 hour profile as well as salivary response to CRF stimulation with or without dexamethasone is an accurate method of diagnosing Cushing s syndrome and (2) the correction of the hypercortisolism will improve the SDB seen in Cushing s syndrome.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
General Clinical Research Centers Program (M01)
Project #
5M01RR000055-46
Application #
7604780
Study Section
National Center for Research Resources Initial Review Group (RIRG)
Project Start
2007-03-01
Project End
2007-09-16
Budget Start
2007-03-01
Budget End
2007-09-16
Support Year
46
Fiscal Year
2007
Total Cost
$10,670
Indirect Cost
Name
University of Chicago
Department
Pathology
Type
Schools of Medicine
DUNS #
005421136
City
Chicago
State
IL
Country
United States
Zip Code
60637
Rosenfield, Robert L; Ehrmann, David A (2016) The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited. Endocr Rev 37:467-520
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