Diagnostic performance of salivary cortisol in the diagnosis of Cushing’s syndrome, adrenal incidentaloma and adrenal insufficiency

Posted on May 1, 2013 by MaryO

Source

F Ceccato, Department of Medicine – DIMED, University of Padova, Endocrinology Unit, Padova, Italy.

Abstract

OBJECTIVE:

Salivary cortisol has been recently suggested for studies on the hypothalamic-pituitary-adrenal (HPA) axis: lack of circadian rhythm is a marker of Cushing’s syndrome (CS), and some authors report that low salivary cortisol levels may be a marker of adrenal insufficiency. The aim of our study was to define the role of salivary cortisol in specific diagnostic setting of HPA axis disease.

SUBJECTS AND METHODS:

We analyzed morning salivary cortisol (MSC) and late night salivary cortisol (LNSC) in 406 subjects: 52 Cushing’s disease (CD), 13 ectopic-CS, 17 adrenal-CS, 27 CD in remission (mean follow-up of 66 ± 39 months), 45 adrenal incidentalomas, 73 patients assessed of CS and then ruled out for endogenous hypercortisolism, 75 patients with adrenal insufficiency and 104 healthy subjects.

RESULTS:

A LNSC value above 5.24 ng/mL differentiated CS from controls with high sensitivity (96.3%) and specificity (97.1%), we found higher LNSC in ectopic-CS than in CD. We found no difference in MSC and LNSC levels between CD in remission and healthy subjects. Both MSC and LNSC were higher in adrenal incidentaloma than in healthy controls. MSC below 2.65 ng/mL distinguished patients with adrenal insufficiency from controls with high sensitivity (97.1%) and specificity (93.3%).

CONCLUSIONS:

salivary cortisol is a useful tool to assess endogenous cortisol excess or adrenal insufficiency and to evaluate stable CD in remission.

PMID:

 

23610124

 

[PubMed – as supplied by publisher]
From PubMed
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Cushing’s Disease and Idiopathic Intracranial Hypertension

Posted on May 2, 2012 by MaryO

Gabriel Zada, Amir Tirosh, Ursula B. Kaiser, Edward R. Laws and Whitney W. Woodmansee

Department of Neurosurgery (G.Z., E.R.L.) and Division of Endocrinology, Diabetes, and Hypertension (A.T., U.B.K., W.W.W.), Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Gabriel Zada, M.D., 15 Francis Street, PBB3, Boston, Massachusetts 02115. E-mail: gzada@usc.edu.

Abstract

Case Illustration: A 33-yr-old woman with Cushing’s disease underwent successful surgical resection of a pituitary adenoma and developed IIH 11 months later after inadvertent withdrawal of oral glucocorticoids.

Methods: A review of the literature was conducted to identify previous studies pertaining to IIH in association with neuroendocrine disease, focusing on reports related to HPA axis dysfunction.

Results: A number of patients developing IIH due to a relative deficiency in glucocorticoids, after surgical or medical management for Cushing’s disease, withdrawal from glucocorticoid replacement, or as an initial presentation of Addison’s disease, have been reported. Hypotheses regarding the underlying pathophysiology of IIH in this context and, in particular, the role of cortisol and its relationship to other neuroendocrine and inflammatory mediators that may regulate the homeostasis of cerebrospinal fluid production and absorption are reviewed.

Conclusion: In a subset of patients, dysfunction of the HPA axis appears to play a role in the development of IIH. Hormonal control of cerebrospinal fluid production and absorption may be regulated by inflammatory mediators and the enzyme 11ß-hydroxysteroid dehydrogenase type 1. Further study of neuroendocrine markers in the serum and cerebrospinal fluid may be an avenue for further research in IIH.

Read the entire article at http://jcem.endojournals.org/content/95/11/4850.full

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