Sialochemistry and cortisol levels in patients with Sjogren's syndrome

Oral Diseases (2012) 18, 255–259 Objectives:  (i) To determine whether salivary cortisol and electrolyte levels differ between patients with Sjogren’s syndrome (SjS) and healthy individuals. (ii) To assess correlations between whole‐saliva cortisol and some clinical manifestations in patients with S...

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Veröffentlicht in:Oral diseases 2012-04, Vol.18 (3), p.255-259
Hauptverfasser: Miller, BE, Deutsch, O, Redlich, M, Konttinen, YT, Benoliel, R, Zaks, B, Davidovich, E, Palmon, A, Aframian, DJ
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Sprache:eng
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Zusammenfassung:Oral Diseases (2012) 18, 255–259 Objectives:  (i) To determine whether salivary cortisol and electrolyte levels differ between patients with Sjogren’s syndrome (SjS) and healthy individuals. (ii) To assess correlations between whole‐saliva cortisol and some clinical manifestations in patients with SjS. Methods:  A total of 24 healthy women (mean age 49.3 ± 9.8) served as controls (C) vis‐à‐vis 17 patients with SjS (mean age 55.5 ± 15.7). Salivary cortisol concentration was determined, and sialochemistry analysis was performed. Results:  Significantly lower saliva flow rates and higher salivary chloride (Cl−), potassium (K+), and Ca2+ levels were found in the SjS group. No significant differences or correlations were found in other parameters, including sodium (Na+), magnesium (Mg2+), phosphate (−), urea (U), and salivary cortisol levels. Conclusion:  Increased whole‐salivary output of Cl− and K+ in SjS may reflect release from apoptotic rests of acinar cells after secondary necrosis. Normal levels of salivary Na+, Mg2+, and − argue against concentration effect, deranged tubular function or cortisol (mineralocorticosteroid) effect as the cause for these findings. Increased salivary Ca2+ levels probably reflect leakage of plasma Ca2+ through the injured oral mucosa in SjS. In spite of disease‐associated stress, salivary cortisol, a stress biomarker, was not increased, suggesting insufficient hypothalamus–pituitary–adrenal (HPA) axis response and/or local consumption of cortisol by lymphocyte infiltrates.
ISSN:1354-523X
1601-0825
DOI:10.1111/j.1601-0825.2011.01866.x