ECE2015 Eposter Presentations Adrenal cortex (94 abstracts)
Reduced salivary cortisone, but similar cortisol day curves in Addison's disease in patients on hydrocortisone replacement
Ian Ross 1 , Miguel Lacerda 1 , Tahir Pillay 1, , Dirk Blom 1 , Gudmundur Johannsson 3 , Joel Dave 1 , Naomi Levitt 1 , David Haarburger 4 & Jan-Stefan van der Walt 5
1University of Cape Town, Cape Town, South Africa; 2NHLS, Tshwane, South Africa; 3University of Gothenburg, Gothenburg, Sweden; 4Ampath Laboratories, Pomona, South Africa; 5Astellas Pharma, Leiden, The Netherlands.
Background: Salivary cortisol, as measured using electro-chemiluminescence has been used to monitor patients with Addison’s disease (AD) on hydrocortisone replacement. Salivary cortisone has been suggested as an alternative to salivary cortisol, as it may accurately reflect plasma free cortisol. We wished to examine the pharmacokinetics of these analytes in patients and controls.
Methods: We measured salivary cortisol and salivary cortisone by liquid chromatography–tandem mass spectrometry using a day curve with 16 time points in patients with AD on hydrocortisone and in healthy controls with endogenous cortisol secretion.
Results: There were 25 patients and 26 healthy controls. The median (interquartile range) area under the curve (AUC) for cortisol was not different for patients, 55.63 (32.91–151.07), compared with controls 37.49 (27.41–52.00) nmol/min per l; P=0.098, whereas the peak cortisol (Cmax) was higher 32.61 (5.75–146.19) nmol/l vs 8.96 (6.96–12.23) nmol/l; P=0.013 and time to peak (Tmax) 1.5 (0.5–2.0), compared with controls 0.0 (0.0–0.5) h; P<0.001. The AUC for cortisone was reduced for patients, 23.65 (6.10–54.76), compared with controls, 227.73 (200.10–280.52) nmol/min per l; P≤0.001, Cmax for cortisone was lower 11.11 (2.91–35.85) nmol/l vs 33.12 (25.97–39.95) nmol/l; P=0.002 and longer Tmax 2.5 (2.0–9.5), compared with 0.25 (0.00–0.50) h, respectively; P<0.001.
Conclusions: Although there was no difference in cortisol exposure, there was less cortisone exposure in patients than controls, possibly due to the pharmacological effect of hydrocortisone on the 11-β-hydroxysteroid dehydrogenase enzymes. Lack of cortisone exposure and less metabolism of cortisol in patients with AD may predispose to metabolic consequences.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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