Dr T.L. Williams’ current address is Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 0ES
Investigation of the pathophysiological mechanism for altered calcium homeostasis in hyperthyroid cats
Version of Record online: 23 JUN 2013
© 2013 British Small Animal Veterinary Association
Journal of Small Animal Practice
Volume 54, Issue 7, pages 367–373, July 2013
How to Cite
Williams, T. L., Elliott, J., Berry, J. and Syme, H. M. (2013), Investigation of the pathophysiological mechanism for altered calcium homeostasis in hyperthyroid cats. Journal of Small Animal Practice, 54: 367–373. doi: 10.1111/jsap.12102
Results from this study were presented at ACVIM Forum 2013, Seattle, USA.
- Issue online: 23 JUN 2013
- Version of Record online: 23 JUN 2013
- Accepted: 20 May 2013
To investigate possible pathophysiological mechanisms (reduced plasma calcitriol concentrations and/or presence of concurrent or masked chronic kidney disease) for hypocalcaemiain hyperthyroid cats.
Prospective cohort study. Routine plasma biochemical parameters, plasma parathyroid hormone and calcitriol concentrations, ionized calcium concentrations, and venous pH, were measured at diagnosis and following treatment of hyperthyroidism. Linear regression analysis was used to determine predictors of ionized calcium concentration.
Hyperthyroid cats (n=45) had lower ionized calcium concentrations than healthy geriatric cats (n=52), however, ionized calcium concentrations were higher in hyperthyroid cats with concurrent or masked chronic kidney disease than non-azotaemic hyperthyroid cats. Plasma calcitriol concentrations were higher in hyperthyroid cats than control cats. Plasma total thyroxine concentration and venous pH were independent predictors of ionized calcium concentration. Plasma total thyroxine concentration was also a predictor of ionized calcium concentration after adjustment for plasma parathyroid hormone and calcitriol concentrations.
Hypocalcaemia in hyperthyroid cats is not associated with the presence of concurrent or masked chronic kidney disease or reduced plasma calcitriol concentrations. Increased thyroid hormone concentrations might influence ionized calcium concentrations through a mechanism, yet to be determined, that is independent of control by parathyroid hormone and calcitriol.