Addison’s disease has always been one of my most rewarding conditions to treat, having seen patients make miraculous recoveries often from the brink of death, by simply administering aggressive fluid therapy and, after performing the necessary diagnostics, a dose of glucocorticoids. However, after watching last week’s webinar, led by Professor Ian Ramsey, I’m now starting to wonder if I may have missed some cases of Addison’s over the years?

As Prof Ramsey explained, Addison’s disease is otherwise known as ‘the great pretender’ and has the variety and vagueness of clinical signs to mimic a number of other diseases. For example an addisonian patient can present with almost exactly the same clinical signs and diagnostic results as a patient in acute renal failure. Both sets of patients will be azotaemic with a low urine specific gravity and both often have a low sodium and high potassium, the classic hallmark of Addison’s disease. Distinguishing between the two can be difficult with only subtle differences existing between them such as the calcium level which is often high in Addison’s disease and normal or low in acute renal failure. Could some of the patients I previously diagnosed with acute renal failure have actually been suffering from Addison’s disease? This is a question I don’t have the answer for but as Professor Ramsey stated in the webinar, the best way to ensure that a diagnosis of Addison’s disease is never missed is to always ask the right questions when working cases up, and once the answers to these questions have been ascertained, to always check to see if they correlate with a possible diagnosis of Addison’s disease.

Of course, the best way to confirm a diagnosis of Addison’s disease is to perform an ACTH stimulation test and Prof Ramsey advises NEVER to give glucocorticoids prior to performing this test. I was in fact wrong earlier, having assumed my injection of glucocorticoids actually saved the lives of my addisonian patients. Prof Ramsey explained it is the aggressive fluid therapy and any additional treatments for addressing the life threatening consequences of hyperkalaemia which actually saves a patient’s life. There is really no excuse to give glucocorticoids prior to performing an ACTH stimulation test, even if it is in the middle of the night. The steroid can always wait till morning when an ACTH stimulation test can be performed prior to its use.

Prof Ramsey also explained that some vets also like to measure basal cortisol as a screening test which, in his opinion, would seem a little pointless. He believes it would be much more cost effective to just go ahead and perform an ACTH stimulation test if you are at all concerned that a patient may be suffering from Addison’s disease. However there may be circumstances where acquiring the ACTH to perform an ACTH stimulation test can be difficult, and in this situation Professor Ramsey advises obtaining a basal cortisol level, but to also place further blood into an EDTA tube, spin it down, remove the supernatant and freeze the remainder. ACTH levels can then be measured alongside basal cortisol and, if the cortisol to ACTH ratio is high, a diagnosis of Addison’s disease can be confirmed.

Treatment for Addison’s disease has changed significantly in the past few months with the development and introduction of the only licensed product, a long acting injectable, desoxycortosterone pivalate (also known as Zycortal). This has replaced the now very expensive unlicensed Fludricortisone, (also known as Florinef). Prof Ramsey provided advice on how to safely and effectively administer Zycortal to either newly diagnosed patients or patients currently stable on Florinef. He did question some of the advice delivered by Dechra about the adjustment of Zycortal’s dose, based on a patient’s sodium to potassium ratios.

Prof Ramsey believes that in-house electrolyte analysers can deliver results of variable accuracy which could have a significant impact on a patient’s sodium to potassium ratio leading to frequent unnecessary dose adjustments. Instead he advised adjusting the Zycortal dose in 10-20% incremental steps. For example, if a patient’s potassium is high or the sodium is low when the electrolytes are measured on day 10, the Zycortal dose should be increased by 20% at day 28. However, if the potassium is too low or the sodium too high, then the dose should be reduced by 10-20%. If, however, on day 28 the potassium is still too low or the sodium too high, then Zycortal should not be injected.

Electrolyte levels should be checked every 7 days in these cases and Zycortal should be injected at a 20% lower dose when a patient’s electrolyte levels return to normal. Once stable, patients should be checked every 4-6 months and owners can be taught to inject at home to save on return trips to the surgery.

Professor Ramsey always delivers excellent, practical and information packed webinars, and last week’s webinar discussing ‘The Great Pretender’ was definitely no exception. If I have missed cases of Addison’s disease in the past, watching this webinar should help to ensure I don’t miss any in the future. It also delivered clarity on a new treatment for Addison’s disease which previously I had used with apprehension and now feel I can use with new found confidence.