scott@vtx-cpd.com

Replying to Rachel H. 05/05/2025 - 13:31

Hi Rachel,

Thanks so much for getting in touch. This is a great case to think through, and I really like your plan. I agree that there are a few red flags that suggest she may not have classic Addison’s, and it makes sense to reassess the diagnosis now that you’ve inherited the case.

The main concern for me is the timing of the ACTH stimulation test. From what you described, the test was performed just five days after stopping prednisolone. Although pred doesn’t interfere analytically with cortisol assays, it absolutely can cause suppression of the hypothalamic-pituitary-adrenal (HPA) axis through feedback inhibition, and five days may not have been long enough to avoid that. Recent data has added some nuance to our understanding here. A 2024 prospective study by Del Baldo et al. looked at HPA axis recovery in 20 client-owned dogs treated with intermediate-acting glucocorticoids like pred or methylpred. They found that while the median time to recovery was just three days, some dogs took much longer, and in one case, the HPA axis remained suppressed for over 18 weeks. That dog showed flat ACTH stim responses for months before eventually regaining a measurable post-stim cortisol. So even though most dogs bounce back quickly, there is significant variability, and a flat cortisol result five days post-pred cannot be considered definitively diagnostic.

The other major factor is the fact that she has never had electrolyte abnormalities. True primary hypoadrenocorticism almost always involves some degree of electrolyte derangement, either at diagnosis or over time. In contrast, dogs with atypical Addison’s have glucocorticoid deficiency only and retain normal sodium and potassium because their mineralocorticoid axis is intact. The fact that she’s needed her Zycortal dose reduced at every recheck, with normal electrolytes throughout, strongly suggests that she may not have any clinically relevant mineralocorticoid deficiency at all.

I think your current approach of continuing the Zycortal but gradually tapering it based on electrolyte monitoring is a very reasonable one. If you reach a dose that’s very low, for example below 0.5 mg/kg, and electrolytes are still normal, I’d absolutely consider a trial off Zycortal. You could skip the next injection, then recheck electrolytes at two to three weeks and again at four to five weeks to watch for any delayed shifts. If her sodium and potassium remain within normal limits and she’s clinically stable, it would support that she does not need mineralocorticoid supplementation.

If you wanted to go a step further, once she’s stable off Zycortal, you could consider repeating the ACTH stimulation test after a longer washout from higher-dose steroids. Including an endogenous ACTH measurement at that time would be helpful too. A truly Addisonian dog should have an elevated endogenous ACTH with a flat cortisol response, whereas a dog with prior suppression will typically have a low to low-normal ACTH as the pituitary axis reawakens.

If she does well off Zycortal, you can just continue low-dose prednisolone long-term and manage her as an atypical Addisonian, assuming her clinical signs remain controlled. Or, if the repeated testing points away from Addison’s altogether, you may even be able to wean her entirely.

You’re already handling this really thoughtfully, and I think you’re absolutely on the right track. Let me know how she gets on or if you want to chat further down the line.

Best,

Scott 🙂

Full reference:

Del Baldo F, Corsini A, Tardo AM, et al. Hypothalamic–pituitary–adrenal axis recovery after intermediate-acting glucocorticoid treatment in client-owned dogs. Journal of Veterinary Internal Medicine. 2024;38(2):942–950. doi:10.1111/jvim.16979

Replying to Samantha T. 07/05/2025 - 19:14

Welcome Sam!

Thank you for your brilliant contribution, and thank you for the cute kitten picture!

Scott 🙂

Replying to Christina Frigast 08/05/2025 - 09:41

Sadly these are all on the more expensive end of treatments!

Thanks again for sharing all these brilliant thoughts.

Scott 🙂

Replying to Rodolfo L. 08/05/2025 - 11:38

Rodolfo!

Thank you so much for joining us and for being part of the course!

We are very lucky to get to work with you!

Scott 🙂

Replying to Christina Frigast 04/05/2025 - 11:04

Hi Christina,

That’s a great question about FIP and transfusions. In general, I do think blood transfusions can have a role in selected cases, particularly when the anaemia is moderate to severe and clearly affecting clinical status. That said, many cats with FIP develop a non-regenerative, inflammatory anaemia that they tolerate reasonably well for some time. If the cat is bright, eating, and stable, I’d often hold off unless there is functional compromise or clear evidence of progression.

Your decision to monitor conservatively, especially with xenotransfusion as the only option, sounds entirely appropriate. Some referral hospitals may opt for early transfusion as a stabilising measure if further procedures or stressors are anticipated, but I think either approach can be valid depending on the context.

I also think the availability of FIP treatment really changes the equation. With GS products and remdesivir now accessible, we’re often able to initiate therapy promptly and see rapid improvement, which can stabilise haematologic parameters and help avoid interventions like transfusion altogether. If antiviral therapy is within reach, I would lean toward starting that and reserving transfusion for cases that are clearly decompensating.

Thanks again for raising such a thoughtful point.

All the best,

Scott 🙂