scott@vtx-cpd.com

Replying to Graeme E. 10/11/2025 - 10:03

Hey Graeme!

Lovely to see you here. I hope all is well your end!

I definitely defer to Liz for this one!

Scott 🙂

Replying to Christina Frigast 21/10/2025 - 10:04

Hi Christina,

I hope all is well with you?

I completely agree, it definitely feels like one of those techniques that could bridge the gap for clients who might otherwise decline wound closure because of cost, or when sedation feels disproportionate to the injury. I was surprised at how simple it looks in practice once you see the step-by-step diagrams.

I think with the right patient temperament (and maybe the right nurse on hand!), it could become a very practical tool for those small, clean wounds we see out of hours. It’ll be interesting to see if a larger follow-up study looks at owner satisfaction, cosmesis, or infection rates longer-term.

All the best,

Scott

Replying to Anna M. 29/10/2025 - 11:46

Hi Anna,

I’m really glad you’re enjoying the course, that’s great to hear!

You’re absolutely right that there’s some nuance in how we approach screening for acromegaly in diabetic cats. The newer data suggest it’s more common than we used to think. The recent German cross-sectional study by Guse et al. (J Feline Med Surg 2025; 27[1]:1098612X241303303) reported increased IGF-1 (>746 ng/mL) in 17.5% of 97 diabetic cats tested, and a positive correlation between IGF-1 and insulin dose (median 1.63 U/kg/day vs 0.86 U/kg/day, P = 0.018). That aligns with earlier findings from the RVC and elsewhere suggesting that 15–25% of diabetic cats may have hypersomatotropism, even though only a subset show overt clinical acromegalic features.

In practice, I don’t test every diabetic cat, I reserve IGF-1 screening for those showing insulin resistance (typically >1.5 U/kg/injection or poor glycaemic control despite good technique, diet, and concurrent disease management). Testing all diabetics will certainly detect mild or subclinical cases, but these often don’t alter management unless there’s genuine insulin resistance or poor control. The review by Scudder & Church (J Feline Med Surg 2024; PMID 38323402) reinforces this selective approach, emphasizing that hypersomatotropism-induced diabetes typically manifests as highly variable or refractory hyperglycaemia.

Regarding comorbidities, pancreatitis remains very common, depending on criteria and assays, around 30–50% of diabetic cats show either historical or concurrent evidence of pancreatitis. Many of these fall under the “triaditis” umbrella (IBD, cholangitis, pancreatitis), and we often suspect at least low-grade pancreatic inflammation in poorly controlled or relapsing diabetics.

Your practical advice for inappetent diabetics is exactly what I suggest:

If they’ve eaten ≥ 50% of their normal meal, it’s generally safe to give the usual insulin dose (or modestly reduce it if there’s concern).

If they’ve eaten < 50%, skip that dose and monitor. Safety always outweighs perfect glycaemic control in these situations, especially if owners don’t have home glucose monitoring. Hope that helps, and I’m delighted you’re finding the material useful. Best, Scott

Replying to Amy G. 14/10/2025 - 15:11

Hi Amy,

That’s a really good question, and one that comes up a lot, particularly when we’re trying to manage IBD in patients that have concurrent or potential endocrine issues. I rarely used budesonide when I worked in the UK, but they love it here in Canada!

In cats, budesonide is generally reserved for cases where we want to limit systemic steroid exposure, such as those with concurrent diabetes mellitus, heart disease, or significant renal compromise. It’s a locally active corticosteroid that undergoes extensive first-pass hepatic metabolism, around 80–90% in people and dogs, which greatly reduces circulating glucocorticoid levels. We presume a similar effect in cats, although there are very limited pharmacokinetic data to confirm it.

Efficacy-wise, there are no robust feline trials directly comparing budesonide with prednisolone, but small case reports and anecdotal experiences suggest that it can provide decent control for many cats, especially those with mild-to-moderate lymphoplasmacytic enteritis or those already induced into remission with prednisolone. In my own experience, and in the broader small-animal literature, it isn’t as potent as prednisolone for induction, but it can maintain clinical control in a fair number of patients.

For dosing, most clinicians use about 0.5 to 1 mg per cat orally once daily, often using compounded capsules. Some cats can move to an every-other-day schedule once stable, but there’s no formal evidence base for tapering. The human enteric-coated formulations such as Entocort or Cortiment may not dissolve predictably in cats because of pH differences along their GI tract, so compounded non-enteric capsules are often more reliable.

Adverse effects can still occur. Even though systemic absorption is reduced, budesonide isn’t free of glucocorticoid activity, and hyperglycaemia or steroid-induced diabetes has been documented in both cats and dogs. The risk is definitely lower than with prednisolone but not zero, so in a cat that previously showed diabetic tendencies on pred, budesonide is a logical next step as long as blood glucose is monitored.

In dogs, the best evidence comes from the randomized controlled trial by Dye and colleagues published in JVIM in 2013. That study compared budesonide and prednisone for induction of remission in canine IBD and found no significant difference in remission rates, roughly 78% for budesonide and 69% for prednisone, and no real difference in the frequency of adverse effects. So in dogs, it’s considered a viable alternative for induction, though most of us still find it slightly “softer” in effect than prednisone.

Overall, budesonide is best thought of as a less systemically active but still clinically useful corticosteroid. It’s often a good compromise in cats that cannot tolerate or have had adverse effects from prednisolone, particularly those prone to hyperglycaemia. In some cases it can be combined with adjunctive therapies such as cobalamin supplementation, dietary management, metronidazole, or chlorambucil if histology shows more severe lymphoplasmacytic inflammation.

So in short, budesonide won’t match prednisolone’s potency for induction, but in cats where hyperglycaemia or other systemic risks are a concern, it’s a very reasonable and commonly used alternative that can still achieve good control in a number of cases.

I love that you are looking for the vitamin B!!!!!!

Scott 🙂