Hypoadrenocorticism in cats – a 40 year update

Practical relevanceAddison’s disease is a very rare condition in cats with only approximately 40 cases documented since it was initially described in the 40 years between 1983 and 2023. Clinical challenges While canine hypoadrenocorticism is a well-recognised disorder with clear diagnostic and treatment guidelines, feline hypoadrenocorticism remains a challenge, due to its rarity, and waxing and waning clinical signs. Furthermore, empirical treatment with corticosteroids, resulting in clinical improvement, contributes to delays in achieving the diagnosis and initiating treatment. Feline hypoadrenocorticism is diagnosed with an ACTH stimulation test (ACTHST); low resting cortisol concentration with an inadequate or absent response to synthetic ACTH is diagnostic. Various ACTH stimulation testing protocols are reported in published cases, with majority using three time-limited blood samples. This can be limiting clinically, depending on cats’ clinical presentation and behaviour at the veterinary practice and tolerance for procedures. Long term treatment, similar to canine hypoadrenocorticism, consists of oral corticosteroids, with several formulations licenced in UK and mineralocorticoids (desoxycorticosterone pivalate) of which the only available formulation is licenced for dogs and its safety has not been assessed in cats (Zycortal, Dechra, UK).Global importanceFeline hypoadrenocorticism occurs worldwide. Although no breed, sex or age association has been reported, cats below 6 years of age are overrepresented. Evidence baseThe information in this review is compiled from 47 reported cases of feline hypoadrenocorticism. Two retrospective multiple case series are included in this review and report investigating clinical presentation, clinicopathological findings and observational treatment outcomes (EBM grade III) with the remaining being single case reports (EBM grade IV). No prospective, randomised, placebo-controlled studies have been performed regarding feline hypoadrenocorticism (EBM grade I). <br/

Recurrent steroid responsive hypertrophic obstructive cardiomyopathy in a Maine Coon.

A 5-year-old, neutered, female Maine Coon with history of eosinophilic enteritis presented for acute deterioration following placement of a subcutaneous ureteral by-pass. Physical examination revealed a new 4/6, left, parasternal, systolic heart murmur. Echocardiography diagnosed hypertrophic obstructive cardiomyopathy with severe left ventricular outflow tract obstruction. Resolution of the hypertrophic obstructive cardiomyopathy phenotype was observed after 3 months of treatment with corticosteroids (1–2 mg/kg/day) implemented for a concurrent chronic enteropathy. Myocardial thickening and moderate left ventricular outflow tract obstruction recurred after discontinuation of steroids. Again, resolution of the cardiac changes was observed after 1 month of treatment with tapering doses of corticosteroids (0.8–2 mg/kg/day). A second recurrence occurred when steroids were decreased to 0.25 mg/kg/day. Due to adverse effects, the dose was only increased to 0.4 mg/kg/day. During follow-up over the next 10 months, this treatment regimen resulted in stabilisation of the disease, with echocardiographic changes compatible with hypertrophic cardiomyopathy stage B1 and minimal left ventricular outflow tract obstruction.</p