Zycortal Symposium Proceedings

and post-ACTH aldosterone in another four dogs with “atypical” hypoadrenocorticism and found it to be below the detection limit of the assay in three of them, one dog had low-normal baseline aldosterone with no increase after ACTH. The finding that aldosterone concentrations were low or undetectable in most dogs with hypoadrenocorticism independently of the degree of electrolyte abnormalities – and even in dogs with normal electrolytes – was striking. This means, that normal electrolytes do not necessarily reflect a normally functioning zona glomerulosa. In human medicine, normal sodium and potassium concentrations are found in 10% and normal potassium in 25% of patients with primary hypoadrenocorticism 30 . The assumption that the zona glomerulosa and the aldosterone secretion are still intact in these patients has been degraded. Increased renin concentrations were found in all of those patients, indicating compensation for a failing zona glomerulosa. Therefore in humans, it is currently assumed that a dissociation between zona glomerulosa and fasciculata/reticularis function occurs very rarely 31 . Possible mechanisms allowing a normal potassium balance without aldosterone are a high tubular flow rate with high delivery of potassium to the collecting duct and/or an increased sensitivity of the tubule to aldosterone due to up-regulation of the receptor. Furthermore, hyperkalaemia itself increases potassium excretion. It is also thought that normal potassium balance can be maintained as long as sodium intake is sufficient to maintain normal extracellular volume and distal tubular flow rate. 32,33 Aldosterone was measured in dogs with “atypical” hypoadrenocorticism in a few other studies. Dunn and Herrtage found normal basal aldosterone but not increase after ACTH in one dog 34 ; Thompson et al reported normal post-ACTH concentration in one dog 15 ; Cartwright et al found normal baseline and post-ACTH aldosterone in a dog with Schmidt syndrome 35 , however, both concentrations were in the lower end of the reference interval. In Zurich dogs with “atypical” hypoadrenocorticism are treated with prednisolone only, i.e. they do not receive mineralocorticoids. Initial dose is 0.5 mg/kg SID or BID (+ IV infusion if necessary), which is tapered to the lowest possible dose within 2-3 weeks after recovery. Most dogs receive 0.05-0.1 mg/kg SID prednisolone long-term. In the majority of dogs electrolytes remain normal. In the largest study so far electrolyte abnormalities developed in 5/35 (14%) dogs with “atypical” hypoadrenocorticism 8 . This finding is in agreement with a 9% and 11% conversion rate of other studies and our own data. 4,12,15 Conversion usually occurs during the first months of therapy, but has also been reported after four years. The risk of conversion requires good client communication and regular re-evaluations. Treatment and follow-up examinations

Redefining ‘atypical’ Addison’s disease?

The topic of “atypical” hypoadrenocorticism is quite complex and the question about the correct definition is challenging. According to currently available data dogs with “atypical” hypoadrenocorticism do not represent a homogenous group and at least three subgroups may be identified. Most dogs with primary hypoadrenocorticism and normal sodium and potassium concentrations have undetectable or very low aldosterone levels. It is very likely, that in those cases not only the zona fasciculata/reticularis but also the zona glomerulosa is destroyed.

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