9 Jan 2017
Stephanie Lalor discusses the case of Ollie, an 18-month-old male entire great Dane, in the latest of our Practice Notes series.
Ollie is an 18-month-old male entire great Dane presented to you with a two-month history of intermittent bilious vomiting and soft faeces, which has been unresponsive to diet change and metronidazole therapy.
Physical examination was unremarkable, apart from a suboptimal body condition score of 4 out of 9. Vital parameters were all within normal limits; temperature was 38.2°C, heart rate was 88bpm and respiratory rate was 24rpm.
Routine haematology and serum biochemistry, including electrolytes (Table 1) was unremarkable, as was canine pancreatic lipase immunoreactivity, folate, cobalamin and faecal analysis.
An adrenocorticotropic hormone (ACTH) stimulation test was performed and this was consistent with hypoadrenocorticism (pre-ACTH cortisol <10nmol/L and post-ACTH cortisol <10nmol/L).
What is the treatment for atypical hypoadrenocorticism (Addison’s disease) and what monitoring is required in the long term?
Ollie has atypical hypoadrenocorticism. This is due to a deficiency in glucocorticoids, and, therefore, electrolytes remain normal. This is usually due to primary adrenal gland failure; however, rarely it can be due to pituitary dysfunction and, therefore, decreased or absent ACTH stimulation. This can result in glucocorticoid deficiency alone, as ACTH has minimal influence on mineralocorticoid secretion.
Some dogs with atypical hypoadrenocorticism may be at risk of developing concurrent mineralocorticoid deficiency. Endogenous ACTH concentration can be measured (prior to ACTH stimulation and steroid therapy commencing) to see which dogs are at risk of progressing to typical hypoadrenocorticism. An ACTH concentration above the reference range is consistent with primary hypoadrenocorticism and these dogs are at risk of progression. If the ACTH concentration is below the reference range, this is consistent with the rarer form of secondary hypoadrenocorticism. In the latter case, no monitoring is required in the future.
Glucocorticoids are the treatment of choice for atypical hypoadrenocorticism.
As Ollie is stable, oral therapy was started on prednisolone dose at 0.2mg/kg SID. He responded well and his vomiting and diarrhoea resolved within seven days. His owner was advised to increase the dose of prednisolone during times of illness or stress, for example, kennelling.
At diagnosis, Ollie’s electrolytes were normal, so mineralocorticoid therapy was not started and endogenous ACTH concentration not measured. Most dogs who do progress to typical hypoadrenocorticism will do so within the first year. Ollie’s electrolytes were, therefore, checked monthly for three months, then every three months thereafter. He remained atypical and has been continued on prednisolone, at a lower dose of 0.15mg/kg SID, due to development of some steroid side effects (polydipsia and polyuria).