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ADDISON'S disease or hypoadrenocorticism generally results from immune-mediated destruction of the adrenal glands and particular dog breeds appear to be overrepresented; for example, West Highland white and wheaten terriers, Portuguese water dogs, duck-tolling retrievers and great danes. Candidate genes for the disease have been identified in several breeds, although at this time the exact contribution of these genes is unclear (Short and others 2014). In most cases of ‘typical’ hypoadrenocorticism there is a lack of production of both mineralocorticoid and glucocorticoid, whereas in the rarer ‘atypical’ Addisonian only glucocorticoid deficiency manifests itself. Mineralocorticoid deficiency results in hyponatraemia and hyperkalaemia, as well as hypovolaemia, whereas glucocorticoid deficiency can lead to weakness, hypoglycaemia and gastrointestinal signs. Once typical hypoadrenocorticism has been diagnosed, both mineralocorticoid and glucocorticoid supplementation is needed.
Mineralocorticoid deficiency is generally treated with either fludrocortisone or desoxycorticosterone pivalate (DOCP). There is an example of a large study of 205 dogs where 95 per cent were initially treated with fludrocortisone. Some of these dogs (14 per cent) were eventually switched to DOCP for a variety of reasons (Kintzer and Peterson 1997). In a paper summarised on p 98 of this issue of Veterinary Record, Roberts and others (2016) were also able to successfully stabilise 90 per cent of their patients with fludrocortisone. There are significant differences between both medications, including cost, and in most countries DOCP is sparingly used, because it is considerably more expensive than fludrocortisone; however, in a small number of countries …
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