References
Primary hypoaldosteronism in a dog with concurrent suspected chronic hepatitis
Abstract
A 3-year-old female spayed English Cocker Spaniel presented with a 2-month history of lethargy. The owner reported a single tonic-clonic seizure 7 months before presentation and intermittent mild gastrointestinal signs for the past 18 months. Initial investigations revealed hyponatraemia, hyperkalaemia and increased levels of liver enzymes. An adrenocorticotropic hormone stimulation test excluded hypocortisolism. The gastrointestinal signs resolved following a dietary change, suggesting that chronic enteropathy and most primary and secondary causes of hepatic disease were excluded, leaving idiopathic chronic hepatitis as the most likely cause of increased levels of liver enzymes. Liver parameters reduced to levels just above reference range after immunosuppressive doses of prednisolone. Aldosterone levels pre- and post-adrenocorticotrophic hormone stimulation were <20 pmol/litre, consistent with mineralocorticoid deficiency. The mineralocorticoid deficiency was treated with desoxycorticosterone pivalate at 1–1.3 mg/kg subcutaneously every 48–87 days, which resulted in immediate and complete resolution of the clinical signs and electrolyte imbalance. Given the dog's signalment and results from clinical investigations, the isolated hypoaldosteronism is speculated to be caused by immune-mediated adrenal gland destruction. Isolated hypoaldosteronism should be considered a differential diagnosis for hyponatraemia in dogs, when an adrenocorticotrophic hormone stimulation test excludes hypocortisolism.
A3-year-old female spayed English Cocker Spaniel was referred for investigations of a 2-month history of lethargy. The owner reported episodes of once-weekly mixed bowel diarrhoea and occasional vomiting over the past 18 months. A single tonic-clonic seizure had occurred 7 months before presentation. The owner telephoned the referral veterinary service to inform them about the seizure episode and was advised to monitor the dog. There was no veterinary visit or blood work performed following this episode. The seizure was suspected to be caused by hyponatraemia; however, toxin ingestion could not be excluded (although no toxin exposure was reported by the owner). Idiopathic, structural or congenital reasons for the seizure were considered at the time. These differentials are now considered less likely given the complete resolution of seizures once the electrolyte imbalance was corrected.
The dog had no history of travelling outside the UK, drug administration or toxin exposure, was up to date with vaccinations and received monthly veterinary prescribed flea and worm treatment. The dog was fed a commercial biologically appropriate raw food diet. No abnormalities were detected on physical and neurological examination. Barrier nursing was implemented while the dog was hospitalised.
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