Hypoadrenocorticism in a 13-year-old-dog
A 13-year-old female spayed Jack Russell Terrier presented to her primary care veterinarian for vomiting and diarrhea 2 days following ingestion of ice cream and cupcakes. The primary veterinarian performed a chemistry panel which was suggestive of pancreatitis (Amylase > 2500 IU/L, ref. range 333-1500 IU/L; Lipase > 6000 IU/L, ref. range 77-750 IU/L). Despite initial symptomatic care, the patient declined and was subsequently referred to the Cornell Emergency Service. She had cranial abdominal pain and prominent mandibular and popliteal lymph nodes. Initial diagnostics were non-specific. Findings included hypoglycemia and a questionable degenerative left shift. Imaging showed no evidence of obstruction or any other obvious cause of vomiting and diarrhea. The patient was managed empirically with pain medications, anti-emetics, antibiotics, and fluids supplemented with dextrose. Additional diagnostics were performed by the Internal Medicine Service. The results were also non-specific and included non-regenerative anemia, a degenerative left shift that improved with antibiotic therapy, intermittent hypoglycemia, elevated amylase that decreased over time, and hypocholesterolemia. Abdominal ultrasound showed a moderately enlarged left adrenal gland with hypoechoic nodules. A baseline cortisol was measured, which was low (Cortisol <0.2 g/dL; Ref. Range 1.8 – 4). An ACTH stimulation was performed, and cortisol was still low leading to a diagnosis of hypoadrenocorticism (Cortisol <0.2 g/dL; Ref. Range 6 – 16). Due to the absence of electrolyte abnormalities that are characteristic of typical hypoadrenocorticism, the patient was presumptively determined to have atypical hypoadrenocorticism. Therefore, she was treated with steroid supplementation only and did not receive mineralocorticoid supplementation. The patient has been doing well at home with medical management.
Hypoadrenocorticism is an uncommon endocrinopathy in dogs, and the atypical form is even less common as it is responsible for approximately 4% of primary hypoadrenocorticism cases. Clinical findings associated with the disease are notoriously vague which makes it a difficult diagnosis. A low cortisol measurement following ACTH stimulation is the gold standard of diagnosis. Patients can be effectively managed with glucocorticoid supplementation alone or glucocorticoid and mineralocorticoid supplementation. With appropriate treatment, the prognosis for hypoadrenocorticism is good.