Hyperadrenocorticism is correct! Results from a repeated serum chemistry profile and complete blood count were normal. Urinalysis and urine culture demonstrated bacteriuria. A thyroid panel showed borderline low serum T4, low normal free T4, and low normal thyroid stimulating hormone levels. An ACTH stimulation test indicated hyperadrenocorticism. This was confirmed with a low-dose dexamethasone suppression test, which was also most consistent with pituitary-dependent hyperadrenocorticism. There are four classic presentations of hyperadrenocorticism to a dermatologist: 1) relapsing pyoderma, 2) failure to regrow hair after clipping, 3) calcinosis cutis, and 4) adult-onset demodicosis. Hypothyroidism is on the list of differential diagnoses for all of these except calcinosis cutis; frequently patients with hyperadrenocorticism have low serum T4, due to sick euthyroid syndrome. Whenever a patient with borderline T4, alopecia, and relapsing pyoderma fails to respond to thyroid supplement, consider hyperadrenocorticism. This patient did not exhibit polyphagia, polyuria, or polydipsia, nor did she have an elevated alkaline phosphatase concentration, stress leukogram, isosthenuria, or hyposthenuria. Specific adrenal function testing is recommended for any patient with dermatologic signs of hyperadrenocorticism even if classic clinical signs of Cushing’s syndrome are not present. Hypertension and bacteriuria secondary to hyperadrenocorticism would be challenging to manage without treating the primary cause. Gracie responded to treatment with cefovecin (Convenia--Pfizer Animal Health) and trilostane (Vetoryl--Dechra; 2 mg/kg daily). ACTH stimulation was used to monitor adrenal function and make modifications to the trilostane dosage. Ongoing antiseptic shampoo therapy minimized relapses of pyoderma. Gracie's hair returned slowly after six weeks of therapy.
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