ABSTRACT
BACKGROUND: Spontaneous hyperadrenocorticism (HAC) is rare in cats. Clinical findings, diagnostic test results, and response to various treatment options must be better characterized. OBJECTIVES: To report the clinical presentation, clinicopathologic findings, diagnostic imaging results, and response to treatment of cats with HAC. ANIMALS: Cats with spontaneous HAC. METHODS: Retrospective descriptive case series. RESULTS: Thirty cats (15 neutered males, 15 spayed females; age, 4.0-17.6 years [median, 13.0 years]) were identified from 10 veterinary referral institutions. The most common reason for referral was unregulated diabetes mellitus; dermatologic abnormalities were the most frequent physical examination finding. Low-dose dexamethasone suppression test results were consistent with HAC in 27 of 28 cats (96%), whereas ACTH stimulation testing was suggestive of HAC in only 9 of 16 cats (56%). Ultrasonographic appearance of the adrenal glands was consistent with the final clinical diagnosis of PDH or ADH in 28 of 30 cats (93%). Of the 17 cats available for follow-up at least 1 month beyond initial diagnosis of HAC, improved quality of life was reported most commonly in cats with PDH treated with trilostane. CONCLUSIONS AND CLINICAL IMPORTANCE: Dermatologic abnormalities or unregulated diabetes mellitus are the most likely reasons for initial referral of cats with HAC. The dexamethasone suppression test is recommended over ACTH stimulation for initial screening of cats with suspected HAC. Diagnostic imaging of the adrenal glands may allow rapid and accurate differentiation of PDH from ADH in cats with confirmed disease, but additional prospective studies are needed.
Subject(s)
Adrenocortical Hyperfunction/veterinary , Cat Diseases/diagnosis , Adrenocortical Hyperfunction/diagnosis , Adrenocortical Hyperfunction/drug therapy , Adrenocortical Hyperfunction/pathology , Adrenocortical Hyperfunction/physiopathology , Animals , Cat Diseases/drug therapy , Cat Diseases/pathology , Cat Diseases/physiopathology , Cats , Dihydrotestosterone/analogs & derivatives , Dihydrotestosterone/therapeutic use , Female , Male , Retrospective Studies , Treatment OutcomeABSTRACT
Hypoadrenocorticism or Addison's disease (AD) is a functional disorder in which insufficient mineralocorticoid and glucocorticoid hormones are produced by the adrenal cortex. Human AD is usually attributed to lymphoplasmacytic adrenalitis with autoimmune destruction of the adrenal cortex. Lymphoplasmacytic adrenalitis is also reported in some descriptions of canine AD; however, the histological aspects of adrenalitis or adrenocortical atrophy have not been well characterized because microscopical examination is not required for diagnosis of AD. In this study, sections of adrenal glands from 33 dogs with adrenalitis were compared with those of 37 dogs without adrenal lesions. The affected dogs were classified clinically as having AD (n = 3), being suspected of having AD (n = 17), not having AD (n = 11) or were unclassified (n = 2). The adrenal inflammation was lymphoplasmacytic in 17 dogs, lymphocytic in four, lymphohistiocytic in one, granulomatous in three and neutrophilic in eight cases. Adrenal glands from control dogs lacked leucocyte infiltration and had a cortical to medullary area ratio of 1.1-7.2. All three dogs with AD, 8/17 dogs with suspected AD and 1/11 dogs without AD had a cortical to medullary area ratio <1.1. Because the area ratio was correlated (r = 0.94) with a linear cortical to medullary thickness ratio, a thickness ratio <1.1 could also indicate severe adrenocortical atrophy. Severe adrenocortical atrophy was associated typically with lymphoplasmacytic infiltration and nearly complete loss of cortical cells; however, the zona glomerulosa was partially spared in three dogs with lymphoplasmacytic adrenalitis and severe cortical atrophy. In contrast, non-lymphoid inflammation was generally part of systemic disease, multifocal and was unaccompanied by severe adrenocortical atrophy.
