Canine hyperadrenocorticism (HAC) is a common condition seen most frequently in middle aged to older dogs. The clinical signs and physical examination findings characteristic for the condition include polyuria, polydipsia, polyphagia, abdominal distension, hepatomegaly and dermatologic changes such as bilaterally symmetrical alopecia. Affected dogs are prone to develop complications from the hypercortisolemia such as pyoderma, urinary tract infections, diabetes mellitus, proteinuric renal disease, and pulmonary thromboembolism.
Editor's Note: In a continuing series of articles, DVM Newsmagazine has teamed up with the American College of Veterinary Internal Medicine, (ACVIM) to bring you the latest in research abstracts on a variety of topics. Every month, an ACVIM diplomate will summarize, in abstract form, the latest research in specialty fields. These articles are coordinated with the help of Dr. Ron Lyman, Ft. Pierce, Fla.
Canine hyperadrenocorticism (HAC) is a common condition seen most frequentlyin middle aged to older dogs. The clinical signs and physical examinationfindings characteristic for the condition include polyuria, polydipsia,polyphagia, abdominal distension, hepatomegaly and dermatologic changessuch as bilaterally symmetrical alopecia. Affected dogs are prone to developcomplications from the hypercortisolemia such as pyoderma, urinary tractinfections, diabetes mellitus, proteinuric renal disease, and pulmonarythromboembolism.
Recently, as more attention has been given to blood pressure measurementin dogs, a new and potentially serious sequela to HAC has been identified:hypertension, which in many instances persists after appropriate therapy.The reported prevalence of hypertension in spontaneously occurring canineHAC is 86 percent. (Ortega et al. JAVMA 1996; 209:1724-1729). Forty percentof these dogs remained hypertensive after adequate control of the disease.Hypertension is associated with life threatening complications such as cardiovascularabnormalities, retinal hemorrhage and detachment, and glomerulopathies inboth human and canine patients. For these reasons, early recognition isnecessary to prevent these potentially disastrous consequences.
The exact mechanism for development of hypertension in canine HAC remainsto be elucidated. Proposed mechanisms include activation of the renin-angiotensinsystem, enhanced vascular sensitivity to endogenous vasopressors, glucocorticoidsacting as mineralocorticoids, and reduced activity of the depressor systems.Human studies support increased sensitivity to endogenous vasopressors asthe major cause for glucocorticoid-induced hypertension.
Recognition of the high prevalence of hypertension in cases of canineHAC has led to increased research in the area. In a recent study, vascularresponsiveness to increasing dose rates of norepinephrine was assessed indogs with HAC induced by administration of hydrocortisone. (Martínezet al., Proceedings of the 20th ACVIM abstract #131). It was found thatalthough there were no significant differences in baseline blood pressuresbetween control dogs and dogs with iatrogenic HAC, dogs in the iatrogenicHAC group appeared more sensitive to the increasing dose rates of norepinephrine.Severe hypertension (systolic blood pressure >240 mmHg) was noted onseven of the eight dogs with iatrogenic HAC and only in one control dog.Systolic blood pressure and heart rate were significantly higher in dogswith iatrogenic HAC than control dogs at low dose rates of norepinephrine.These results were in agreement with studies in human HAC. In another study,the role of aldosterone as a cause for hypertension was evaluated in dogswith pituitary-dependent HAC. (Goy-Thollot et al., JSAP 2002;43:489-492).In this study, cortisol, aldosterone, plasma sodium and potassium concentrations,and systolic blood pressure were evaluated in dogs with pituitary dependenthyperadrenocorticism before and after treatment with mitotane. Nine of 13dogs (69 percent) had a systolic arterial blood pressure above 200 mmHg.Mitotane treatment did not appear to modify systolic arterial blood pressure.Aldosterone levels were lower in affected dogs both pre and post ACTH stimulationwhen compared to normal dogs. No significant difference was found in plasmapotassium concentrations between affected and control dogs. These resultsare in concordance with results of a previous study in which aldosteronelevels were not found to be elevated in dogs with HAC (Golden et al. JVIM1988; 2:121-125) but opposite to the findings of another study in whichaldosterone levels were found to be significantly greater than normal indogs with untreated pituitary-dependent HAC. (Ortega et al. Proceedingsof the 13th ACVIM abstract #10). More studies are needed to determine themechanism for cortisol-induced hypertension in canine HAC.
Regardless of the cause, the high prevalence of hypertension in canineHAC makes accurate measurement of arterial blood pressure in affected dogsan essential part of the initial work-up and follow-up if we want to preventthe potentially severe complications of hypertension. Although measurementof direct arterial blood pressure is considered the gold standard for bloodpressure measurement, a recent study showed that noninvasive blood pressuremethods such as oscillometric and Doppler techniques give results that arecomparable to those obtained by the direct arterial puncture technique andprovided a cut off value of systolic arterial blood pressure above 160 mmHgfor the diagnosis of canine hypertension. (Stepien et al. JVIM 2003; 17:65-72).A final diagnosis of hypertension should not be made based on a single measurementbut with a combination of a detailed history and physical examination findings,including fundic examination before deciding if initiation of therapy isindicated.