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Hypertension - a common but underdiagnosed complication in Cushing´s patients
Canine hyperadrenocorticism (HAC) is a common systemic disease seen most frequently in middle aged to older dogs. The reported prevalence of hypertension in spontaneously occurring canine HAC is 86 percent, and this is associated with life threatening complications such as cardiovascular abnormalities. Controls are strongly recommended!

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.

Recently, as more attention has been given to blood pressure measurement in dogs, a new and potentially serious sequela to HAC has been identified: hypertension, which in many instances persists after appropriate therapy. . (Ortega et al. JAVMA 1996; 209:1724-1729). Forty percent of these dogs remained hypertensive after adequate control of the disease. Hypertension is associated with life threatening complications such as cardiovascular abnormalities, retinal hemorrhage and detachment, and glomerulopathies in both human and canine patients. For these reasons, early recognition is necessary to prevent these potentially disastrous consequences.

The exact mechanism for development of hypertension in canine HAC remains to be elucidated. Proposed mechanisms include activation of the renin-angiotensin system, enhanced vascular sensitivity to endogenous vasopressors, glucocorticoids acting as mineralocorticoids, and reduced activity of the depressor systems. Human studies support increased sensitivity to endogenous vasopressors as the major cause for glucocorticoid-induced hypertension.

Recognition of the high prevalence of hypertension in cases of canine HAC has led to increased research in the area. In a recent study, vascular responsiveness to increasing dose rates of norepinephrine was assessed in dogs with HAC induced by administration of hydrocortisone. (Martínez et al., Proceedings of the 20th ACVIM abstract #131). It was found that although there were no significant differences in baseline blood pressures between control dogs and dogs with iatrogenic HAC, dogs in the iatrogenic HAC group appeared more sensitive to the increasing dose rates of norepinephrine. Severe hypertension (systolic blood pressure >240 mmHg) was noted on seven of the eight dogs with iatrogenic HAC and only in one control dog. Systolic blood pressure and heart rate were significantly higher in dogs with 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 dogs with 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 dependent hyperadrenocorticism before and after treatment with mitotane. Nine of 13 dogs (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 stimulation when compared to normal dogs. No significant difference was found in plasma potassium concentrations between affected and control dogs. These results are in concordance with results of a previous study in which aldosterone levels were not found to be elevated in dogs with HAC (Golden et al. JVIM 1988; 2:121-125) but opposite to the findings of another study in which aldosterone levels were found to be significantly greater than normal in dogs with untreated pituitary-dependent HAC. (Ortega et al. Proceedings of the 13th ACVIM abstract #10). More studies are needed to determine the mechanism for cortisol-induced hypertension in canine HAC.

Regardless of the cause, the high prevalence of hypertension in canine HAC makes accurate measurement of arterial blood pressure in affected dogs an essential part of the initial work-up and follow-up if we want to prevent the potentially severe complications of hypertension. Although measurement of direct arterial blood pressure is considered the gold standard for blood pressure measurement, a recent study showed that noninvasive blood pressure methods such as oscillometric and Doppler techniques give results that are comparable to those obtained by the direct arterial puncture technique and provided a cut off value of systolic arterial blood pressure above 160 mmHg for 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 measurement but with a combination of a detailed history and physical examination findings, including fundic examination before deciding if initiation of therapy is indicated.

Source: Nivia I. Martínez (2003): Hypertension in canine hyperadrenocorticism more common than previously thought. In: DVM Newsmagazine April 1, 2003. www.dvmnewsmagazine.com/dvm/






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