Prevalence of Systemic Hypertension and Control of Systolic Blood Pressure in a Cohort of 14 Dogs with Adrenal-Dependent Hypercortisolism during the First Year of Trilostane Treatment or after Adrenalectomy.

Hypercortisolism in dogs is frequently associated with systemic hypertension (SH). However, there are no studies evaluating the changes in systolic blood pressure (SBP) in dogs with adrenal-dependent hypercortisolism (ADH) during trilostane treatment or after adrenalectomy and their response to antihypertensive treatments. For this reason, the objectives of this study were to evaluate the changes in SBP in dogs with ADH during the first year of trilostane treatment or after adrenalectomy, the relation with clinical control of hypercortisolism and certain laboratory parameters, and the response to antihypertensive drugs. Fourteen dogs newly diagnosed with ADH were prospectively included and evaluated at diagnosis (T0) and 1, 3, 6, and 12 months after (T1, T3, T6, and T12, respectively). Dogs were classified as hypertensive (HT; SBP ≥ 160 mmHg) and non-hypertensive. In HT dogs, benazepril was considered as the first-line drug, and, if necessary, amlodipine was prescribed. The prevalence of SH at T0 was 79%, and it was reduced to 25% at T12. Blood pressure (BP) was not associated with disease control or selected laboratory parameters at any endpoint. Only 22% of dogs with SH needed more than one drug to normalize their SBP. In all dogs surgically treated that were HT at T0, BP normalized at T3.

Survival of dogs with pituitary-dependent hyperadrenocorticism treated twice daily with low doses of trilostane.

BACKGROUND: Twice daily low trilostane doses have proven to be effective to manage canine Cushing's syndrome. However, survival and prognostic factors in dogs treated with this protocol have not been evaluated. The aim of the study was to evaluate survival and prognostic factors, including systolic blood pressure (SBP) at diagnosis, in dogs with pituitary-dependent hypercortisolism (PDH) treated with low trilostane doses. METHODS: Medical records of 91 dogs newly diagnosed with PDH initially treated with 0.2-1.1 mg/kg of trilostane twice daily were retrospectively included. Survival times were calculated using the Kaplan-Meier estimator. Univariable and multivariable analysis were performed using the Cox proportional hazard regression analysis. RESULTS: Overall, median survival was 998 days (range 26-1832 days, 95% confidence interval = 755-1241 days). In the multivariable analysis, age (hazard ratio [HR] = 1.337, p < 0.001), presence of calcinosis cutis (HR = 5.271, p < 0.001), body condition score (BCS) ≤3/9 (HR = 8.100, p < 0.001) and higher platelet count (HR = 1.002, p = 0.022) were negatively correlated with survival. SBP was not associated with survival. CONCLUSIONS: Low-dose trilostane treatment twice daily provides slightly longer survival than previously reported for dogs with PDH treated once or twice daily at higher doses. Older age, presence of calcinosis cutis, low BCS and higher platelet count, but not systemic hypertension, are predictive of poorer prognosis in dogs with PDH.

Changes in systolic blood pressure in dogs with pituitary dependent hyperadrenocorticism during the first year of trilostane treatment.

BACKGROUND: Systemic hypertension (SH) is common in dogs and humans with hypercortisolism and can persist after treatment. OBJECTIVES: To evaluate changes in prevalence of SH and systolic blood pressure (SBP) in dogs with pituitary-dependent hyperadrenocorticism (PDH) during the first year of trilostane treatment, its relationship with disease control and selected laboratory variables, and their response to antihypertensive treatment. ANIMALS: Fifty-one dogs with PDH treated with trilostane Q12h. METHODS: Prospective case series study. Dogs were evaluated at diagnosis (T0) and 1, 3, 6, and 12 months (T12). Dogs were classified as nonhypertensive (SBP < 160 mm Hg) or hypertensive (SBP≥160 mm Hg) and subclassified according to target organ damage (TOD) risk. Hypertensive dogs were treated with benazepril and, if control of SH was not achieved, amlodipine was added. RESULTS: Prevalence of SH decreased from T0 (36/51) to T12 (17/37; P = .01). Changes in SBP during the study were influenced by the risk of TOD at T0. In severely hypertensive (SBP ≥ 180 mm Hg) dogs, the decrease in SBP was more pronounced whereas in normotensive (SBP < 140 mm Hg) dogs SBP increased slightly (P = .00). Blood pressure was not associated with disease control. Antihypertensive treatment was needed in 31/51 dogs, and in 13/31 dogs additional SH control with amlodipine was required. One third of nonhypertensive dogs at T0 required treatment with benazepril because SH developed during follow-up. CONCLUSIONS AND CLINICAL IMPORTANCE: In dogs with PDH, SBP should be measured at every visit, regardless of disease control or SBP at diagnosis. More than 1 drug may be necessary to manage SH in affected dogs.

Prevalence and risk factors associated with systemic hypertension in dogs with spontaneous hyperadrenocorticism.

BACKGROUND: Systemic hypertension (SH) is common in dogs with hyperadrenocorticism (HAC) however there are not many studies assessing its prevalence and risk factors. OBJECTIVES: To determine the prevalence and severity of SH in dogs with HAC and its association with clinical and laboratory findings to identify potential risk factors. ANIMALS: Sixty-six client owned dogs with spontaneous HAC. METHODS: Retrospective cross-sectional study. Medical records of dogs with HAC were reviewed. Systolic blood pressure (SBP) was measured using Doppler ultrasonography. Clinical signs, physical examination findings and clinicopathologic data (CBC, serum biochemistry and electrolytes, urinalysis and urinary culture, and adrenal function tests) were reviewed for analysis. RESULTS: Prevalence of SH (≥150 mm Hg) was 82% (54/66) and prevalence of severe SH (≥180 mm Hg) was 46% (30/66). All dogs with thrombocytosis had SH (P = .002), and a platelet count ≥438 × 103 /µL was 100% specific and 61.1% sensitive to predict SH (AUC = .802, P = .001). Median potassium levels were lower in hypertensive dogs (4.1 mEq/L, range 3.1-5.4 mEq/L) than in normotensive ones (4.5 mEq/L, range 4.0-5.0 mEq/L) (P = .007). Dogs with UPC ≥ 0.5 had higher median SBP than those without proteinuria (P = .03). Dogs with concurrent diabetes mellitus seemed to have a reduced risk of SH (OR = .118, 95%CI = .022-.626, P = .02). CONCLUSIONS AND CLINICAL IMPORTANCE: Systemic hypertension is common in dogs with HAC and is frequently severe. Blood pressure should be routinely assessed in these dogs, especially if thrombocytosis, proteinuria or low potassium concentrations are present.

Laboratory assessment of trilostane treatment in dogs with pituitary-dependent hyperadrenocorticism.

BACKGROUND: Results of ACTH stimulation test (ACTHst), pre- and post-trilostane serum cortisol concentrations (SCCs), urine concentration (urine-specific gravity [USG]), and urine cortisol : creatinine ratios (UCCRs) are common variables used to monitor trilostane treatment of dogs with pituitary-dependent hyperadrenocorticism (PDH). However, none has consistently discriminated dogs receiving an adequate dose (A) from those overdosed (O) or underdosed (U). OBJECTIVES: To assess and compare recommended monitoring variables, including serial SCCs in a cohort of dogs with PDH treated with trilostane. ANIMALS: Privately owned dogs with PDH (n = 22) and 3 healthy dogs (controls). METHODS: Prospective, multicenter, 2-day study. On day "a" (randomized): ACTHst was completed. Day "b" (>2 to <7 days later): SCCs were assessed -0.5 hours, immediately before, and 1, 2, 2.5, 3, 3.5, 4, 6, 8, and 12 hours after trilostane administration. On the first study day, urine collected at home was assessed for USG, UCCR and owner opinions regarding PDH were categorized as: A (clinical signs resolved), U (remains symptomatic), or ill (possible O). RESULTS: At 27 pairs of evaluations, 7 dogs were categorized as A, 19 U, and 1 possible O (excluded from the study). There was overlap in SCC results from the A and U dogs at every time point. Results of USG, UCCR, and ACTHst did not discriminate A from U dogs. Trilostane suppresses SCC within 1 hour of administration and its duration of action in most PDH dogs is <8 hours. CONCLUSIONS AND CLINICAL IMPORTANCE: No single variable or group of variables reliably discriminated A dogs from U dogs during trilostane treatment for PDH.