Canine hyperadrenocorticism associations with signalment, selected comorbidities and mortality within North American veterinary teaching hospitals.

OBJECTIVE: To describe a large population of dogs with a diagnosis of hyperadrenocorticism at the time of death in North American veterinary teaching hospitals, and to identify comorbid conditions associated with hyperadrenocorticism. MATERIALS AND METHODS: Retrospective cohort study of 1519 dogs with hyperadrenocorticism from a population of 70,574 dogs reported to the Veterinary Medical Database. Signalment, presence or absence of hyperadrenocorticism, aetiology of hyperadrenocorticism (if described), frequency of select comorbidities and causes of death were evaluated in dogs with and without hyperadrenocorticism. RESULTS: Hyperadrenocorticism was more frequent in females. Neutering was associated with a minor, but significant, increase in the odds of hyperadrenocorticism. Hyperadrenocorticism was the presumed cause of death of 393 (25∙9%) of affected dogs. When aetiology was specified (527 dogs, corresponding to 34∙7% of the cases), pituitary-dependent hyperadrenocorticism [387 (73∙4%) out of 527 dogs] was more common than functional adrenocortical tumour [136 (25∙8%) out of 527 dogs). Hyperadrenocorticism was over-represented in certain expected (miniature poodle, dachshund) and unexpected (Irish setter, bassett hound) breeds compared with the population at large. Of the select comorbidities investigated, dogs with hyperadrenocorticism were at increased risk for concurrent diabetes mellitus, urinary tract infection, urolithiasis, hypertension, gall bladder mucocoele and thromboembolic disease compared with dogs without hyperadrenocorticism. CLINICAL SIGNIFICANCE: Hyperadrenocorticism is significantly associated with certain comorbid conditions but is not a major cause of mortality in affected dogs. Documented patterns now provide targets for prospective clinical research.

Assessment of coagulation and potential biochemical markers for hypercoagulability in canine hyperadrenocorticism.

BACKGROUND: Anecdotal accounts and limited research suggest that dogs with spontaneous hyperadrenocorticism (HAC) are at risk of developing thromboembolic complications. Detailed description of coagulation status and identification of subsets of dogs at greatest risk would impact therapeutic recommendations for these patients. HYPOTHESIS: A subset of dogs with HAC will have a hypercoagulable tendency as identified by increased procoagulant activity, decreased fibrinolysis, or both. Objective 1: To document the existence of this hypercoagulable tendency in HAC dogs using assays of individual coagulation factors, fibrinolytic activity, and systemic coagulation. Objective 2: To evaluate clinical and biochemical markers in HAC dogs to identify a subset of HAC patients at increased risk of this hypercoagulable tendency. ANIMALS: Seventeen dogs newly diagnosed with HAC. METHODS: Prospective study. Medical history, physical examination findings, routine diagnostic tests, and comprehensive coagulation testing were performed at the time of HAC diagnosis. Coagulation parameters were assessed individually and as panels for each dog. Historical and clinical variables were correlated with coagulation parameters to identify risk factors. RESULTS: The majority (88.2%) of HAC dogs exhibited a hypercoagulable tendency. Abnormalities in 1 coagulation assay did not predict abnormalities in others. Duration of clinical signs of HAC did not predict hypercoagulability. Comorbid conditions or abnormal clinicopathologic parameters that predicted hypercoagulability were not identified. CONCLUSIONS AND CLINICAL IMPORTANCE: Although HAC dogs may demonstrate a hypercoagulable tendency individually and as a group, comorbid conditions or biochemical variables that would predict more severe coagulation abnormalities were not identified.

Generalised peripheral oedema associated with amlodipine therapy in two dogs.

This report details two cases of adverse drug reactions to amlodipine. The first case presented with diffuse peripheral oedema and a history of amlodipine therapy. Haematology, clinical chemistry, endocrine testing, thoracic, abdominal and cardiac imaging revealed no cause for oedema. Amlodipine therapy was discontinued and oedema diminished markedly within 72 hours. The second case presented for bilateral retinal detachments secondary to systemic hypertension. Haematology, clinical chemistry, thoracic and abdominal imaging were unremarkable and amlodipine therapy was begun. Within 72 hours, diffuse peripheral oedema developed that was unresponsive to therapy and the dog was euthanised. Veterinarians should be aware of the potential serious adverse events associated with commonly used drugs; severe, diffuse oedema is a possible adverse drug event in dogs treated with amlodipine.

Treatment of canine idiopathic immune-mediated haemolytic anaemia with mycophenolate mofetil and glucocorticoids: 30 cases (2007 to 2011).

OBJECTIVE: To compare short-term outcome and frequency of adverse events for dogs with idiopathic immune-mediated haemolytic anaemia treated with glucocorticoids and mycophenolate mofetil vs alternate immunosuppressive protocols. METHODS: A retrospective study of medical case records of dogs with immune-mediated haemolytic anaemia was conducted. Data collected included signalment, clinicopathological data, medications administered, duration of hospitalization, short-term survival and adverse events. Variables were compared between dogs treated with glucocorticoids and mycophenolate mofetil (mycophenolate mofetil group) vs dogs treated with other two-drug immunosuppressive protocols (combined group). RESULTS: Sixty-four cases of idiopathic immune-mediated haemolytic anaemia were identified. Two dogs were euthanased without treatment, three received glucocorticoids alone, and seven received two additional drugs. Fifty-two dogs received glucocorticoids and additional immunosuppressive medications: 30 mycophenolate mofetil, 15 cyclosporine, 6 azathioprine and 1 human immunoglobulin. There was no significant difference between the discharge rate, 30-day or 60-day survival rates between the mycophenolate mofetil and the combined groups (Fisher's exact; P=0·272, 0·518, 1·000, respectively). The sole adverse event observed in the mycophenolate mofetil group was diarrhoea (n=5). CLINICAL SIGNIFICANCE: Administration of mycophenolate mofetil appears safe in dogs with idiopathic immune-mediated haemolytic anaemia. The combination of glucocorticoids and mycophenolate mofetil has similar efficacy to alternate immunosuppressive protocols used to treat this disease.

Mortality in north american dogs from 1984 to 2004: an investigation into age-, size-, and breed-related causes of death.

BACKGROUND: Anecdotal beliefs and limited research suggest variable patterns of mortality in age, size, and breed cohorts of dogs. Detailed knowledge of mortality patterns would facilitate development of tailored health-maintenance practices and contribute to the understanding of the genetic basis of disease. HYPOTHESIS/OBJECTIVES: To describe breed-specific causes of death in all instances of canine mortality recorded in the Veterinary Medical Database (VMDB)(a) between 1984 and 2004. We hypothesized that causes of death, categorized by organ system (OS) or pathophysiologic process (PP), would segregate by age, body mass, and breed. ANIMALS: 74,556 dogs from the VMDB for which death was the outcome of the recorded hospital visit. METHODS: Retrospective study. Causes of death from abstracted VMDB medical records were categorized by OS and PP and analyzed by age, breed, and breed-standard mass of dog. RESULTS: Causes of death, categorized by OS or PP, segregated by age, breed, and breed-standard mass. Young dogs died more commonly of gastrointestinal and infectious causes whereas older dogs died of neurologic and neoplastic causes. Increasing age was associated with an increasing risk of death because of cardiovascular, endocrine, and urogenital causes, but not because of hematopoietic or musculoskeletal causes. Dogs of larger breeds died more commonly of musculoskeletal and gastrointestinal causes whereas dogs of smaller breeds died more commonly of endocrine causes. CONCLUSIONS AND CLINICAL IMPORTANCE: Not all causes of death contribute equally to mortality within age, size, or breed cohorts. Documented patterns now provide multiple targets for clinical research and intervention.

Evaluation of plasma time-activity curves of technetium-99m-mebrofenin for measurement of hepatic function in dogs.

In this study, plasma time-activity curves of 99mTc-mebrofenin were used to quantify hepatic function in dogs before and after induction of hepatic damage using a hepatotoxic agent. Nine dogs were determined to be healthy on the basis of physical examination, laboratory data and hepatic imaging. Plasma samples were collected 1, 3, 5, 7, 9, 15, 20, 30, 40, 50, and 60 minutes following a peripheral venous injection of 111-222 MBq (3-6 mCi) of 99mTc-mebrofenin. The area under the plasma time-activity curve (AUC) was calculated using two different methods and compared to direct measurement of the hepatic extraction efficiency. First pass hepatic extraction efficiency of 99mTc-mebrofenin was calculated from differential equation analysis of a two-compartment model following mesenteric venous injection of the radiopharmaceutical. In 7 of the original 9 dogs and 2 additional healthy dogs, plasma clearance and hepatic extraction efficiency determination were repeated following induction of hepatic injury by thiacetarsamide (3 mg/kg IV twice daily for 1 day). In one additional dog, hepatic injury was induced using carbon tetrachloride (0.3 ml/kg IP). Plasma time-activity curves of 99mTc-mebrofenin had kinetics of a two compartment model. Area under the curve was highly correlated with hepatic extraction efficiency. The AUC integrated from 1-60 minutes (AUC60) had the best correlation with hepatic extraction efficiency (r2 = 0.978, p < 0.001). A formula for calculation of hepatic extraction efficiency was derived using linear regression analysis: hepatic extraction efficiency = 105.583 - 3.099 x 10(5) x AUC60. Plasma clearance of a peripheral venous injection of 99mTc-mebrofenin is a simple, non-invasive, convenient method to quantify hepatic function which can be performed without a gamma camera.