Search

Liver disease is frequently cited as a cause of gastroduodenal ulceration (GDU) in dogs but studies regarding GDU and liver disease are limited.To document the presence of GDU in dogs with liver disease.Forty dogs that underwent liver biopsy, computed tomographic (CT) angiography or both at the University of Florida Small Animal Hospital to diagnose congenital or acquired liver disease.Cross-sectional study. Dogs had gastroduodenoscopy performed with photographic and video documentation in a standardized fashion. Lesions (hemorrhage, erosions, ulcers) in the esophagus, stomach, and duodenum were scored based on a grading scale. Presence of esophageal varices was recorded. Dogs were categorized into 4 groups according to cause of liver disease (inflammatory disease, cirrhosis, congenital, other). Presence or absence of ulcers, erosions or both as well as total endoscopic scores were compared among groups.Forty dogs were enrolled with the following distribution: 13 congenital, 13 inflammatory, 3 cirrhosis, and 11 other. Four dogs had GDU (10%; 95% confidence interval [CI], 3%-24%) and 6 dogs had erosions (15%; 95% CI, 6%-30%). No difference was found in total endoscopic score (P = .21) or in the proportion of dogs with ulcers, erosions or both versus those without (P = .25) among the groups.Gastroduodenal ulceration was found in 10% of dogs with liver disease in this population. Additional studies are warranted to confirm these findings in larger numbers of dogs with specific disease etiologies.

Background Concurrent exocrine pancreatic dysfunction and decreased pancreatic organ size are common findings in various stages of human type 1 diabetes mellitus (DM). Exocrine pancreatic insufficiency (EPI) is incompletely described in diabetic dogs. Objective To compare canine trypsin-like immunoreactivity (cTLI) of diabetic dogs with that of healthy controls. A secondary aim was to evaluate the correlation between duration of DM and cTLI. Animals Thirty client-owned diabetic dogs and thirty client-owned control dogs. Methods Cross-sectional study. Diabetic and healthy control dogs were included if they had no clinical evidence of pancreatitis and if serum samples obtained after food was withheld were available. Serum cTLI was measured at a reference laboratory and compared between groups. Canine pancreatic lipase immunoreactivity (cPLI) was analyzed concurrently as an indicator of pancreatitis. Results The median cTLI concentration in all diabetic dogs (36.4 μg/L [range, 7.0-288 μg/L]) did not differ from control dogs (28.7 μg/L [range, 12.8-58.6 μg/L]) (P = .07; difference -7.8 μg/L [95% Confidence Interval (CI), -23.5 to 0.6 μg/L]). There was still no difference in cTLI between groups after exclusion of dogs with cPLI consistent with pancreatitis (n = 8 diabetic dogs). There was no correlation between cTLI and DM duration in all diabetic dogs (r = -0.07, [95% CI, -0.43 to 0.3], P = .7). Conclusions and clinical importance There was no evidence of EPI as evaluated using cTLI in this cohort of diabetic dogs, but concurrent increases in cPLI suggest cTLI might not be the optimal indicator of exocrine pancreatic dysfunction in dogs with DM.

Objectives To quantify anti-insulin antibodies in diabetic dogs treated with recombinant human insulin and to determine if insulin dosage or duration of treatment differed between anti-insulin antibody-positive and -negative diabetic dogs. Materials and methods Descriptive preliminary study using serum from 24 client-owned diabetic dogs treated for a minimum of 2 weeks with recombinant human insulin, and 24 client-owned healthy control dogs without diabetes. Sera were analysed by radioimmunoassay for anti-insulin antibodies. The proportion of antibody positive dogs was compared between groups by Fisher's exact test. Results Four diabetic (16.6%) and no control dogs were anti-insulin antibody positive. Clinical significance These results indicate that treatment with recombinant human insulin may induce anti-insulin antibodies in dogs, although this finding needs to be re-investigated in a larger study to investigate the impact of anti-insulin antibodies on glycaemic control.

Canine diabetes has been considered a potential model of human type 1 diabetes (T1D), however the detection of autoantibodies common in humans with T1D in affected dogs is inconsistent. The aim of this study was to compare autoantibody responses in diabetic and healthy control dogs using a novel nucleic acid programmable protein array (NAPPA) platform. We performed a cross-sectional study of autoantibody profiles of 30 diabetic and 30 healthy control dogs of various breeds. Seventeen hundred human proteins related to the pancreas or diabetes were displayed on NAPPA arrays and interrogated with canine sera. The median normalized intensity (MNI) for each protein was calculated, and results were compared between groups to identify candidate autoantibodies. At a specificity of 90%, six autoantibodies had sensitivity greater than 10% (range 13–20%) for distinguishing diabetic and control groups. A combination of three antibodies (anti-KANK2, anti-GLI1, anti-SUMO2) resulted in a sensitivity of 37% (95% confidence interval (CI) 0.17–0.67%) at 90% specificity and an area under the receiver operating characteristics curve of 0.66 (95% CI 0.52–0.80). While this study does not provide conclusive support for autoimmunity as an underlying cause of diabetes in dogs, future studies should consider the use of canine specific proteins in larger numbers of dogs of breeds at high risk for diabetes.

INTRODUCTION: Dogs with naturally occurring diabetes mellitus represent a potential model for human type 1 diabetes, yet significant knowledge voids exist in terms of the pathogenic mechanisms underlying the canine disorder. Untargeted metabolomic studies from a limited number of diabetic dogs identified similarities to humans with the disease. OBJECTIVE: To expand and validate earlier metabolomic studies, identify metabolites that differ consistently between diabetic and healthy dogs, and address whether certain metabolites might serve as disease biomarkers. METHODS: Untargeted metabolomic analysis via liquid chromatography-mass spectrometry was performed on serum from diabetic (n=15) and control (n=15) dogs. Results were combined with those of our previously published studies using identical methods (12 diabetic and 12 control dogs) to identify metabolites consistently different between the groups in all 54 dogs. Thirty-two candidate biomarkers were quantified using targeted metabolomics. Biomarker concentrations were compared between the groups using multiple linear regression (corrected P

While predominant as a disease entity, knowledge voids exist regarding the pathogenesis of canine diabetes. To test the hypothesis that diabetic dogs have similar metabolomic perturbations to humans with type 1 diabetes (T1D), we analyzed serum metabolomic profiles of breed- and body weight-matched, diabetic (n=6) and healthy (n=6) dogs by liquid chromatography-mass spectrometry (LC-MS) profiling. We report distinct clustering of diabetic and control groups based on heat map analysis of known and unknown metabolites. Random forest classification identified 5/6 dogs per group correctly with overall out of bag error rate=16.7%. Diabetic dogs demonstrated significant upregulation of glycolysis/gluconeogenesis intermediates (e.g., glucose/fructose, C6H12O6, keto-hexose, deoxy-hexose, (PAbbreviationsAA(amino acid)AAb(autoantibody)FA(fatty acid)HILIC(hydrophilic interaction liquid interaction chromatography)LC-MS(liquid chromatography mass spectrometry)OOB(out of bag)T1D(type 1 diabetes)T2D(type 2 diabetes)UF(University of Florida)

Despite decades of research in humans and mouse models of disease, substantial gaps remain in our understanding of pathogenic mechanisms underlying the development of type 1 diabetes. Furthermore, translation of therapies from preclinical efforts capable of delaying or halting β-cell destruction has been limited. Hence, a pressing need exists to identify alternative animal models that reflect human disease. Canine insulin deficiency diabetes is, in some cases, considered to follow autoimmune pathogenesis, similar to NOD mice and humans, characterized by hyperglycemia requiring lifelong exogenous insulin therapy. Also similar to human type 1 diabetes, the canonical canine disorder appears to be increasing in prevalence. Whereas islet architecture in rodents is distinctly different from humans, canine pancreatic endocrine cell distribution is more similar. Differences in breed susceptibility alongside associations with MHC and other canine immune response genes parallel that of different ethnic groups within the human population, a potential benefit over NOD mice. The impact of environment on disease development also favors canine over rodent models. Herein, we consider the potential for canine diabetes to provide valuable insights for human type 1 diabetes in terms of pancreatic histopathology, impairment of β-cell function and mass, islet inflammation (i.e., insulitis), and autoantibodies specific for β-cell antigens.

INTRODUCTION: We recently identified variances in serum metabolomic profiles between fasted diabetic and healthy dogs, some having similarities to those identified in human type 1 diabetes. OBJECTIVES: Compare untargeted metabolomic profiles in the non-fasted state. METHODS: Serum from non-fasted diabetic (n=6) and healthy control (n=6) dogs were analyzed by liquid chromatography-high resolution mass spectrometry. RESULTS: Clear clustering of metabolites between groups were observed, with multiple perturbations identified that were similar to those previously observed in fasted diabetic dogs. CONCLUSION: These findings further support the development of targeted assays capable of detecting metabolites that may be useful as biomarkers of canine diabetes.

Objective—To determine the effects of oral prednisone administration with or without ultralow-dose acetylsalicylic acid on coagulation parameters in healthy dogs and to assess intraindividual variation in thromboelastography results. Animals—14 healthy research dogs and 10 healthy client-owned dogs. Procedures—In a randomized controlled trial, research dogs underwent thromboelastography twice (3 days apart), and intraindividual variation in test results was calculated. Dogs were given prednisone (2 mg/kg/d, PO) plus acetylsalicylic acid (0.5 mg/kg/d, PO) or prednisone (2 mg/kg/d, PO) plus a placebo for 14 days, after which thromboelastography and other tests were repeated. Differences from preadministration (baseline) test results between and within groups were compared. In a separate trial, client-owned dogs also underwent thromboelastography twice 2 days apart to assess intraindividual variation in untreated dogs. Results—Intraindividual variation in thromboelastography results for research dogs was ≤ 10% for maximum amplitude (MA) and α angle. In the research dogs, MA and fibrinogen values significantly increased from baseline, whereas percentage lysis 30 minutes after attainment of the MA as well as antithrombin activity significantly decreased within each group. In the dogs that received prednisone plus a placebo, percentage lysis 60 minutes after attainment of the MA was significantly lower than at baseline. For all parameters for research dogs, there was no difference between groups for change from baseline. Intraindividual variation in findings for client-owned dogs was similar to the variation for research dogs. Conclusions and Clinical Relevance—Prednisone administration resulted in hypercoagulability in healthy dogs as indicated by an increase in MA and plasma fibrinogen concentration and a decrease in antithrombin activity. Concurrent ultralow-dose acetylsalicylic acid use had no effect on measured thromboelastography values. The high intraindividual variation in some thromboelastography parameters may preclude routine use of this technique in clinical practice.

A 3-year-old Labrador retriever was presented to the Western College of Veterinary Medicine for a tibial plateau levelling osteotomy. While performing a pre-operative epidural, thiopental was inadvertently administered into the epidural space. Treatment included epidural saline flushing and intravenous methylprednisolone sodium succinate. No neurologic deficits were detected.

BACKGROUND: Sterile nodular panniculitis (SNP) is an uncommon inflammatory condition of subcutaneous fat that can be idiopathic, but has also been associated with underlying conditions such as pancreatic disease or systemic lupus erythematosus (SLE). The pathogenesis and clinical course of the condition are not well understood. OBJECTIVES: To retrospectively review cases of SNP associated with systemic signs, concurrent disease, or both and characterize the clinical, laboratory, imaging, and histopathologic findings, treatment, and response to treatment. ANIMALS: Fourteen dogs with histologically confirmed SNP diagnosed between 1996 and 2008. METHODS: Retrospective study. RESULTS: Skin lesions were ulcerated or draining nodules in 9 dogs and nonulcerative subcutaneous nodules in 5. Most dogs had systemic signs, such as fever, inappetence, lethargy, and multiple lesions. Common clinicopathologic findings included neutrophilia with or without left shift, increased alkaline phosphatase activity, mild hypoglycemia, hypoalbuminemia, and proteinuria. Concurrent diseases included pancreatic disease, SLE, rheumatoid arthritis, polyarthritis, lymphoplasmacytic colitis, and hepatic disease. Dogs responded to immunosuppressive doses of corticosteroids when administered. Prognosis for recovery was related to the underlying disease process. CONCLUSIONS AND CLINICAL IMPORTANCE: SNP is not a single disease. Rather, it is a cutaneous marker of systemic disease in many cases. After thorough evaluation for concurrent disease and infectious causes, immunosuppressive treatment is often effective.