Background: Chronic enteropathies (CE) predispose dogs to thromboembolic disease, but the underlying mechanisms are poorly understood. Humans with CE have decreased activity of a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13), a von Willebrand factor (vWF) cleaving enzyme, and increased circulating vWF. The primary aim of this study is to assess plasma ADAMTS13 activity, vWF antigen (vWF:Ag) concentration, and vWF collagen binding activity (vWF:CBA) in dogs with CE.
Hypotheses: Dogs with CE have reduced plasma ADAMTS13 activity, increased vWF:Ag, and increased vWF:CBA compared to healthy control dogs.
Animals: Twenty privately-owned dogs with CE and 40 healthy dogs were recruited from a specialty hospital population.
Methods: Prospective observational study. Dogs were confirmed to have CE using histopathology. ADAMTS13 activity was measured using a commercially available ELISA kit (DiapharmaⓇ) in 20 dogs with CE and 40 healthy control dogs. Plasma vWF:Ag was assessed in 20 dogs with CE and 20 healthy control dogs. Plasma vWF:CBA was assessed in 19 dogs with CE and 20 healthy control dogs. For statistical analysis, an unpaired t-test was used for normally distributed data and Wilcoxon rank sum was used for non-Gaussian distribution. Significance was set at P < 0.05.
Results: Plasma ADAMTS13 activity and vWF:Ag were not significantly different compared to healthy dogs (P = 0.07, P = 0.16, respectively). Plasma vWF:CBA was significantly decreased compared to healthy dogs (P = 0.007).
Conclusions and clinical relevance: Plasma ADAMTS13 activity was not significantly different in dogs with CE compared to healthy dogs and is unlikely to be the primary mechanism for hypercoagulability associated with CE. Forty-three percent of CE dogs with hypoalbuminemia had ADAMTS13 activity below reference interval. Further studies are warranted to evaluate ADAMTS13 activity in a subset of dogs with CE, including those with protein losing enteropathy and thromboembolism. / Master of Science / Background: Dogs with chronic gastrointestinal disease, or chronic enteropathies (CE), often have abnormal blood clotting which predisposes to thrombosis. The mechanisms leading to this abnormal blood clotting are poorly understood. Humans with CE also suffer from abnormal blood clotting and thrombosis. Decreased activity of a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13), a von Willebrand factor (vWF) cleaving enzyme, and increased circulating vWF have been reported as contributors to this abnormal blood clotting in people. Von Willebrand factor is a protein that allows platelets to stick together and adhere to damaged tissue to facilitate blood clot formation. The concentration of vWF can be measured using vWF antigen (vWF:Ag) and the activity of vWF can be measured using vWF collagen binding activity (vWF:CBA).
Hypothesis: Dogs with CE have reduced plasma ADAMTS13 activity, increased vWF:Ag, and increased vWF:CBA compared to healthy control dogs.
Animals: Twenty privately-owned dogs with CE and 40 healthy dogs were recruited from a hospital population.
Methods: Prospective observational study. Plasma ADAMTS13 activity, vWF:Ag and vWF:CBA were assessed in dogs with CE and compared to healthy control dogs.
Results: There was no difference in plasma ADAMTS13 activity and vWF:Ag between the two groups. The mean vWF:CBA was significantly lower in CE dogs compared to healthy dogs.
Conclusions and clinical relevance: Reduced ADAMTS13 activity is unlikely to be the primary mechanism for abnormal blood clotting in dogs with CE.
| Identifer | oai:union.ndltd.org:VTETD/oai:vtechworks.lib.vt.edu:10919/116196 |
| Date | 01 September 2023 |
| Creators | Barth, Samantha Irene |
| Contributors | Biomedical and Veterinary Sciences, Wilkinson, Ashley, Demonaco, Stefanie, Boes, Katie Mae, Conner, Bobbi Jo |
| Publisher | Virginia Tech |
| Source Sets | Virginia Tech Theses and Dissertation |
| Language | English |
| Detected Language | English |
| Type | Thesis |
| Format | ETD, application/pdf |
| Rights | Creative Commons Attribution 4.0 International, http://creativecommons.org/licenses/by/4.0/ |
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