Platelet function in dogs with congenital portosystemic shunt

Kalbantner, Kerstin; Meyer‐Lindenberg, Andrea; Mischke, R.

doi:10.1016/j.tvjl.2010.04.002

Cited by 8 publications

(10 citation statements)

References 19 publications

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“…Our studies and those of others have shown prolonged PT and aPTT and mild to moderate decreases in platelet count in dogs with CPSS . Furthermore, some studies show mild decreases in platelet aggregability and decreases in the concentrations of factors II, V, VII, and X . Despite the presence of these abnormalities traditionally associated with hypocoagulablity, TEG analysis suggests that concurrent procoagulant alterations (decreases in AT and PC activities and increases in factor VIII activity) may have a greater impact on global coagulation status in dogs with CPSS.…”

Section: Discussionsupporting

confidence: 58%

“…Although it is not clear how platelet counts within the reference range might contribute to hypercoagulability, the association could be explained by the presence of platelet hyperreactivity. We did not investigate platelet function in this study, but a single previous study has shown a tendency toward hypoaggregability in dogs with CPSS . We also were able to show a weak but statistically significant association of G value with serum fibrinogen concentration.…”

Section: Discussionmentioning

confidence: 57%

See 1 more Smart Citation

Thromboelastographic Evaluation of Dogs with Congenital Portosystemic Shunts

Kelley

Lester

deLaforcade

et al. 2013

Veterinary Internal Medicne

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Background: On plasma-based assays, dogs with congenital portosystemic shunts (CPSS) have changes in serum concentrations of both pro-and anticoagulant proteins, but how these abnormalities affect whole blood coagulation assays (eg, thromboelastography) are unknown.Objectives: To conduct kaolin-activated thromboelastography (TEG) analysis in dogs with CPSS and to compare TEG coagulation status with clinical presentation, routine serum biochemistry, and plasma-based coagulation tests.Animals: Twenty-one client-owned dogs with CPSS confirmed by ultrasound examination or nuclear scintigraphy. Methods: In a prospective study, signalment, clinical presentation, TEG analysis, CBC, serum biochemistry, and hemostatic tests (platelet count, prothrombin time [PT], activated partial thromboplastin time [aPTT], quantitative fibrinogen, antithrombin [AT] activity, protein C [PC] activity, d-dimers, and factor VIII activity) were analyzed in dogs with CPSS.Results: Dogs with CPSS had significantly shorter K values and increased angle, maximum amplitude (MA), and G values compared with the reference population. On plasma-based coagulation testing, dogs with CPSS had significantly prolonged PT, lower platelet counts, lower AT and PC activities, and increased d-dimers and factor VIII activity. Evaluation of G value defined 9/21 dogs with CPSS as hypercoagulable. These dogs were more likely to have hepatic encephalopathy (HE) than CPSS dogs that had normal coagulation.Conclusions and Clinical Importance: TEG analysis detected hemostatic abnormalities consistent with a hypercoagulable state in some dogs with CPSS. The presence of a hypercoagulable state was 40 times more likely in dogs with symptomatic HE.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 57%

Thromboelastographic Evaluation of Dogs with Congenital Portosystemic Shunts

Kelley

Lester

deLaforcade

et al. 2013

Veterinary Internal Medicne

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“…Unfortunately the reason for this elevation remains unclear . Kalbantner et al recently highlighted the absence of severe primary hemostasis disorder and concluded that decreased platelet count may result from consumptive coagulopathy.…”

Section: Discussionmentioning

confidence: 99%

Comparative outcomes between ameroid ring constrictor and cellophane banding for treatment of single congenital extrahepatic portosystemic shunts in 49 dogs (1998‐2012)

et al. 2017

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“…Recently, platelet function was assessed in dogs with CPSS and while no abnormalities were detected in bleeding time and platelet response to ADP, platelet aggregation in response to collagen and arachidonic acid was moderately impaired. Proposed mechanisms for platelet hypoaggregability in hepatobiliary disease include changes in platelet plasma membrane lipid composition that impair transmembrane signaling or decrease thromboxane synthesis, storage pool defects of ATP and serotonin, and the presence of circulating inhibitors, such as bile acid and FDPs . Additional studies are necessary to evaluate the presence and significance of platelet function defects in veterinary patients with hepatobiliary disease.…”

Section: Coagulation Abnormalities In Hepatobiliary Diseasementioning

confidence: 99%