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Prevalence of reduced fibrinogen binding to platelets in a population of Thoroughbreds

Jeffrey W. NorrisDepartments of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California, Davis, CA 95616

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Suzanne M. PrattDepartment of Veterinary Pathobiology, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907

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Jessica F. HunterDepartments of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California, Davis, CA 95616

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Ian A. GardnerDepartments of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616

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Fern TablinDepartments of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California, Davis, CA 95616

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Abstract

Objective—To measure the frequency and magnitude of reduced fibrinogen binding in a population of horses from a Thoroughbred breeding farm.

Animals—444 Thoroughbred horses, 1 to 27 years old, including 316 females, 72 geldings, and 56 sexually intact males.

Procedures—Blood was collected from horses into tubes containingacid citrate dextrose adenine, and washed platelets were examined by use of flow cytometry for their ability to bind fibrinogen.

Results—Data regarding fibrinogen binding to activated platelets were normally distributed, with nearly identical amounts of variation regardless of sex. In 3 horses, fibrinogen binding to platelets was reduced from 67.6% to 83.4%, compared with normal platelets, which indicated an inability of platelets to aggregate in response to thrombin (0.1 U/mL).

Conclusions and Clinical Relevance—Platelet fibrinogen binding of the affected horses identified in this study was characteristic of a reported heritable bleeding disorder in which the reduction in fibrinogen binding correlated with prolonged bleeding times in template bleeding assays. The bleeding disorder is distinct from Glanzmann thrombasthenia, in which platelets fail to bind fibrinogen because of lack of αllb-β3 integrin on their surface. The prevalence of affected horses within the small sample population studied here (0.7% [n = 3]) is considerably higher than the prevalence of bleeding disorders within more genetically diverse groups.

Abstract

Objective—To measure the frequency and magnitude of reduced fibrinogen binding in a population of horses from a Thoroughbred breeding farm.

Animals—444 Thoroughbred horses, 1 to 27 years old, including 316 females, 72 geldings, and 56 sexually intact males.

Procedures—Blood was collected from horses into tubes containingacid citrate dextrose adenine, and washed platelets were examined by use of flow cytometry for their ability to bind fibrinogen.

Results—Data regarding fibrinogen binding to activated platelets were normally distributed, with nearly identical amounts of variation regardless of sex. In 3 horses, fibrinogen binding to platelets was reduced from 67.6% to 83.4%, compared with normal platelets, which indicated an inability of platelets to aggregate in response to thrombin (0.1 U/mL).

Conclusions and Clinical Relevance—Platelet fibrinogen binding of the affected horses identified in this study was characteristic of a reported heritable bleeding disorder in which the reduction in fibrinogen binding correlated with prolonged bleeding times in template bleeding assays. The bleeding disorder is distinct from Glanzmann thrombasthenia, in which platelets fail to bind fibrinogen because of lack of αllb-β3 integrin on their surface. The prevalence of affected horses within the small sample population studied here (0.7% [n = 3]) is considerably higher than the prevalence of bleeding disorders within more genetically diverse groups.

Contributor Notes

Supported by the Oak Tree Racing Association, the State of California Pari-Mutuel Fund, and contributions by private donors (Center for Equine Health, University of California, Davis).

Address correspondence to Dr. Norris.