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Keywords:

  • Anemia;
  • Antiphospholipid syndrome;
  • Beta-2 glycoprotein 1;
  • Lupus anticoagulant;
  • Thromboembolism

Background

The pathophysiology of thrombus formation in canine IMHA and other diseases remains unclear. Antiphospholipid antibodies (aPL) are an important cause of thrombosis in humans and might cause thrombosis in dogs.

Hypothesis

Dogs with IMHA, spontaneous thrombosis, and hyperadrenocorticism will have increased levels of aPL and lupus anticoagulants (LA), compared with healthy and sick dogs.

Animals

Thre aPL were measured in healthy controls (n = 40–45); sick dogs without thrombosis (n = 86); IMHA (n = 37); spontaneous thrombosis (ST, n = 11); and hyperadrenocorticism (n = 17). Four groups of dogs were also tested for the presence of LA: healthy controls (n = 40); sick dogs without thrombosis (n = 13); IMHA (n = 13); and ST (n = 5).

Methods

Prospective cohort study. Dogs were tested for aPL by an ELISA and for LA by the dilute Russell's Viper venom time (dRVVT). Median values were compared by Kruskal–Wallis (aPL) or ANOVA (LA), and an odds ratio for development of thrombosis in dogs positive for aPL was calculated.

Results

aPL are uncommon in healthy dogs. A total of 13/86 sick dogs without thrombosis, 7/37 dogs with IMHA, 1/11 dogs with ST, and 3/17 dogs with HAC were positive for protein binding-dependent aPL. There was no significant difference in the number of dogs positive for aPL for any of the study groups, and there was no increased risk for thrombosis in dogs positive for aPL. No dogs had LA.

Conclusions

Our preliminary research does not support a strong role for aPL for the development of thrombosis in dogs with IMHA and other thombotic diseases, although future studies are warranted.