Results suggest that development of nonspecific clinical signs of vomiting, lethargy, and anorexia in conjunction with high serum hepatic enzyme activities and mature neutrophilia in a medium-sized or large-breed dog should increase the index of suspicion for LLT. Abdominal ultrasonography with Doppler assessment may be useful in establishing the diagnosis. The long-term outcome for dogs that survive the hospitalization period is excellent.
Background: Dogs with protein-losing enteropathy (PLE) have previously been reported to present with thromboembolism; however, the prevalence and pathogenesis of hypercoagulability in dogs with PLE have not been investigated so far.Hypothesis: Dogs with PLE are hypercoagulable compared with healthy control dogs. Animals: Fifteen dogs with PLE. Thirty healthy dogs served as controls (HC). Methods: A prospective study was performed including 15 dogs with PLE. All dogs were scored using the canine chronic enteropathy activity index (CCECAI). Thromboelastography (TEG) and other measures of coagulation were evaluated. Recalcified, unactivated TEG was performed and reaction time (R), kinetic time (K), alpha angle (a), and maximum amplitude (M A ) values were recorded. Nine dogs were reassessed after initiation of immunosuppressive treatment.Results: All dogs with PLE in the study were hypercoagulable with decreased R ( [33.5-49]) (all P o .001). Median antithrombin (AT) concentration was borderline low in PLE dogs; however, mean serum albumin concentration was severely decreased (mean 1.67 g/dL AE 5.1, reference range 2.8-3.5 g/dL). Despite a significant improvement in serum albumin and CCECAI, all 9 dogs with PLE were hypercoagulable at re-examination.Conclusions and Clinical Importance: The hypercoagulable state in dogs with PLE cannot be solely attributed to loss of AT. Despite good clinical response to treatment, dogs remained hypercoagulable and could therefore be predisposed to thromboembolic complications.
Sepsis, the systemic inflammatory response to infection, represents the major cause of death in critically ill veterinary patients. Whereas important advances in our understanding of the pathophysiology of this syndrome have been made, much remains to be elucidated. There is general agreement on the key interaction between pathogen‐associated molecular patterns and cells of the innate immune system, and the amplification of the host response generated by pro‐inflammatory cytokines. More recently, the concept of immunoparalysis in sepsis has also been advanced, together with an increasing recognition of the interplay between regulatory T cells and the innate immune response. However, the heterogeneous nature of this syndrome and the difficulty of modeling it in vitro or in vivo has both frustrated the advancement of new therapies and emphasized the continuing importance of patient‐based clinical research in this area of human and veterinary medicine.
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