Characterization of thrombelastography over time in dogs with hyperadrenocorticism

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Canine hyperadrenocorticism (HAC) is a common endocrinopathy often associated with hypercoagulability, thrombosis and thromboembolism and it can contribute to increased morbidity and mortality. The condition results in increased, unregulated secretion of glucocorticoids (GCs). While prospective identification of hypercoagulability is challenging, thrombelastography (TEG) is a diagnostic tool that enables the detection of hypercoagulability in a clinical setting. The objective of this prospective cohort study was to serially assess coagulation in dogs with HAC using TEG to test the hypothesis that dogs with HAC have increased TEG maximal amplitude (MA) and that the MA would normalize once clinical control was achieved. Twenty-three dogs with naturally occurring HAC were enrolled and hemostatic (including TEG, platelet function, thrombin-antithrombin complexes and coagulation panel) and hematological variables were measured at presentation. TEG was serially monitored until clinical resolution of HAC was attained.At presentation, most dogs with HAC had increased MA values, increased thrombin-antithrombin complexes and many were hyperfibrinogenemic. Platelet function analyzer-100 (PFA-100) closure times were significantly prolonged. TEG tracings did not normalize in either medically- or surgically-managed dogs, but fibrinogen concentrations decreased. It seems that dogs with HAC have a complex coagulopathy in which hypercoagulability and platelet hyporeactivity or dysfunction might occur simultaneously. As TEG tracings did not normalize in well-controlled dogs, it is unlikely that increased blood GCs are solely responsible for TEG alterations seen in dogs with HAC.

Original languageEnglish (US)
Pages (from-to)675-681
Number of pages7
JournalVeterinary Journal
Volume197
Issue number3
DOIs
StatePublished - Sep 2013

Fingerprint

Adrenocortical Hyperfunction
Thrombelastography
hyperadrenocorticism
Dogs
Thrombophilia
dogs
Blood Platelets
thrombin
Glucocorticoids
glucocorticoids
coagulation
Thromboembolism
Hemostatics
thrombosis
fibrinogen
Fibrinogen
cohort studies
Canidae
Thrombosis
Cohort Studies

Keywords

  • Canine
  • Coagulation
  • Hyperadrenocorticism
  • Thrombelastography
  • Thrombosis

ASJC Scopus subject areas

  • Animal Science and Zoology
  • veterinary(all)

Cite this

Characterization of thrombelastography over time in dogs with hyperadrenocorticism. / Kol, Amir; Nelson, Richard W; Gosselin, R. C.; Borjesson, Dori L.

In: Veterinary Journal, Vol. 197, No. 3, 09.2013, p. 675-681.

Research output: Contribution to journalArticle

@article{f9cc8496a2474c0e9626156327bbcd58,
title = "Characterization of thrombelastography over time in dogs with hyperadrenocorticism",
abstract = "Canine hyperadrenocorticism (HAC) is a common endocrinopathy often associated with hypercoagulability, thrombosis and thromboembolism and it can contribute to increased morbidity and mortality. The condition results in increased, unregulated secretion of glucocorticoids (GCs). While prospective identification of hypercoagulability is challenging, thrombelastography (TEG) is a diagnostic tool that enables the detection of hypercoagulability in a clinical setting. The objective of this prospective cohort study was to serially assess coagulation in dogs with HAC using TEG to test the hypothesis that dogs with HAC have increased TEG maximal amplitude (MA) and that the MA would normalize once clinical control was achieved. Twenty-three dogs with naturally occurring HAC were enrolled and hemostatic (including TEG, platelet function, thrombin-antithrombin complexes and coagulation panel) and hematological variables were measured at presentation. TEG was serially monitored until clinical resolution of HAC was attained.At presentation, most dogs with HAC had increased MA values, increased thrombin-antithrombin complexes and many were hyperfibrinogenemic. Platelet function analyzer-100 (PFA-100) closure times were significantly prolonged. TEG tracings did not normalize in either medically- or surgically-managed dogs, but fibrinogen concentrations decreased. It seems that dogs with HAC have a complex coagulopathy in which hypercoagulability and platelet hyporeactivity or dysfunction might occur simultaneously. As TEG tracings did not normalize in well-controlled dogs, it is unlikely that increased blood GCs are solely responsible for TEG alterations seen in dogs with HAC.",
keywords = "Canine, Coagulation, Hyperadrenocorticism, Thrombelastography, Thrombosis",
author = "Amir Kol and Nelson, {Richard W} and Gosselin, {R. C.} and Borjesson, {Dori L}",
year = "2013",
month = "9",
doi = "10.1016/j.tvjl.2013.05.047",
language = "English (US)",
volume = "197",
pages = "675--681",
journal = "Veterinary Journal",
issn = "1090-0233",
publisher = "Bailliere Tindall Ltd",
number = "3",

}

TY - JOUR

T1 - Characterization of thrombelastography over time in dogs with hyperadrenocorticism

AU - Kol, Amir

AU - Nelson, Richard W

AU - Gosselin, R. C.

AU - Borjesson, Dori L

PY - 2013/9

Y1 - 2013/9

N2 - Canine hyperadrenocorticism (HAC) is a common endocrinopathy often associated with hypercoagulability, thrombosis and thromboembolism and it can contribute to increased morbidity and mortality. The condition results in increased, unregulated secretion of glucocorticoids (GCs). While prospective identification of hypercoagulability is challenging, thrombelastography (TEG) is a diagnostic tool that enables the detection of hypercoagulability in a clinical setting. The objective of this prospective cohort study was to serially assess coagulation in dogs with HAC using TEG to test the hypothesis that dogs with HAC have increased TEG maximal amplitude (MA) and that the MA would normalize once clinical control was achieved. Twenty-three dogs with naturally occurring HAC were enrolled and hemostatic (including TEG, platelet function, thrombin-antithrombin complexes and coagulation panel) and hematological variables were measured at presentation. TEG was serially monitored until clinical resolution of HAC was attained.At presentation, most dogs with HAC had increased MA values, increased thrombin-antithrombin complexes and many were hyperfibrinogenemic. Platelet function analyzer-100 (PFA-100) closure times were significantly prolonged. TEG tracings did not normalize in either medically- or surgically-managed dogs, but fibrinogen concentrations decreased. It seems that dogs with HAC have a complex coagulopathy in which hypercoagulability and platelet hyporeactivity or dysfunction might occur simultaneously. As TEG tracings did not normalize in well-controlled dogs, it is unlikely that increased blood GCs are solely responsible for TEG alterations seen in dogs with HAC.

AB - Canine hyperadrenocorticism (HAC) is a common endocrinopathy often associated with hypercoagulability, thrombosis and thromboembolism and it can contribute to increased morbidity and mortality. The condition results in increased, unregulated secretion of glucocorticoids (GCs). While prospective identification of hypercoagulability is challenging, thrombelastography (TEG) is a diagnostic tool that enables the detection of hypercoagulability in a clinical setting. The objective of this prospective cohort study was to serially assess coagulation in dogs with HAC using TEG to test the hypothesis that dogs with HAC have increased TEG maximal amplitude (MA) and that the MA would normalize once clinical control was achieved. Twenty-three dogs with naturally occurring HAC were enrolled and hemostatic (including TEG, platelet function, thrombin-antithrombin complexes and coagulation panel) and hematological variables were measured at presentation. TEG was serially monitored until clinical resolution of HAC was attained.At presentation, most dogs with HAC had increased MA values, increased thrombin-antithrombin complexes and many were hyperfibrinogenemic. Platelet function analyzer-100 (PFA-100) closure times were significantly prolonged. TEG tracings did not normalize in either medically- or surgically-managed dogs, but fibrinogen concentrations decreased. It seems that dogs with HAC have a complex coagulopathy in which hypercoagulability and platelet hyporeactivity or dysfunction might occur simultaneously. As TEG tracings did not normalize in well-controlled dogs, it is unlikely that increased blood GCs are solely responsible for TEG alterations seen in dogs with HAC.

KW - Canine

KW - Coagulation

KW - Hyperadrenocorticism

KW - Thrombelastography

KW - Thrombosis

UR - http://www.scopus.com/inward/record.url?scp=84884988534&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84884988534&partnerID=8YFLogxK

U2 - 10.1016/j.tvjl.2013.05.047

DO - 10.1016/j.tvjl.2013.05.047

M3 - Article

C2 - 23838206

AN - SCOPUS:84884988534

VL - 197

SP - 675

EP - 681

JO - Veterinary Journal

JF - Veterinary Journal

SN - 1090-0233

IS - 3

ER -