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Cited by 162Venous Thromboembolism Diagnosis and ManagementBlood Coagulation and Thrombosis MechanismsPituitary Gland Disorders and Treatments

Hypercoagulability in C ushing's syndrome: prevalence, pathogenesis and treatment

van der Pas, R., Leebeek, F.W.G., Hofland, L.J., de Herder, W.W., Feelders, R.A.·2013·Clinical Endocrinology
DOI 10.1111/cen.12094
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Abstract

Summary: Cushing's syndrome is not only accompanied by an increased prevalence of cardiovascular disease but also by a hypercoagulable state that is reflected by an increased incidence of venous thromboembolism. Overall, patients with CS have been reported to have a more than 10‐fold increased risk of developing venous thromboembolism. Moreover, the incidence of postoperative thrombosis has been shown to be comparable to the risk after major orthopaedic surgery. Hypercoagulability in CS is due to both increased production of procoagulant factors with activation of the coagulation cascade and an impaired fibrinolytic capacity, resulting in a shortened activated partial thromboplastin time and an increased clot lysis time respectively. Although these abnormalities seem to improve 1 year following successful surgery, they do not yet normalize. Therefore, sustained biochemical remission might be required to fully resolve the hypercoagulable state in CS. Considering the risk of venous thromboembolism in uncontrolled CS there may be a rationale to give patients with active CS thromboprophylaxis. So far this seems warranted following surgical interventions. However, further studies are needed to determine the optimal dosage and duration of thromboprophylaxis.

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Crossref · 10.1111/cen.12094

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  • The high venous thromboembolism risk in Cushing syndrome is due to glucocorticoid-induced activation of the coagulation cascade, whereas fibrinolysis is impaired.

    “The high VTE risk is due to glucocorticoid-induced activation of the coagulation cascade, whereas fibrinolysis is impaired (3, 24).”

    From Approach to the Patient: Diagnosis of Cushing Syndrome (2022) · cites this paper as [24]

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Authors
van der Pas, R., Leebeek, F. W. G., Hofland, L. J., de Herder, W. W., & Feelders, R. A.
Affiliations
  • Department of Internal Medicine Division of Endocrinology Erasmus MC Rotterdam the Netherlands
  • Erasmus MC (NL)
ORCID
Venue
Clinical Endocrinology
Publisher
Wiley
Published
2013-03-12
Volume
78
Issue
4
Pages
481-488
ISSN
  • 0300-0664 (ISSN-L)
  • 1365-2265
DOI
10.1111/cen.12094
OpenAlex
W2162435639
Cited by
162
References
3
Citations by year
2026: 4 · 2025: 7 · 2024: 13 · 2023: 15 · 2022: 27 · 2021: 15 · 2020: 8 · 2019: 11 · 2018: 14 · 2017: 10 · 2016: 9 · 2015: 20 · 2014: 8 · 2013: 1
FWCI
1.86
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Clinical Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
  • EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
Topics
  • Health Sciences › Medicine › Internal Medicine › Venous Thromboembolism Diagnosis and Management
  • Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
Keywords
Cushing's syndrome, hypercoagulability, venous thromboembolism, thromboprophylaxis, postoperative thrombosis, procoagulant factors, coagulation cascade, fibrinolysis, activated partial thromboplastin time, biochemical remission, pathogenesis
MeSH terms
Cushing Syndrome, Hemostasis, Humans, Models, Biological, Preventive Medicine, Incidence, Prevalence, Thrombophilia, Venous Thromboembolism

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