Thrombin generation in Cushing's Syndrome: do the conventional clotting indices tell the whole truth?

S Koutroumpi1, L Spiezia, N Albiger

  • 1Endocrinology Unit, Department of Medicine-DIMED, University of Padua, Via Ospedale, 105, 35128, Padua, Italy.

Pituitary
|February 15, 2013
PubMed

Insights

Cushing's Syndrome (CS) and Metabolic Syndrome (MetS) patients exhibit a prothrombotic state, with altered thrombin generation parameters. While CS patients show increased endogenous anticoagulants, suggesting a potential protective mechanism, their hypercoagulability is less pronounced than in MetS.

Area of Science:

  • Endocrinology
  • Hematology
  • Thrombosis Research

Background:

  • Cushing's Syndrome (CS) is linked to increased mortality, with hypercoagulability playing a key role in thrombosis.
  • Understanding the hemostatic balance in CS is crucial for managing associated risks.

Purpose of the Study:

  • To evaluate in vitro thrombin generation (TG) and clotting markers in CS patients.
  • To compare these markers with those in Metabolic Syndrome (MetS) patients and healthy controls.
  • To investigate correlations between TG parameters, cortisol levels, and clinical factors like BMI and comorbidities.

Main Methods:

  • Assessed TG parameters (lag time, peak thrombin, ETP) and clotting markers (PT, PTT).
  • Included 33 CS patients, 28 MetS patients, and 31 healthy individuals.
  • Analyzed correlations with night salivary cortisol, urinary free cortisol, BMI, obesity, diabetes, and hypertension.

Main Results:

  • CS and MetS patients showed shorter lag time and higher peak thrombin/ETP than controls; CS lag time was less shortened than MetS.
  • PT was prolonged in both CS and MetS; PTT was shorter in CS.
  • Elevated Factor VIII (FVIII), Antithrombin (AT), protein C, and S were observed exclusively in CS patients.
  • Cortisol levels, BMI, obesity, diabetes, and hypertension correlated significantly with TG parameters and clotting markers.

Conclusions:

  • CS and MetS patients present a prothrombotic state, with distinct patterns in thrombin generation.
  • Elevated endogenous anticoagulants in CS may offer a partial protective effect against hypercoagulability.
  • These findings highlight the complex hemostatic alterations in CS and their relationship with endocrine and metabolic factors.

Related Concept Videos

Cushing Syndrome I: Introduction01:26

Cushing Syndrome I: Introduction

Cushing syndrome refers to the collection of clinical manifestations that arise when tissues are exposed to excessive amounts of cortisol or cortisol-like medications over an extended period. Cortisol, a glucocorticoid produced by the adrenal cortex, regulates metabolism, immune responses, and the body’s adaptation to stress. When its concentration remains chronically elevated, these physiological pathways become dysregulated, resulting in the characteristic features of the syndrome.Exogenous...
Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Venous Thrombosis III: Interprofessional Care01:29

Venous Thrombosis III: Interprofessional Care

Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
Venous Thrombosis II: Clinical Manifestations and Diagnostic Studies01:20

Venous Thrombosis II: Clinical Manifestations and Diagnostic Studies

The key difference between Superficial Vein Thrombosis (SVT) and Deep Vein Thrombosis (DVT) lies in their location and severity.Clinical ManifestationsSVT typically presents with localized pain, tenderness, and redness along the course of a superficial vein, often accompanied by a palpable, cord-like structure under the skin. This condition is usually less dangerous than DVT but can be uncomfortable and may lead to complications such as cellulitis or, rarely, a clot extension into the deep...