Editorial - Hematology and Blood Disorders (2025) Volume 8, Issue 2

Clotting Chaos: How Liver Disease Disrupts Hemostasis

Rini Santoso ^*

Department of Medicine, University of Beirut, Lebanon

*Corresponding Author:

Rini Santoso
Department of Medicine,
University of Beirut, Lebanon
E-mail: rinis@ui.ac.id

Received: 01-Aug-2025, Manuscript No. AAHBD-24-171317; Editor assigned: 03-Aug-2025, PreQC No. AAHBD-24-171317(PQ);Reviewed:16-Aug-2025, QC No. AAHBD-24-171317; Revised:18-Aug-2025, Manuscript No. AAHBD-24-171317(R); Published: 24-Aug-2025, DOI:10.35841/AAHBD-8.2.220

Citation: Santoso R. Clotting chaos: How liver disease disrupts hemostasis. Hematol Blood Disord. 2025;8(2):220

Introduction

The liver, often hailed as the body's biochemical powerhouse, plays a central role in maintaining hemostasis—the delicate balance between bleeding and clotting. When liver function deteriorates, this equilibrium is thrown into chaos, leading to a paradoxical state where patients are simultaneously at risk for hemorrhage and thrombosis. This phenomenon, known as coagulopathy of liver disease, is a complex and evolving area of clinical medicine that demands greater awareness and nuanced understanding. Hemostasis involves three interconnected processes: primary hemostasis (platelet plug formation), secondary hemostasis (coagulation cascade), and fibrinolysis (clot breakdown). The liver orchestrates this symphony by synthesizing nearly all clotting factors (except von Willebrand factor), natural anticoagulants (like protein C and antithrombin), and fibrinolytic proteins (such as plasminogen) [1].

Additionally, the liver produces thrombopoietin (TPO), a hormone that regulates platelet production. Any disruption in hepatic function can therefore have cascading effects on all phases of hemostasis. Contrary to traditional belief, liver disease does not simply cause a bleeding tendency. Instead, it creates a “rebalanced” but fragile hemostatic state. This rebalancing occurs because reductions in procoagulant factors are often matched by decreases in anticoagulant proteins. However, this balance is precarious and can be tipped toward bleeding or clotting depending on additional stressors like infection, trauma, or invasive procedures [2].

Platelet transfusions are considered when counts fall below 50,000/μL for invasive procedures. Thrombopoietin receptor agonists (e.g., eltrombopag) may be used in select cases. Despite elevated INR, anticoagulation may be indicated for PVT or DVT. Low-molecular-weight heparin is preferred, but bleeding risk must be closely monitored. Endoscopic band ligation and non-selective beta-blockers are frontline therapies. In acute bleeding, vasoactive agents and antibiotics are essential. Liver disease is a global health challenge, with rising rates of cirrhosis due to alcohol, hepatitis, and non-alcoholic fatty liver disease (NAFLD). Understanding its impact on hemostasis is crucial for improving outcomes. Emerging research is exploring: Biomarkers for bleeding/thrombotic risk, Novel anticoagulants tailored for cirrhosis. Especially vitamin K-dependent factors II, VII, IX, and X. Due to splenic sequestration (from portal hypertension), bone marrow suppression, and decreased TPO production. Even when platelet counts are normal, their function may be impaired. Compensates for platelet defects but may promote thrombosis. Can be either increased or decreased, contributing to bleeding or clotting risks [3].

Standard coagulation tests like prothrombin time (PT), activated partial thromboplastin time (aPTT), and international normalized ratio (INR) are often misleading in liver disease. These tests measure only isolated aspects of coagulation and do not reflect the full hemostatic picture [4].

For example, an elevated INR is traditionally interpreted as a bleeding risk. However, in cirrhotic patients, it may not correlate with actual hemorrhagic tendencies. Global assays like thromboelastography (TEG) and thrombin generation tests offer a more comprehensive view but are not yet widely available or standardized. However, bleeding risk varies widely and is influenced by factors beyond coagulation tests, such as infection, renal dysfunction, and endothelial integrity. Surprisingly, liver disease also increases the risk of thrombosis, including: Portal vein thrombosis (PVT).  This paradox arises from elevated VWF, reduced anticoagulants, and endothelial dysfunction. Clinicians must carefully weigh the risks and benefits of anticoagulation in these patients. Managing hemostasis in liver disease requires individualized, evidence-informed approaches: Administering fresh frozen plasma (FFP) to normalize INR before procedures is often unnecessary and may increase volume overload or thrombosis risk [5].

Conclusion

Liver disease disrupts hemostasis in a uniquely chaotic way—creating a tightrope walk between bleeding and clotting. Traditional diagnostic tools fall short, and management requires a nuanced, patient-centered approach. As research advances, clinicians must stay informed to navigate this complex terrain and ensure safer outcomes for patients.

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