Fibrinogen and D-dimer alterations in thyroid dysfunction: implications for bleeding and thrombotic risk
- 1Department of Medical Laboratory Sciences, College of Medicine and Health Sciences, Debre Berhan University
- 2Department of Hematology and Immunohematology, School of Biomedical and Laboratory Sciences, College of Medicine and Health Sciences, University of Gondar
Abstract
Thyroid dysfunction can disrupt the balance of the hemostatic system, predisposing affected individuals to either bleeding or thrombotic complications, depending on the nature and severity of the disorder. In hyperthyroidism, a prothrombotic state is commonly observed, characterized by increased fibrinogen concentrations, elevated D-dimer levels, and enhanced coagulation activation. Conversely, hypothyroidism may impair coagulation and fibrinolysis, resulting in variable bleeding or thrombotic manifestations depending on disease severity. Raised D‑dimer levels reflect increased thrombin generation with secondary fibrinolysis and therefore serve as markers of a hypercoagulable state. Fibrinogen concentrations above 4.0 g/L are independently associated with a higher risk of venous thromboembolism, although a direct causal role has not been established. In patients with hyperthyroidism, fibrinogen levels are increased by approximately 20% on average, suggesting an elevated thrombotic risk, potentially mediated by reduced fibrinolytic capacity. Hyperthyroid patients consistently demonstrate higher plasma D‑dimer concentrations, indicating concurrent activation of coagulation and fibrinolysis. Previous studies have documented increased D‑dimer levels in both overt and subclinical hyperthyroidism, consistent with upregulation of the fibrinolytic pathway. D‑dimer values in the range of approximately 450–650 ng/mL are frequently observed in this population. In moderate hypothyroidism, relatively lower D‑dimer levels have been linked to diminished fibrinolytic activity. Bleeding manifestations have been frequently reported in patients with hypothyroidism, although their prevalence varies considerably depending on the study population and clinical criteria used. In contrast, thrombotic complications are more commonly associated with hyperthyroidism, with reported frequencies varying widely across studies due to differences in disease severity, population characteristics, and outcome definitions. In summary, thyroid dysfunction disturbs hemostatic equilibrium and leads to characteristic changes in fibrinogen and D‑dimer levels. Abnormal concentrations of these markers may signal impaired hemostatic function and could help identify patients at increased risk of bleeding or thrombosis.
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BibTeX
@article{mandefro2026fibrinogen,
title = {{Fibrinogen and D-dimer alterations in thyroid dysfunction: implications for bleeding and thrombotic risk}},
author = {Befikad Mandefro and Amanuel Kelem and Tiruneh Adan},
journal = {Thyroid Research},
year = {2026},
month = jul,
doi = {10.1186/s13044-026-00312-8},
url = {https://doi.org/10.1186/s13044-026-00312-8},
note = {CC BY},
}
RIS
TY - JOUR
TI - Fibrinogen and D-dimer alterations in thyroid dysfunction: implications for bleeding and thrombotic risk
AU - Befikad Mandefro
AU - Amanuel Kelem
AU - Tiruneh Adan
PY - 2026
DA - 2026/07/01
JO - Thyroid Research
DO - 10.1186/s13044-026-00312-8
UR - https://doi.org/10.1186/s13044-026-00312-8
AB - Thyroid dysfunction can disrupt the balance of the hemostatic system, predisposing affected individuals to either bleeding or thrombotic complications, depending on the nature and severity of the disorder. In hyperthyroidism, a prothrombotic state is commonly observed, characterized by increased fibrinogen concentrations, elevated D-dimer levels, and enhanced coagulation activation. Conversely, hypothyroidism may impair coagulation and fibrinolysis, resulting in variable bleeding or thrombotic manifestations depending on disease severity. Raised D‑dimer levels reflect increased thrombin generation with secondary fibrinolysis and therefore serve as markers of a hypercoagulable state. Fibrinogen concentrations above 4.0 g/L are independently associated with a higher risk of venous thromboembolism, although a direct causal role has not been established. In patients with hyperthyroidism, fibrinogen levels are increased by approximately 20% on average, suggesting an elevated thrombotic risk, potentially mediated by reduced fibrinolytic capacity. Hyperthyroid patients consistently demonstrate higher plasma D‑dimer concentrations, indicating concurrent activation of coagulation and fibrinolysis. Previous studies have documented increased D‑dimer levels in both overt and subclinical hyperthyroidism, consistent with upregulation of the fibrinolytic pathway. D‑dimer values in the range of approximately 450–650 ng/mL are frequently observed in this population. In moderate hypothyroidism, relatively lower D‑dimer levels have been linked to diminished fibrinolytic activity. Bleeding manifestations have been frequently reported in patients with hypothyroidism, although their prevalence varies considerably depending on the study population and clinical criteria used. In contrast, thrombotic complications are more commonly associated with hyperthyroidism, with reported frequencies varying widely across studies due to differences in disease severity, population characteristics, and outcome definitions. In summary, thyroid dysfunction disturbs hemostatic equilibrium and leads to characteristic changes in fibrinogen and D‑dimer levels. Abnormal concentrations of these markers may signal impaired hemostatic function and could help identify patients at increased risk of bleeding or thrombosis.
SN - 1756-6614
ER -