Key result
The rate of thyroid dysfunction did not differ significantly between patients with unprovoked and provoked deep vein thrombosis (15.4% vs 5.9%, p=0.844).
Why the study?
Coagulation anomalies in thyroid dysfunction range from subclinical laboratory abnormalities to life-threatening thrombosis, prompting investigation into the effect of thyroid dysfunction on thrombophilia in patients with acute and subacute deep vein thrombosis.
Is there a difference in the rate of thyroid dysfunction between patients with provoked versus unprovoked acute and subacute deep vein thrombosis?
Case-Control (n=30)
No
Is there a difference in the rate of thyroid dysfunction between patients with provoked versus unprovoked acute and subacute deep vein thrombosis?
Absolute Event Rate: 15.4% vs 5.9%
p-value: p=0.844
This small case-control study found no significant correlation between acute/subacute DVT and thyroid dysfunction, though PAI-1 gene mutations were highly prevalent in the cohort.
No association seen between thyroid dysfunction and DVT thrombophilia; leaves open need for larger prospective studies.
Objective: Coagulation anomalies in patients with thyroid dysfunction may vary from subclinical disorders in laboratory tests to life threatening thrombotic events or bleeding. We aimed to determine the effect of thyroid dysfunction on thrombophilia in patients with acute and subacute deep vein thrombosis (DVT). Materials and Methods: A number of 30 patients with the diagnosis of DVT between November 2015 and June 2016 included in this case - control study. The patients divided into two groups as provoked (with known ethiology, n = 13) and unprovoked (with un-known ethiology, n = 17) patients. Provoked patients group divided as the patients with acquired risk factors (predisposition) and/or the patients with genetic risk factors. Results: The difference of the rate of the thyroid dysfunction between the provoked and unprovoked groups was not significant (p=0.844). The PAI – 1 gene mutation was detected in 70% of the study cohort and none of the patients had prothrombin gene mutation. The most provocative factors for DVT were male gender and undergoing a major surgery in the last three months. Conclusions: There was no correlation between acute – subacute DVT and thyroid dysfunction in this study. Therefore, we think that the ‘provocative factors’ may support the relation of thyroid dysfunction and venous thromboembolism (VTE). We think that more studies with larger cohorts and prospective should be conducted about this subject.
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Sungur et al. (2022) conducted a case-control in Acute and subacute deep vein thrombosis (n=30). Unprovoked deep vein thrombosis vs. Provoked deep vein thrombosis was evaluated on Rate of thyroid dysfunction (p=0.844). The rate of thyroid dysfunction did not differ significantly between patients with unprovoked and provoked deep vein thrombosis (15.4% vs 5.9%, p=0.844).
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