Key result
Protein S deficiency was associated with a significantly higher risk of arterial thrombosis compared to patients without the deficiency (OR 1.888; 95% CI 1.041-3.422; P=0.036).
Why the study?
The role of natural anticoagulant deficiency in the development of arterial thrombosis remains controversial.
Does deficiency of natural anticoagulants increase the risk of arterial thrombosis in patients without prior thrombosis or anticoagulant therapy?
Cross-Sectional (n=585)
Does deficiency of natural anticoagulants increase the risk of arterial thrombosis in patients without prior thrombosis or anticoagulant therapy?
Odds Ratio: 1.888 (95% CI 1.041–3.422)
p-value: p=0.036
Protein S deficiency is associated with an increased risk of arterial thrombosis, suggesting a potential role for natural anticoagulant screening in these patients.
PS deficiency was associated with arterial thrombosis; leaves open causal role of natural anticoagulant deficiencies in AT pending prospective confirmation.
Background The role of natural anticoagulant deficiency in the development of arterial thrombosis (AT) is controversial. Objective Our objectives were to assess the deficiency of natural anticoagulants, including protein S (PS), protein C (PC), antithrombin III (AT III) and their involvement in the occurrence of AT. Design Retrospective cross-sectional study. Methods This study was conducted in 585 patients who were examined with PS, PC, and AT III tests. The activity of PC, PS (men, women), and ATIII under 70%, 75%, 60%, and 80% was recognized as a deficiency, respectively. Peripheral blood cell and coagulation tests were performed before starting treatment. Patients with previous AT, venous thromboembolism (VTE) or anticoagulant therapy were excluded. Results Patients without thrombosis were 222 (38%), patients with newly diagnosed VTE were 281 (48%), and patients with newly diagnosed AT were 82 (14%). The most common AT sites were in the lungs, brain, and lower extremities (31.2%, 20.8%, and 20.8%, respectively). Compared to the nonthrombosis group, the AT group had a lower PS activity (%) (82.77 ± 24.09 vs 91.31 ± 27.27), a higher fibrinogen (g/L) (4.25 ± 1.68 vs 3.74 ± 1.51), a higher D-dimer (mg/L FEU) (6.16 vs 1.95), and a higher neutrophil count (G/L) (8.57 vs 6.50) with P < .05. Compared to the VTE group, the AT group had higher hemoglobin (g/L) (135.95 ± 23.75 vs 129.02 ± 25.22) and a higher neutrophil count (G/L) (8.57 vs 7.28) ( P < .05). In the AT group, the frequencies of PC, PS, and AT III deficiency were 23.1%, 28%, and 17.1%, respectively. The AT group had a higher frequency of PS deficiency than the nonthrombosis group (28% vs 17.1%, P = .035). Patients with PS deficiency had a higher risk of AT compared to those without PS deficiency (OR = 1.888, 95% CI [1.041-3.422], P = .036). Conclusion PS deficiency may be considered a factor in increasing the risk of AT.
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Nguyen et al. (2023) conducted a cross-sectional in Arterial thrombosis (n=585). Protein S deficiency vs. Without Protein S deficiency was evaluated on Occurrence of arterial thrombosis (OR 1.888, 95% CI 1.041-3.422, p=0.036). Protein S deficiency was associated with a significantly higher risk of arterial thrombosis compared to patients without the deficiency (OR 1.888; 95% CI 1.041-3.422; P=0.036).
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