To the editor

I read with great interest the original article by Piróg et al¹ published recently in Polish Archives of Internal Medicine. Through a rigorous cohort design, this study systematically explored the association between fibrin clot properties and the risk of thromboembolic events (TEs) in patients with obstetric antiphospholipid syndrome (OAPS). It was the first to confirm the predictive value of plasma fibrin clot permeability (K_s) for TEs in OAPS patients, providing a crucial new perspective on risk assessment and clinical management in this field, with notable academic and clinical significance.

The core findings of this study are highly insightful: OAPS patients exhibited a prothrombotic phenotype characterized by denser fibrin clots (16.4% reduction in K_s) and impaired fibrinolysis (16.9% prolongation in clot lysis time [CLT]). These changes were more pronounced in the patients with a high‑risk antiphospholipid antibody (aPL) profile (eg, lupus anticoagulant or multiple aPL positivity). During follow‑up, the incidence of TEs in the OAPS patients was significantly higher than that in the control group (16.1% vs 3.2%), and K_s values equal to or below 6.1 × 10^-9 cm² could effectively predict TE risk (hazard ratio, 3.59). This result not only reveals the potential mechanism of thrombosis in OAPS—abnormal fibrin clot structure and function—but also provides a quantifiable biological marker, offering an objective basis for clinically identifying OAPS patients at a high thrombotic risk, and promising to improve the precision of risk‑stratified management for OAPS.

However, to further deepen the clinical translation and popularization of the study conclusions, several points are worth discussing. First, fibrin clot properties were only measured at baseline, whereas the immune status and coagulation–fibrinolysis system function of OAPS patients may actually fluctuate over time (eg, during concurrent infections or exacerbations of autoimmune disease). Whether dynamic monitoring of changes in K_s and CLT can more accurately reflect TE risk warrants verification in subsequent studies. Second, the authors did not clarify the impact of different treatment regimens (eg, dose adjustment of low‑molecular‑weight heparin combined with aspirin, application of direct oral anticoagulants) on fibrin clot properties in OAPS patients. If interventions can be shown to improve the prothrombotic clot phenotype and reduce TE risk, it would provide more robust evidence for optimizing OAPS treatment strategies.² Third, all study samples were from a single regional center, and high‑risk OAPS patients accounted for 75.8% of the OAPS group, which may introduce selection bias. Future multicenter, large‑sample cohort studies should include more low‑risk patients and diverse ethnic populations to assess the generalizability of the results.³

In addition, the authors mentioned a correlation between antiphosphatidylserine / prothrombin (aPS/PT) antibodies and K_s values in OAPS patients, which expands the role of aPL in thrombosis. However, the molecular mechanism via which aPS/PT antibodies affect fibrin clot structure remains unclear. Subsequent basic research can further explore the interaction of these antibodies with fibrinogen, or their impact on thrombin generation and plasmin activity, to improve the mechanism network of thrombosis in OAPS.⁴

Despite the aforementioned areas for further exploration, the study by Piróg et al¹ has laid an important foundation for thromboembolic risk assessment and mechanism research in OAPS. The K_s cutoff value proposed in this study is expected to serve as a supplementary indicator for routine risk screening of OAPS patients, facilitating early intervention in high‑risk populations. It is anticipated that future studies focused on the above issues will further improve the diagnosis and treatment of OAPS and enhance the long‑term prognosis of patients.