LAUSR

POLISH ARCHIVES OF INTERNAL MEDICINE 2020; 130 (12) antiphospholipid syndrome (APS).7 Antiphos­ pholipid antibodies can be measured with 2 types of assays: LAs interfere with phospholipid­ ­dependent coagulation tests in vitro, while oth­ er types of aPLs are measured with various im­ munoassays. Both LAs and aCLs can be directed against β2GPI or other antigenic targets such as prothrombin, protein C, protein S, tissue plas­ minogen activator, and annexin.1 The prevalence of elevated aPL levels has been reported in 1% to 5% of healthy young people, increasing by up to 50% in older patients with chronic diseases. The clinical significance of aPLs in healthy peo­ ple remains elusive. Of note, not every test pos­ itive for aPLs is of clinical significance and pa­ tients with aPLs are at different levels of risk of adverse events associated with aPLs. There­ fore, patients having aPLs together with other cardiovascular risk factors, such as high blood pressure, elevated cholesterol levels, diabetes, smoking status, or obesity, are at higher risk of adverse events. According to the current labora­ tory criteria for APS, aPLs should be present in tests performed twice at least 12 weeks apart.7 The medium ­to ­high titers of aPLs are clinical­ ly more significant than lower levels, and dou­ ble or triple positivity increases the risk of ad­ verse events. A systematic review of observa­ tional studies excluding patients with autoim­ mune diseases reported a pooled prevalence rate of aPLs in up to 23.3% of patients with stroke, 23% with myocardial infarction, 15.8% with deep vein thrombosis, and 13% of women with ad­ verse events during pregnancy.6 A high prevalence of aCLs, anti ­β2GPIs, LAs, antiphosphatidylcholine, antiphosphatidylser­ ine, antiphosphatidylinositol, antiphosphatidyl­ ethanolamine, and antiprothrombin antibodies was observed in patients with various types of hematological malignancies and solid tumors.2 Therefore, an already increased risk of develop­ ing thrombosis in cancer patients is even higher in the aPL carriers. The reported prevalence of The association between thrombosis and cancer was first observed by Trousseau in 1865. Since then, numerous studies have shown that throm­ boembolism is a common complication of cancer, occurring in 15% of all cancer patients.1,2 Despite extensive research and modern interventions, thromboembolic disorders are still the major cause of morbidity and mortality in this popula­ tion. The risk of thromboembolic events is 4 ­fold higher in patients with cancer than in the general population and this risk is further increased in pa­ tients undergoing chemotherapy.2,3 Much of this high risk is attributed to cancer itself. However, patient ­related factors such as age, performance status, body mass index, underlying comorbid­ ities, and therapy also represent considerable factors. The biological origin of thromboembol­ ic events is related to the procoagulant, hypoxic, and inflammatory state associated with tumors, especially at advanced stages.4 Multiple mecha­ nisms contribute to the hypercoagulable state ob­ served in cancer, which leads to complex interac­ tions among various factors, such as tissue fac­ tors, platelet and endothelial activation, coagu­ lation abnormalities, procoagulants secreted by tumor cells, abnormal blood flow, and abnormal tumor angiogenesis.1,5 The question arises wheth­ er antiphospholipid antibodies (aPLs) additional­ ly increase the thromboembolic risk in patients with malignant diseases. Antiphospholipid antibodies constitute a het­ erogeneous group of autoantibodies directed against phospholipids or certain phospholipid­ ­binding plasma proteins and their elevated lev­ els in an individual are associated with a predis­ position to thrombus formation.6 The occurrence of one or more clinical episodes of thrombosis and / or complications during pregnancy, such as miscarriage or preterm delivery, in conjunc­ tion with significant levels of aPLs including lu­ pus anticoagulants (LAs), anticardiolipin anti­ bodies (aCLs), and anti–β2 ­glycoprotein I anti­ bodies (anti ­β2GPIs) indicates the presence of EDITORIAL