The impact of direct oral anticoagulants (DOACs) on laboratory assays used for thrombophilia testing (e.g., antithrombin, protein S, protein C, lupus anticoagulant and activated protein-C resistance) is a well-known issue and may cause false-positive and -negative results. Therefore, the correct interpretation of tests that are performed in patients taking DOACs is mandatory to prevent misclassification and the subsequent clinical consequences. We aimed at evaluating the efficiency of a new and simple procedure (DOAC-Stop®; Haematex Research, Hornsby, Australia) to overcome the effect of all DOACs in real-life settings and to assess the percentage of erroneous results due to the presence of DOACs on thrombophilia screening tests. For this purpose, 135 DOAC-treated patients (38 apixaban, 40 dabigatran, 15 edoxaban, and 42 rivaroxaban) and 20 control patients were enrolled. A significant drop in apixaban, dabigatran, edoxaban, and rivaroxaban plasma concentrations following the DOAC-Stop® treatment was observed (74.8–8.2 ng/mL [p < 0.0001], 95.9–4.7 ng/mL [p < 0.0001], 102.1–8.8 ng/mL [p = 0.001], and 111.3–7.0 ng/mL [p < 0.0001], respectively). The DOAC-Stop® treatment was mostly effective to overcome the effect of DOACs on PTT-LA, dilute Russell's viper venom time (dRVVT) screen, and dRVVT confirm tests. Using our procedures, false-positive results due to DOACs were observed only with lupus anticoagulant tests (up to 75%) and fell to zero after the DOAC-Stop® procedure, regardless of the DOAC considered. In conclusion, the DOAC-Stop® adsorbent procedure appeared to be an effective and simple way to overcome the interference of DOAC on coagulation tests and should facilitate the interpretation of thrombophilia screening tests in patients taking DOACs.

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Pseudothrombocytopenia (PTCP), a relative common finding in clinical laboratories, can lead to diagnostic errors, overtreatment, and further (even invasive) unnecessary testing. Clinical consequences with potential life-threatening events (e.g., unnecessary platelet transfusion, inappropriate treatment including splenectomy or corticosteroids) are still observed when PTCP is not readily detected. The phenomenon is even more complex when occurring with different anticoagulants. In this review we present a case of multi-anticoagulant PTCP, where we studied different parameters including temperature, amikacin supplementation, measurement methods, and type of anticoagulant. Prevalence, clinical risk factors, pre-analytical and analytical factors, along with clinical implications, will be discussed. The detection of an anticoagulant-dependent PTCP does not necessarily imply the presence of specific disorders. Conversely, the incidence of PTCP seems higher in patients receiving low molecular weight heparin, during hospitalization, or in men aged 50 years or older. New analytical technologies, such as fluorescence or optical platelet counting, will be soon overturning traditional algorithms and represent valuable diagnostic aids. A practical laboratory approach, based on current knowledge of PTCP, is finally proposed for overcoming spuriously low platelet counts.

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