LAUSR

2533 presumptively targets the cytokine storm phase of the disease by inhibiting the IL-6 pathway (2). However, IL-6 has a multifaceted role in venous thromboembolism, and Zhang et al. has reported that upregulation of IL-6 as the result of aberrant downregulation of miR-338-5p may lead to venous thromboembolism (3). Conversely, using a rat model, Nosaka et al. demonstrated the importance of iIL-6 in resolving thrombi through macrophage recruitment and proteolytic enzymes induction (4). The absence of IL-6, in fact, leads to the thrombus growing (4). Moreover, tocilizumab has been reported to decrease factor XIII, chemerin, and plasminogen activator inhibitor levels (5). Factor XIII is involved in fibrin stabilization; blocking this factor may lead to fibrin clot instability, causing microthrombi to dislodge, increasing the likelihood of thrombophilia. The association of tocilizumab with thrombosis is not clearly understood. However, the potential for adverse effects that we describe may warrant a short period of therapeutic anticoagulation before and after administering tocilizumab. The hypercoagulable state reported in the findings by Griffin et. al. may represent a side effect of tocilizumab rather than being a condition secondary to COVID-19, or it could result from a combination of both.