We report on a patient with coagulation abnormalities induced by a wasp sting anaphylaxis. First, we observed an unclottable activated partial thromboplastin time and a significant anti-Xa activity (equivalent to a therapeutic heparin range), whereas the patient had received no heparin. This phenomenon is probably due to activated mast cells that release mediators such as heparin and tryptase. Heparin can then act as an anticoagulant by binding to antithrombin. This "heparinization" explains the anti-Xa activity contributing to the unclottable activated partial thromboplastin time detected in our patient. Second, we noted an extremely low fibrinogen level in the presence of normal platelet count and only a slight increase of D-dimers (absence of important disseminated intravascular coagulation). This is probably due to serum tryptase released during massive mast cell activation. Tryptase cleaves the alpha and beta chains of fibrinogen. This results in the removal of the thrombin cleavage site and of the critical polymerization site from the fibrinogen beta chain. Thrombin- initiated clot formation is therefore inhibited. Tryptase also acts directly on the fibrinolytic pathway by activating the single-chain urinary-type plasminogen activator, resulting in conversion of plasminogen into plasmin and therefore degradation of fibrinogen and other coagulation factors. This hyperfibrinogenolysis explains both the prolonged clotting times and the low fibrinogen level observed. Although our patient did not bleed, in other settings (trauma, during surgery) patients with anaphylaxis may present bleeding disorders. Although the mechanisms underlying these abnormalities have been described in vitro and in vivo animal trials, this is the first time they are described in a human clinical setting.