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.