The
venoms from 3 snakes have been shown to induce defibrinogenation:
ancrod from the
venom of Calloselasma rhodostoma (formerly known as Agkistrodon rhodostoma),
batroxobin from the
venom of Bothrops atrox moojeni, and
crotalase from the
venom of Crotalus adamanteus. The purified fractions of
ancrod,
batroxobin, and
crotalase possess
coagulant, proteolytic and esterolytic properties, although their primary mechanism of action is a proteolytic effect on circulating
fibrinogen.
Ancrod cleaves only the A-fibrinopeptides, but not the B-fibrinopeptides, from
fibrinogen; this contrasts with
thrombin,
batroxobin and
crotalase, which cleave both
fibrinopeptides A and B. Within minutes of administration of
ancrod or
batroxobin, there is a significant reduction in plasma
fibrinogen levels, and these remain exceedingly low with repeated administration (once or twice daily). The rapid fall in plasma
fibrinogen levels is accompanied by a slightly delayed but marked rise in the level of
fibrinogen-
fibrin degradation products.
Plasminogen levels are decreased and blood viscosity is reduced, but formed elements in the circulating blood remain unaltered.
Ancrod and
batroxobin have been investigated in patients with
stroke,
deep-vein thrombosis,
myocardial infarction, peripheral arterial
thrombosis,
priapism, and sickle-cell crisis;
crotalase has not been administered to humans. However, results have been difficult to interpret, and additional well designed trials are needed to better define the optimum role of
ancrod and
batroxobin in the management of these conditions. Overall, treatment is well tolerated and serious adverse events are infrequent. In the coagulation laboratory,
ancrod,
batroxobin and
crotalase may be used as
reagents to perform coagulation studies on specimens of blood that contain
heparin. These
venom fractions can be substituted for
thrombin in performing the thrombin time and in removing
fibrinogen from plasma for accurate determination of
fibrinogen-
fibrin degradation products.