Biology Reference
In-Depth Information
be underappreciated. For example, streptokinase failed to dissolve postmortem clot-
ted blood from a patient fatally envenomated by a
T. kirtlandii
(Mebs et al., 1978).
The clinical pathology of the venom disease in the patient described by Mebs et al.
(1978) suggests development of
purpura fulminans
from microvascular thrombosis.
Therefore, this case featured some pathology in common with endotoxemia-induced
DIC.
Interestingly, Wang et al. (2009) described a recombinant fibrinogenase derived
from
Deinagkistrodon acutus
(Chinese snorkel-nosed viper or “hundred-pacer”)
venom that protected rabbits against lipopolysaccharide (LPS; endotoxin)-induced
DIC. This recombinant also decreased renal fibrin deposition in the LPS-treated
animals. It is not surprising that some venoms contain components that oppose the
pharmacological effects of other venom toxins; some may even represent potential
scaffolds for future therapeutics useful in the management of venom-induced DIC.
As noted by Dempfle (2004), no randomized trials have demonstrated evidence-
supported therapies for consumptive coagulopathy. This author suggested recom-
mendations similar to those of Wada et al. (2010), but reinforced the lack of proven
clinical efficacy for most of these treatments. Therefore, recommendations for endo-
toxin-induced DIC present a guide that reflects some of the management strategies
suggested by case studies of venom-induced consumptive coagulopathy/DIC. In
summary, these are treatment of the specific cause of the coagulopathy (provision of
antivenom if available); avoidance of unproven and possibly harmful therapies (hep-
arin, vitamin K, antifibrinolytics, etc.); cautious provision of replacement therapy
as clinically indicated and use, at the discretion of the physician, of therapeutics of
unproven efficacy that have a low-risk profile (e.g., SPI).
