The effects of green pit viper (Trimeresurus albolabris and Trimeresurus macrops) venom on the fibrinolytic system in human.
Green pit viper (Trimeresurus albolabris and Trimeresurus macrops) venom was found to have a thrombin-like effect in vitro but cause a defibrination syndrome in vivo. The effects of venom on fibrinolytic system have not been well characterized. This knowledge can help to define the roles of antifibrinolytic therapy, give insights in fibrinolytic system regulation and potentially lead to identification of a new profibrinolytic agent from this venom. Forty-six cases of green pit viper bites were studied for various coagulation and fibrinolytic parameters and correlated with serum venom levels measured by ELISA. Fibrinolytic system activation is very common as indicated by low plasminogen (50%), low antiplasmin (56.5%) and elevated fibrin-fibrinogen degradation products (FDPs, 97.4%) levels. FDP test is very sensitive and a normal level is useful for exclusion of systemic envenomation. In contrast to some other models of defibrination syndrome, such as Russell viper (Daboia russelli siamensis), elevation of plasminogen activator activity (PA) was found indicating a hyperfibrinolytic state. Definite increase in tissue-type plasminogen activator (t-PA) antigen (p = 0.00075) with a modest elevation of its inhibitor plasminogen activator inhibitor-1 (PAI-1) (p = 0.27) probably contributes to this effect. This supports the idea that the balance between plasminogen activators and inhibitors can determine fibrinolytic responses in pathologic states. Fibrinopeptide A levels were markedly elevated (68.43 +/- 51.57 ng/ml in cases and 2.83 +/- 3.80 ng/ml in control, p < 0.0001) and correlated well with clinical severity suggesting that the fibrin deposition from the thrombin-like effect is the main mechanism of fibrinolysis. Therefore, antifibrinolytic agents probably have no role in treatment. However, the components of green pit viper venom that have these profibrinolytic effects in human are interesting and should be further identified.
Rojnuckarin
P
P
Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. ponlapat@u.washington.edu
Intragumtornchai
T
T
Sattapiboon
R
R
Muanpasitporn
C
C
Pakmanee
N
N
Khow
O
O
Swasdikul
D
D
D000328:Adult; D000818:Animals; D000997:Antivenins / Q000627:therapeutic use; D001778:Blood Coagulation Disorders / Q000139:chemically induced* / Q000503:physiopathology / Q000628:therapy; D003435:Crotalid Venoms / Q000009:adverse effects* / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005342:Fibrinolysis / Q000187:drug effects* / Q000502:physiology; D005343:Fibrinolytic Agents / Q000032:analysis; D006801:Humans; D008297:Male; D010958:Plasminogen / Q000032:analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis; D010974:Platelet Aggregation / Q000187:drug effects*; D012909:Snake Bites / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D013921:Thrombocytopenia / Q000139:chemically induced; D010959:Tissue Plasminogen Activator / Q000032:analysis; D017819:Viperidae; D000979:alpha-2-Antiplasmin / Q000032:analysis
D000997:Antivenins; D003435:Crotalid Venoms; D005338:Fibrin Fibrinogen Degradation Products; D005343:Fibrinolytic Agents; D017395:Plasminogen Activator Inhibitor 1; C029748:Trimeresurus venoms; D000979:alpha-2-Antiplasmin; D010958:Plasminogen; D010959:Tissue Plasminogen Activator