Colchicine Overdose—The Need for a Specific Antidote

Abstract

Purpose To report the case of a colchicine overdose to highlight current limitations in the treatment of this toxicologic emergency. Summary A 23-year-old man was admitted to the intensive care unit (ICU) after attempting suicide via polypharmacy ingestion, which included 80 to 100 colchicine 0.6 mg tablets (approximately 0.9 mg/kg of body weight). He was taken to the emergency department where gastric decontamination was initiated. Because attempts to obtain a colchicine-specific antibody fragment (Fab) were unsuccessful, only supportive therapies were provided throughout his hospitalization. Over the course of several days, the patient experienced the 3 separate evolutionary phases of colchicine toxicity ultimately leading to multiple organ failure and hemodynamic collapse, and death. Conclusion Acute colchicine intoxication is a rare, but potentially life-threatening event. Although 1 case report demonstrated the successful use of a colchicine-specific Fab fragment in the management of acute colchicine overdose, there is presently no commercially-available antidote for colchicine toxicity. Prompt recognition of the overdose, aggressive gastrointestinal decontamination, and supportive therapies directed at the multi-organ failure remain the standard of care.

Thrombin and Thrombin‐Incorporated Biomaterials for Disease Treatments

“…[38,40] Bovine thrombin, human thrombin, and recombinant human thrombin have been utilized for hemostasis control when blood oozing from venules and capillaries is approachable, as well as when typical surgical procedures are not able to control the bleeding. [37,[41][42][43] Thrombin can be combined with various hemostatic agents like absorbable materials (including oxidized regenerated cellulose, gelfoam, and microfibrillar collagen), or further mixed with fibrinogen in the formation of fibrin glues. [44][45][46][47] Because of their porous structures, the above-mentioned absorbable materials-containing hemostats offer the essential architecture for the aggregation of platelets and the activation of coagulation factors.…”