Mechanism of thrombosis caused by sclerotherapy of esophageal varices using sodium tetradecyl sulphate.
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Jacobson BF, Franz RC, Hurly EM, Norman GL, Becker P, Myburgh JA, Mendelow BV
Mechanism of thrombosis caused by sclerotherapy of esophageal varices using sodium tetradecyl sulphate.
Surg Endosc. 1992 Jan-Feb;6(1):4-9.
- PubMed ID
- 1344580 [ View in PubMed]
- Abstract
The mechanism of thrombosis following intravariceal injection of sodium tetradecyl sulphate (S.T.D.) was investigated with respect to effects on the vascular endothelium, the coagulation cascade, and platelet function. Using an umbilical cord model designed to simulate blood flow over the endothelium, it was found that S.T.D. is a potent toxin for endothelial cells in that brief exposure to even low concentrations of the agent were effective in stripping endothelium over a considerable distance, exposing highly thrombogenic endothelium in the process. Effects on coagulation and platelet function were found to be dependent on concentration. Diluted S.T.D. induced a hypercoagulable state, possibly in consequence of a selective inhibition of the physiological anticoagulant, protein C, and promoted platelet aggregation. Higher concentrations inactivated the coagulation cascade and lysed platelets completely. These results suggest that intravariceal infusion of S.T.D. at considerable dilution may be at least as effective in inducing thrombosis as standard dosage, and possibly more so.
DrugBank Data that Cites this Article
- Drug Targets
Drug Target Kind Organism Pharmacological Action Actions Sodium tetradecyl sulfate Vitamin K-dependent protein C Protein Humans YesInhibitorDetails Sodium tetradecyl sulfate Vitamin K-dependent protein S Protein Humans YesInhibitorDetails