Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifteen patients with severe intermittent claudication were treated by therapeutic defibrination with subcutaneous injections of ancrod for 5 weeks. Mean plasma-fibrinogen was maintained below 50% of the initial value throughout the treatment period. This reduction in plasma-fibrinogen was accompanied by a parallel fall in whole-blood viscosity and a pronounced clinical improvement. Objective measurements showed maximum benefit on the 21st day of treatment, when the mean resting ankle/arm pressure index had increased by 37%, the post-exercise pressure index had increased by 50%, and the time taken for the pressure index to return to a resting value after a constant exercise had decreased by 33%. (The claudication-count had increased by 59%).
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PMID:Treatment of severe intermittent claudication by controlled defibrination. 6 29

Two thirds of the patients with peripheral arterial occlusive disease have to be treated conservatively, for only up to 30% can be revascularized by operative methods. Using the pharmacological differential treatment the grade of compensation and localization of the obliterative process has to be considered. Ignoring the usual basic therapy (elimination of heart failure and pathological bradycardia, systemic walking-exercise, anticoagulation etc.) intrafemoral long-term application of energetic phosphate (i.e. nucleotid-nucleosid-mixtures) leads to a positive result in nearly two thirds (n = 97 legs) with a degree of II to IV of Fontaine. Whereas the snakes' encyme Ancrod with the effect of defibrination was successful in almost 70% of the patients with arterial insufficiency (n = 45) including the degree II B (painless walking-distance under 100 meters). Energetic phosphates, applied to the arteria femoralis, are most successful in degree II with claudication intermittens. Ancrod should be used respectively for patients with pain during rest. These results are discussed with respect to compensation and localization of arterial occlusive disease, acute and chronic measurements of the hemodynamics by use of Doppler ultrasound and strain gauge plethysmography and with respect to variation of the concentration of the metabolic parameters lactate and pyruvate--the latter when defibrination was performed.
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PMID:[Pharmacological treatment of chronic arterial occlusive disease (author's transl)]. 49 58

Ancrod is a purified coagulant venom which renders blood incoagulable by cleaving fibrinopeptide A (FPA) from fibrinogen, but the mechanism involved in the clearance of fibrin from the circulation is unknown. To investigate the fibrinolytic response to ancrod, and to increase understanding of clearance mechanisms, six patients with peripheral vascular disease causing claudication were infused with ancrod at 2 u/kg over 6 h followed by 2 u/kg at 12 h intervals for 38 h. Venous blood samples were taken at time 0, 3, 6, 25 and 49 h for assay of fibrinogen (Fbg), fibrinopeptide A (FPA), total fibrin(ogen) degradation products (TDP), fibrin degradation products (FbDP), fibrinogen degradation products (FgDP), cross-linked fibrin degradation products (XL-FDP), tissue plasminogen activator (tPA), urinary type plasminogen activator (u-PA), plasminogen, alpha 2 antiplasmin (alpha 2 AP) and plasminogen activator inhibitor-1 (PAI-1). Fibrinogen (median and range) was 2.3 (1.4-3.90) g/l at time 0 and thereafter was undetectable. FPA rose from 2.5 (1.8-3.6) to 600 and 188 pmol/l at 3 h and 6 h and remained elevated. TDP, FbDP and FgDP increased greatly following ancrod while there was no evidence of XL-FDP. The surprising increase in FgDP during defibrination suggests either that fibrinogen is digested following its incorporation into circulating fibrin protofibrils or that some of the fibrin subunits in the photofibril retain one of the two fibrinopeptide A's. tPA and uPA remained unchanged. Plasminogen fell from 125 (100-155)% to 79 (40-118)% at 49 h and alpha 2 AP fell from 91 (75-107)% to 24 (10-35)% at 49 h. The level of PAI-1 was depressed during defibrination, with the exception of the 6 h data. The results demonstrate that ancrod removes FPA from fibrinogen to produce non-cross-linked (soluble) fibrin. This is cleared from the circulation without evidence of an increase in the circulating activities of the plasminogen activators, tPA or UK, but with evidence of plasminogen activation and consumption.
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PMID:The fibrinolytic response to ancrod therapy: characterization of fibrinogen and fibrin degradation products. 845 76