DMB March 2010

March 2010 Newsletter

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FEATURE ARTICLE

Fibrinolysis 202: Dissolve that Fibrin

by David Berg

Fibrin formation has many useful functions, especially when you cut or injure yourself. Sealing a wound via cross-linked fibrin (a scab or blood clot) is a routine function of the coagulation system and may result in an inflammatory response. The degree of response depends on the level of trauma and potential exposure to pathogens.

Similarly when a body is exposed to pathogens (viral, bacterial, fungal, etc), fibrin formation occurs to wall off pathogens and keep an infection localized. Then when the infection is contained and cleaned up by the immune system, the fibrinolytic system goes to work to dissolve the fibrin and debris of the wound.

Problems occur when there are defects in the proteins of the coagulation system. This may be in the clotting and/or fibrinolytic proteins. Thrombophilic defects allow the body to clot too easily or quickly, while fibrinolytic defects prevent the cleanup of fibrin and may allow a small amount of fibrin to grow into a blood clot.Fibrin formation is the conversion of fibrinogen into soluble fibrin strands by the enzyme thrombin(factor IIa). A burst of thrombin activates factor XIII, which cross-links soluble fibrin strands into insoluble fibrin, a.k.a., a blood clot.

The break down of a clot can be measured using the Quantitative D-Dimer (QDD) test in the laboratory. Elevated D-dimer results show the presence of a clot that is being broken down. Kinase therapy can help dissolve fibrin as previously discussed in Fibrinolysis 101, Part II (DMB 2009 September issue). Dosing of lumbrokinase (Boluoke) is based on the Alpha-2-AntiPlasmin (A2AP) assay.

There are two special quantitative tests that give a clear picture of the current status of the clotting and fibrinolytic states in a patient. Prothrombin Fragment 1+2 (F1+2) is an activation peptide that is cleaved from prothrombin when it is converted to thrombin. Elevated F1+2 values show current coagulation activation and thrombin generation. When thrombin is generated, AntiThrombin (AT) binds with thrombin to control its generation. This forms Thrombin/AntiThrombin (TATs) complexes, which are removed from the blood in the liver.

When thrombin is generated (increased F1+2), the TATs should be elevated. This is the normal way to control thrombin generation, a normal physiological state. When the F1+2 is elevated and the TATs are normal, this is evidence of the lack of fibrinolysis. The lower the TATs, the worse the fibrinolysis. Good fibrinolysis should be above a 2.0 value.

These two tests, F1+2 and inside TATs, can aid a clinician to decide whether or not to use anticoagulant
therapy (low dose heparin) and/or kinase therapy to encourage fibrinolysis.

NOTE: A PDF file of coagulation pathways, F1+2 & TATs interpretation and therapy guidelines are available by sending a request for the file to davidberg@azrf.org.

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BIO

David E. Berg, MS, CLS(NCA), FAHA was the director Arizona Coagulation Consultants (ACC) and HEMEX Laboratories in Phoenix, Arizona for 25 years. HEMEX performed special coagulation testing
throughout North America. This led to new findings about chronic illnesses, fibrin deposition in these illnesses, and low level coagulation activation. A frequent workshop moderator and speaker, Mr. Berg’s research has been published in leading journals. He now consults with clinicians and patients through ACC.

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Dragon's Medical Bulletin

FEATURE ARTICLE

Fibrinolysis 202: Dissolve that Fibrin

by David Berg

BIO