Resistance to activated protein C is a congenital inherited hypercoagulable disease. The problem here is that normally protein C with a co-factor of protein S controls the activity, if you will, down the coagulation pathway starting with number 11, then 12, 9, 8 and so on as the cascade moves down. This system here normally protein C co-factor S inactivates number 5 and number 8 coagulation factor proteins. They are kind of keeping a balance here to prevent ongoing conversion of soluble fibrinogen to insoluble fibrin. That’s the whole idea of this system.
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We see here that here is factor V and normally this undergoes degradation. But in resistance to activated protein C there is at position 506 in the factor V molecule, arginine moiety is replaced by glutamine, and this is what identifies this. The factor V gene also has an abnormality in it at position 1691. The factor V at 506, the factor V molecule, this arginine is replaced by a glutamine, it’s resistant now to the normal degradation of activated protein C, and the factor V gene here at 1691 a glutamine is replaced by an arginine with a single point mutation.
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This problem is variously reported in different articles and publications to be at a frequency rate in some places of 30, 40, 50, 60% of the populations that are studied. However you and I all know that thrombosis is not in any way shape or form found in that frequency. So one must be somewhat concerned about this and the absolute direct connection that it may have. This may not always really be the answer for this situation, but of the things that you can look for today, it’s certainly going to be high on the list for an etiologic or diagnostic test that can be done. So don’t forget about this population of resistance to activated protein C. The presence of the factor V Leyden molecule, which does not undergo normal degradation as it should, by protein C with a co-factor of protein S.
Feb 06
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