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PostPosted: Sun Nov 07, 2010 9:18 am 
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The reduction of MS relapses in preganancy is a well documented phenomenon and the reasons for it are not known. I propose that it is secondary to increased fibrinolytic activity during pregnancy. Fibrinolytic activity is the bloods ability to break down fibrin. I a prevous post, I explain how fibrin may be key in the development of MS symptoms and lesions. http://www.thisisms.com/ftopict-14475.html

One measure of fibrinolytic activity is the level of fibrin degradation products (FDP) in the blood. Logically, FDP should be increased in states of increased fibrinolysis as fibrin is broken down into its degradatation products. This is exactly what was shown in the following study; ‘”Prospective, sequential, longitudinal study of coagulation changes during pregnancy in Chinese women " (Xing-hui et al., International Journal of Gynecology & Obstetrics,Vol 105, Issue 3, June 2009).

http://www.ncbi.nlm.nih.gov/pubmed/19342052

Fibrin degradation products were shown to increase progressively in pregnancy and decreased post partum. Consistent with these finding is another phenomenon during pregnancy, the progressive increase in D-dimer levels. D-dimer is another product of the breakdown of fibrin.

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PostPosted: Sun Nov 07, 2010 9:25 am 
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I need to understand fibrin before I can understand some of this. I will work on that. But another piece of the puzzle with pregnancy is that there are many circulatory system changes during the pregnancy included a marked increase in blood volume.


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PostPosted: Sun Nov 07, 2010 9:50 am 
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Last edited by Lyon on Sun Nov 20, 2011 5:26 pm, edited 1 time in total.

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PostPosted: Sun Nov 07, 2010 10:37 am 
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Last edited by LR1234 on Tue Mar 06, 2012 8:28 am, edited 1 time in total.

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PostPosted: Sun Nov 07, 2010 10:53 am 
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I thought it was contradictory initially as well. But after a bit of thought it wasn't. Here's my reasoning:

What I stated was that there was active fibrinolysis in pregnancy. I suspect this happens in the small vessels where fibrin is formed and results in fewer ms lesions and symptoms. During fibrinolysis plasminogen gets converted to plasmin which is its active form. Plasmin then complexes with fibrin to degrade it. What is happening here is that plasminogen is being used up in the small vessels. The result is that in the larger vessels, plasminogen levels are very low (because it it used up in the small vessels) and blood will therefore clot too easily as fibrinloysis will not be able to take place in the larger vessels. This predisposes to clotting of the larger vessels in pregnancy. I think this is how you can have very active fibrinolysis in pregnancy but still be hypercoagulable and require heparin. Make sense?

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PostPosted: Sun Nov 07, 2010 12:59 pm 
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Besides the increased blood volume I think pregnancy causes vasodilation.

An IR I spoke with about blood vessels in pregnancy said that the veins get bigger and in some people that makes it so the valves can't shut like they should. They get too far apart. He was talking about varicose veins, but the same thing should apply to the rest of the veins in the body you would think?

MS doesn't always get better during pregnancy :(


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