If you have "a history of excessive clotting or clotting for no reasons" then a hematological work-up would be in order. But otherwise, he says it's not helpful or cost-effective.
Cece wrote:thanks, Cheer. If anyone investigated the right things, it was you. So you are saying that people with MS may have higher likelihood than normal people of having hypercoaguability. And we already know that if you have it, then it is a risk factor for increased clotting after the procecure.
I had a CBC done last winter, I'll have to go dig out the results and look it over again.
cheerleader wrote:(I believe hypercoagulation in pwCCSVI is due to the coagulation cascade initiated by diffuse cerebral hypoxia...but this is only a theory.)
Look to your SED rates, d-dimer, ESR...see if there's anything out of range. Simply having MS means that you will most likely have have higher levels of fibrin in your blood, higher inflammation and this will cause hypercoagulation.
patientx wrote:Look to your SED rates, d-dimer, ESR...see if there's anything out of range. Simply having MS means that you will most likely have have higher levels of fibrin in your blood, higher inflammation and this will cause hypercoagulation.
My SED rate was completely normal.
eric593 wrote:patientx wrote:Look to your SED rates, d-dimer, ESR...see if there's anything out of range. Simply having MS means that you will most likely have have higher levels of fibrin in your blood, higher inflammation and this will cause hypercoagulation.
My SED rate was completely normal.
Me too. Is there research that shows that MSer's 'most likely' have higher levels of fibrin? If this were so, it would increase the risks of angio and/or stenting for MSer's - if that were so - why aren't ALL MS angio patients being put on the likes of comoudin, heparin or warfarin? Wouldn't one of the treating doctors have reported this by now since it changes medications given after angio to prevent coagulation and the risk factors of the treatment itself? Wouldn't they be instituting pre-testing of levels beforehand if hypercoagulation is "most likely" in MSer's?
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system and is the most common cause of neurologic disability in young adults. In this study, the coagulation status and biochemical and non-specific inflammatory markers in patients with MS were investigated. Plasma prothrombin time, activated partial thrombin time, fibrinogen, D-dimer, serum high sensitive C-reactive protein, homocysteine, blood urea nitrogen, creatinine, calcium, total protein, albumin, total cholesterol, vitamin B12, folate levels and erythrocyte sedimentation rate were measured in 42 patients with MS and 31 healthy subjects as a control group. There was a positive correlation between homocysteine and D-dimer levels (r=0.84, p<0.01). However, there was no significant correlation between homocysteine, vitamin B12 (r=0.18) and folate (r=0.23) levels. Serum total protein, albumin and calcium levels of MS patients were lower than the control group. There are some alterations in the coagulation and biochemical status in MS patients. These findings may contribute to better understanding of the etiopathogenesis and clinical characteristics of this disease.
Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium (lining of the vessel). Exposure of the blood to proteins such as tissue factor initiates changes to blood platelets and the plasma protein fibrinogen, a clotting factor. Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously: Proteins in the blood plasma, called coagulation factors or clotting factors, respond in a complex cascade to form fibrin strands, which strengthen the platelet plug.
Fibrin, as the final product of the coagulation cascade, plays a major role in blood clotting. However, the role of fibrin is not restricted to the blood, since components of the coagulation cascade reside within tissues and can stimulate extravascular fibrin formation (1). Studies of fibrin deposition in human diseases (2-5), in combination with experiments from gene-targeted mice deficient in fibrin (6), have shown that a wide range of pathological conditions, such as glomerulonephritis, lung ischemia, and rheumatoid arthritis, are exacerbated by fibrin deposition.
Compromised vasculature in the nervous tissue is a pathogenic manifestation apparent in traumatic injuries, such as spinal cord, optic nerve, and sciatic nerve injury, as well as in central nervous system (CNS) diseases with autoimmune characteristics, such as multiple sclerosis (MS) (7). Blood-brain barrier (BBB) disruption precedes clinical symptoms in MS patients , and fibrin is deposited in the lesions (9, 10), apparently before cerebral tissue injury and demyelination (11). Fibrin deposition also coincides with areas of demyelination (12), as well as with areas of axonal damage (13). In addition, in experimental autoimmune encephalomyelitis (EAE), an autoimmune animal model of MS, there is increased coagulation activation before symptom development (14). Pharmacologic depletion of fibrin in EAE ameliorates clinical symptoms, suggesting that fibrin plays a role in CNS inflammatory demyelination (15, 16). Furthermore, inhibition of fibrin formation by attenuation of thrombin activity is protective in the injured optic nerve (17).
MS is closely related to antiphospholipid syndrome, which became a differential diagnosis in the 1980s when Dr. Hughes detected APS.
MaggieMae wrote:My husband is on a list for treatment for CCSVI. He and his sister have MS. His niece was diagnosed with antiphospholipid syndrome. His neurologist doesn't believe in CCSVI. Should we see his GP and ask for specific tests before angioplasty treatment?
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