From Journal of Neuroinflammation
Antiphospholipid Antibodies: Paradigm in Transition
Posted 03/18/2009
Lawrence L Horstman; Wenche Jy; Carlos J Bidot; Yeon S Ahn; Roger E Kelley; Robert Zivadinov; Amir H Maghzi; Masoud Etemadifar; Seyed Ali Mousavi; Alireza Minagar
http://www.medscape.com/viewarticle/587338_1
ACMS is an inflammatory disorder believed to be autoimmune in etiology, and can present with features resembling APS.[294-297] Several reviews of the neurological symptoms of APS/SLE are available,[298-300] and many case reports, e.g., cerebral ischemia.[301] However, MS is not thought to involve ischemia, although elements of the coagulation cascade are present in MS lesions, including fibrinogen and recently, tissue factor and protein C inhibitor.[302]
In 2000, our collaborative investigation demonstrated elevated endothelial microparticles (EMP) during exacerbations of MS.[303,304] Those findings motivated further investigations, this time of aPL in MS, with the hypothesis that aPL might be involved in endothelial activation in MS. Several prior reports had established that aPL commonly occur in MS, but in most of them the patient population was heterogeneous or inadequately defined, and there was no indication of a relation between aPL and the pathophysiology of MS.
To examine the relationship more closely, we tested samples of well-defined, treatment-naive MS patients in either exacerbation or remission, documented by neurological as well as brain MRI with and without contrast. The central finding was that all aPL measured were significantly elevated in acute phases vs. remission, and correlated strongly with MRI imaging, p = 0.002.[136] The antigens tested included β2GPI, FVII, and four pure PL (CL, PC, PS, PE). Of interest, aFVII was never detected in remission but was present in 60% of acute MS; and anti-β2GPI was positive in 80% of acute MS. It is possible that unidentified and possibly MS-specific auto antibodies were also present, judging by the strong reaction to the pure PL in acute, but not remission, cases. Unexpectedly, aPL in MS were exclusively of IgM class, with no IgG detected.
Because that work showed a direct relation between aPL and clinical state in MS, it is plausible to suspect that aPL may be involved in the pathogenesis of MS. Of course, the possibility exists that aPL in acute MS are epiphenomenal; but the same argument could be levelled against the hypothesis that aPL cause thrombosis. In further support, Shoenfeld and colleagues clearly demonstrated neuropathological effects of aPL in animal models.[305-307]
Since some aPL have been identified with anti-endothelial (anti-EC) antibodies (earlier cited), and since our group[303] and others have documented endothelial activation in MS, it is relevant to note that anti-EC have been detected in MS and were proposed to contribute to its pathogenesis. In 1989, Tsukada et al. found anti-EC in 75% of active MS but in only 4% of remission.[308] However, a 1992 report found only 13% positive[309] and a later report found only 10% reactive to human umbilical vein EC (HUVEC).[310] On the other hand, another report around the same time, but using brain microvascular EC rather than HUVEC, found that 12/16 active vs 0/15 inactive MS reacted to EC.[311] This suggests that anti-EC in MS are specific for brain microvessels, and would be consistent with the fact that CNS lesions in MS tend to develop around brain microvessels (Dawson fingers).[312] Thus, brain-specific anti-EC could be a pivotal pathogenic mechanism of aPL in MS.
The picture now emerging is that aPL are part of a large spectrum of autoantibodies, including, for example, those of ITP, and that APS is just one manifestation of a particular constellation of aPL. We may be better served by abandoning the concept that aPL are exclusively thrombogenic.
In regard to the cause of aPL-associated pathologies, a promising hypothesis is dysregulation of anti-idiotype networks. Many of the consequences appear to be best explained in terms of complement-mediated effects. However, full understanding of the aPL phenomenon remains a challenge for the future.
My point was if you have one finding rather than 2 you still have evidence of a venous problem as Zamboni describes it and you and your doctor may want to talk about venograms 
fingers crossed! 
