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These observations suggest that the loss of endothelial cell antithrombotic function combined with the induction of a procoagulant state may contribute to the vascular disorders linked to moderate hyperhomocysteinemia
No specific safety data could be identified
8 essential labs with optimal ranges and testing schedule
The reduction in SAM tissue concentrations resulting from the altered homocysteine remethylation might be compensated for by the increase in SAM synthesis with the methionine supply (Miller et al, 1994a)
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