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- W20493609 abstract "Current evidence indicates that plasma fibrinogen is synthesized by the Jiver; that genetic and environmental factors regulate plasma fibrinogen levels; that interleukin-6 (IL-6) affects the synthesis of plasma fibrinogen by mechanisms involving protein kinase C, and that during the acute-phase response, monocytes generate a variety of monokines including IL-6. Certain drugs and nutrients have been reported to lower plasma fibrinogen levels. The mechanism(s) involved in this effect is poorly understood. However, since most of these substances quantitatively and/or qualitatively affect monocytes, the possibility that these drugs affect plasma fibrinogen levels via these cells should be considered. In addition to fibrinogen,IL-6 also regulatees the synthesis of other acute-phase proteins. Especially when combined, major risk factors for atherosclerosis cause vascular injury that triggers inflammatory events. This raises the issue of whether high plasma fibrinogen levels are just the epiphenomenon of as yet unknown events in thrombosis and atherosclorosis. Thus, the issue to be addresed is whether high plasma fibrinogen concentrations should be lowered or should they deserve to suggest strong interventions on established risk factors. As for other risk factors, fibrinogen measurements in population-bsed studies, in parallel with measurements of established risk factors will help define appropriate directions to be followed to gain insight into the issue and define new antithrombotic stratergies." @default.
- W20493609 created "2016-06-24" @default.
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- W20493609 date "1996-01-01" @default.
- W20493609 modified "2023-10-16" @default.
- W20493609 title "Drugs affecting plasma fibrinogen levels. Implications for new antithrombotic strategies" @default.
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- W20493609 doi "https://doi.org/10.1007/978-3-0348-8996-4_4" @default.
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