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Are platelet factor 4 and beta-thromboglobulin markers of cardiovascular disorders?
Beta-thromboglobulin and platelet factor 4 are the two best characterized platelet-specific proteins. They are stored in the platelet alpha-granules and released during platelet activation. Their physiological function is unknown. PF4 has high anti-heparin activity, whilst beta-TG does not. Certain factors can affect the plasma level of one or both of these two proteins and these must be borne in mind whenever the evaluation of beta-TG and PF4 are thought to represent true in vivo platelet activation: their artificial release due to sample collection and processing, the in vivo release of PF4 induced by heparin, and the elevation of beta-TG due to renal failure. What really represents an abnormal level of beta-TG and PF4 is unknown, since we do not know their pathophysiology. At present, however, the platelet-specific proteins, even if they are considered as 'markers' of platelet activation, do not necessarily reflect the severity of the cardiovascular disorders nor do they signal thrombus formation, as thrombosis is a consequence of several interacting factors.
Beta-thromboglobulin and platelet factor 4 are the two best characterized platelet-specific proteins. They are stored in the platelet alpha-granules and released during platelet activation. Their physiological function is unknown. PF4 has high anti-heparin activity, whilst beta-TG does not. Certain factors can affect the plasma level of one or both of these two proteins and these must be borne in mind whenever the evaluation of beta-TG and PF4 are thought to represent true in vivo platelet activation: their artificial release due to sample collection and processing, the in vivo release of PF4 induced by heparin, and the elevation of beta-TG due to renal failure. What really represents an abnormal level of beta-TG and PF4 is unknown, since we do not know their pathophysiology. At present, however, the platelet-specific proteins, even if they are considered as 'markers' of platelet activation, do not necessarily reflect the severity of the cardiovascular disorders nor do they signal thrombus formation, as thrombosis is a consequence of several interacting factors.