Abstract
Platelets play a pivotal role in both hemostasis and thrombosis. Increased platelet
volume has several etiologies and may be secondary to a genetic variant, platelet
activation, increased platelet turnover, or in response to inflammatory stimuli. There
are several hereditary syndromes in which an increased mean platelet volume (MPV)
occurs in association with a reduction in platelet number and function. An acquired
increase in platelet size is often associated with increased platelet reactivity,
shortened bleeding time, and increased platelet aggregation. Many studies have shown
that high MPV is associated with increased risk of venous and arterial thrombosis,
but genome-wide association analyses found a weak inverse association between the
risk of coronary heart disease and MPV. The disease associations of MPV suggest that
it could provide a useful contribution to risk assessment algorithms for both venous
thromboembolism and arterial thrombosis. However, owing to the problems associated
with reliably assessing MPV, it does not yet constitute a practically useful biomarker
for this purpose. Before MPV can be adopted for wider clinical use, the methodological
problems involved in obtaining accurate and interlaboratory comparable results must
be resolved. In particular, a major degree of standardization is required, as are
local reference ranges calculated with respect to specified time intervals from venipuncture
to laboratory analysis. We discuss here the potential role of MPV in predicting the
risk of acquired thrombotic disorders in addition to roles in congenital thrombocytopenic
disorders, as well as the problems and pitfalls associated with use of MPV in these
settings.
Keywords
platelets - mean platelet volume - thrombosis - quality control - standardization
