Platelets are intimately involved in hemostasis, inflammation, innate and adaptive immunity, tissue regeneration and other
physiological and pathological processes. Their granular structure is programmed to release a wide range of bioactive substances in response
to agonists. Upon activation, platelet membranes display thrombotic and inflammatory agents, which may take an active part in
the pathophysiology of autoimmune and autoinflammatory disorders.
The aim of this review is to analyze current evidence of platelet (dys)function in inflammatory rheumatic diseases and overview platelettargeting
mechanisms of antirheumatic drug therapies.
A comprehensive search through Medline/PubMed, SciVerse/Scopus and Web of Science was performed for English-language original
research papers, using the keywords related to platelets in autoimmune and autoinflammatory rheumatic disorders. Additionally, the
Cochrane Collaboration database was searched for the literature on the effects of antirheumatic drugs on platelet function.
A variety of platelet markers have been tested in systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, spondyloarthropathies,
vasculitides, and some autoinflammatory disorders. It has been shown that platelets circulate in an activated state in most
of these disorders and tend to form complexes with other inflammatory and immune cells. Thrombotic and inflammatory agents, released
from platelets, may trigger disease-specific complications (e.g., extraarticular features, fibrosis in systemic sclerosis) and propagate endothelial
dysfunction. Whether platelet activation is a primary or secondary feature in rheumatic disorders remains to be elucidated. Some
widely used antirheumatic drugs may suppress thrombopoiesis and platelet activity, however the clinical implications of this effect have
yet to be examined in specifically designed prospective studies. Large retrospective cohort studies supported the use of low-dose aspirin
for suppressing platelet function and preventing cerebrovascular events in giant-cell arteritis. However, emerging data suggest that the release
rate of activated platelets applied topically to the inflamed cartilage in arthritis or skin ulcers in scleroderma may suppress the inflammation
and facilitate tissue repair. Taken together, current evidence necessitates a balanced approach to platelet-activating and suppressing
drug therapies in inflammatory rheumatic diseases.