CRP and autoimmune thrombocytopenic purpura: C-reactive protein is markedly upregulated during acute infections and inflammation (178), and it has been shown that C-reactive protein, via binding to platelet phosphorylcholine residues, enhanced the IgG-mediated phagocytic responses against platelets and thereby thrombocytopenia, which has implications in the pathogenesis of both ITP and FNAIT (123, 124).