Table 1.

Studies evaluating the effect of the available anti-inflammatory agents on platelet activation parameters.

Study	Agent	Population	Findings
Di Sabatino et al. [165]	Infliximab	IBD	↓ TX biosynthesis ↓ sCD40L
Manfredi et al. [86]	Anti-TNF-α	RA	↓ platelet-leukocyte and platelet-monocyte aggregates ↓ P-selectin
Menchen et al. [166]	Infliximab	CD	↓ sCD40L Non-significant reduction of the enhanced binding of FITC–fibrinogen
Padfield et al. [157]	Etanercept	AMI	Non-significant effects on platelet activation parameters
Nielsen et al. [158]	Adalimumab	In vitro	↑ TRAP-induced platelet aggregation ≥20%
	Tocilizumab		↓ ADP- and collagen-induced platelet aggregation ≥20%
Canzano et al. [128]	Tocilizumab	COVID-19 (in vitro)	↓ P-Selectin ↓ Platelet-granulocyte and platelet-neutrophil aggregates
Shah et al. [159]	Colchicine	Healthy	↓ P-Selectin and PAC-1 ↓ Platelet-granulocyte and platelet-neutrophil aggregates No effect on homotypic platelet aggregation
Cirillo et al. [162]	Colchicine	CAD	↓ TRAP-induced platelet aggregation
Cimmino [163]	Colchicine	CAD (in vitro)	ADP/Collagen/TRAP-induced platelet aggregation due to cytoskeleton reorganization
Pennings [164]	Colchicine	Healthy (in vitro)	↓ P-Selectin ↓ collagen-induced platelet aggregation
DeSena et al. [167]	Canakinumab	Case of epilepsy	Downregulation of genes associated with platelet activation

TX: thromboxane, sCD40L: soluble cluster of differentiation 40 ligand, FITC: Fluorescein isothiocyanate, AMI: acute myocardial infarction, TRAP: Thrombin Activating Receptor Peptide, ADP: adenosine diphosphate. ↓ indicates decreased and ↑ indicates increased