BACKGROUND: Microparticles (MPs) are increased in diseases characterised by endothelial injury. Kawasaki disease (KD) damages the endothelium provoking life-threatening involvement of coronary arteries. OBJECTIVES: To compare KD MPs vs. controls. METHODS. Thirty KD and 20 controls were enrolled. MPs were stained with monoclonal antibodies against platelets, endothelial cells (EC), monocytes, T and B cells, neutrophils, and quantified by FACS. RESULTS: The total number of MPs was significantly increased in KD versus controls (193x105±0.6x105 vs. 94x105±0.9x105 million/ml plasma p=0.01) and vs. KD after IVIG therapy (132x105±0.4x105million/ml plasma p=0.01). EC and T cells were the major source of MPs in KD (72x105±1x105 vs. 3x105±0.9x105million/ml plasma for T cells p=0.005; 76x105±0.7x105 vs. 45x105±0.4x105 million/ml plasma for EC p<0.02) followed by MPs derived from platelets (13x105±0.3x105 vs. 3x105±0.9x105 million/ml plasma p=0.028). Cell-derived MPs B were 17x105±0.4x105 vs. 20x105±0.8x105million/ml plasma in controls (p=0.7). No significant differences were observed in KD MPs derived from monocytes and neutrophils. After IVIG administration, a significant decrease of MPs derived from platelets (3x105±0.2x105 million/ml plasma p=0.03), EC (9x105±0.4x105 million/ml plasma p=0.01), T cells (72x105±1x105 million/ml plasma p=0.02) and B cells (7x105±0.3x105 million/ml plasma p=0.02) was observed. CONCLUSIONS: The number of KD MPs is significantly increased and EC and T cells are the major source. MPs may develop from endothelial damage and cell activation. Their role as markers of disease activity or as contributors to endothelial derangement in KD has to be further investigated.
BACKGROUND: Microparticles (MPs) are increased in diseases characterised by endothelial injury. Kawasaki disease (KD) damages the endothelium provoking life-threatening involvement of coronary arteries. OBJECTIVES: To compare KD MPs vs. controls. METHODS. Thirty KD and 20 controls were enrolled. MPs were stained with monoclonal antibodies against platelets, endothelial cells (EC), monocytes, T and B cells, neutrophils, and quantified by FACS. RESULTS: The total number of MPs was significantly increased in KD versus controls (193x105±0.6x105 vs. 94x105±0.9x105 million/ml plasma p=0.01) and vs. KD after IVIG therapy (132x105±0.4x105million/ml plasma p=0.01). EC and T cells were the major source of MPs in KD (72x105±1x105 vs. 3x105±0.9x105million/ml plasma for T cells p=0.005; 76x105±0.7x105 vs. 45x105±0.4x105 million/ml plasma for EC p<0.02) followed by MPs derived from platelets (13x105±0.3x105 vs. 3x105±0.9x105 million/ml plasma p=0.028). Cell-derived MPs B were 17x105±0.4x105 vs. 20x105±0.8x105million/ml plasma in controls (p=0.7). No significant differences were observed in KD MPs derived from monocytes and neutrophils. After IVIG administration, a significant decrease of MPs derived from platelets (3x105±0.2x105 million/ml plasma p=0.03), EC (9x105±0.4x105 million/ml plasma p=0.01), T cells (72x105±1x105 million/ml plasma p=0.02) and B cells (7x105±0.3x105 million/ml plasma p=0.02) was observed. CONCLUSIONS: The number of KD MPs is significantly increased and EC and T cells are the major source. MPs may develop from endothelial damage and cell activation. Their role as markers of disease activity or as contributors to endothelial derangement in KD has to be further investigated.