Abstract
To examine the possible correlation between mucocutaneous lymph node syndrome (MCLS) and thromboarteritis, we studied the capacity of polymorphonuclear leukocytes (PMNs) from 31 pediatric patients with MCLS to generate active oxygens (AO) and to release lysosomal enzymes. Cultured endothelial cells from human umbilical cord vein were also incubated with PMNs to assess AO-induced tissue. injury. Within five days of MCLS onset, AO production, except for chemiluminescence generation, was markedly increased and the 51Cr release from labeled endothelial cells was significantly elevated. The lysosomal enzyme release was slightly, but significantly, higher. In the presence of superoxide dismutase and catalase, the 51Cr release was reduced to the control level, indicating the specificity of the effect of AO endothelial cell damage. At more than six to seven days after MCLS onset, the PMN functions were normal or decreased and the 51Cr release was reduced. The grade of an increase in AO generation by PMNs from the patients with bacterial infections was lower than that from MCLS patients within five days of onset. Further PMNs from bacterial patients did not induce significant increase in 51Cr release from cultured endothelial cells. In view of reports that coronary occlusion may appear one week after MCLS onset, we suggest that in the early stage of MCLS, a marked increase in AO generation induced by activated PMNs gives rise to coronary vascular injury, possibly leading to thromboarteritis and aneurysm formation.
