[Reduced "oxidative burst" in a granulocyte subpopulation in a case of Sweet syndrome]

Oxidative burst was defective in 50% of peripheral blood neutrophils in a case of Sweet syndrome with leukemoid granulocytosis. Phagocytosis was normal. We suggest that the decreased ability to produce oxygen radicals observed in this patient might lead to a compensatory recruitment of hematopoietic growth factors. Consecutive activation, increased chemotaxis and adhesion of polymorphonuclear granulocytes might be the cause of the neutrophilic dermal infiltrate of Sweet syndrome.