Zinc correction of defective chemotaxis in acrodermatitis enteropathica.
Three patients with acrodermatitis enteropathica (AE), a disorder of zinc metabolism, demonstrated a zinc-responsive defect in chemotaxis of neutrophils and monocytes. Monocyte chemotaxis was depressed during a controlled period of zinc deficiency and increased to normal values after administration of oral zinc sulfate supplements that was sufficient to restore normal plasma zinc levels. In the only patient in whom neutrophils were also studied, a similar defect in chemotaxis of neutrophils was corrected by administration of zinc sulfate supplements. Preincubation of defective cells in vitro with zinc sulfate increased chemotaxis in an almost linear dose-response relationship. These findings suggest an important role for zinc in neutrophil and monocyte chemotaxis and demonstrate a correctable immune defect in AE.
D000169:Acrodermatitis / Q000188:drug therapy / Q000276:immunology*; D000328:Adult; D002634:Chemotaxis, Leukocyte / Q000187:drug effects*; D002648:Child; D002675:Child, Preschool; D005260:Female; D006801:Humans; D008297:Male; D009000:Monocytes / Q000276:immunology; D015032:Zinc / Q000008:administration & dosage* / Q000097:blood
D015032:Zinc