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April 1977

Zinc Correction of Defective Chemotaxis in Acrodermatitis Enteropathica

Author Affiliations

From the Departments of Dermatology (Drs Weston, Huff, and Neldner), Pediatrics (Drs Humbert, Hambidge, and Walravens), and Biophysics and Genetics (Dr Humbert), University of Colorado Medical Center, Denver.

Arch Dermatol. 1977;113(4):422-425. doi:10.1001/archderm.1977.01640040030002

• 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.

(Arch Dermatol 113:422-425, 1977)