In a group of 22 patients with second and third degree burns, seven were found to have impaired chemotaxis. The chemotactic defect was present from two to 68 days and eventually became normal. The impairment was found to be due to a primary transient defect in polymorphonuclear leukocytes and not to an inhibitor or inactivator in the serum.
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Fikrig et al. (1977) studied this question.
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