In Reply.—We thank Drs Özsoylu and Akgün tor bringing attention to our results on the defect of neutrophil motility in children with chronic liver disease. We draw attention to the existence of the defect of chemotaxis also in children without liver cirrhosis: this was evident for children with hepatitis B virus chronic hepatitis, who showed impaired chemotaxis despite the inflammatory activity of the disease, the presence of cirrhosis, and active replication of virus. Moreover, neutrophil chemotaxis of children with biliary atresia was normal despite severe cholestasis, cirrhosis, portal hypertension, and liver insufficiency. Perhaps the problem is in a deficit of some serologic factors, as suggested by Drs Özsoylu and Akgün, which can occur in some patients but not in others. Zinc is involved intricately with numerous enzyme activities and with stability and permeability of biomembranes.1 It is possible that a deficit of the intracellular zinc, as well as other oligoelements and
GIACOMO CD, SACCHI F, MAGGIORE G. Defective Neutrophil Motility-Reply. Am J Dis Child. 1985;139(1):10–11. doi:10.1001/archpedi.1985.02140030012008
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