Prolonged impairment of polymorphonuclear cells functions in one infant with transient zinc deficiency: a case report.

Background: Zinc is an essential trace element for the immune system. The zinc deficiency diminishes antibody- and cell-mediated responses in man. Lymphopenia and thymic atrophy are usually the early hallmarks of zinc deficiency. Surprisingly, only scarce data are available about polymorphonuclear cells (PMNs) functions in infants with zinc deficiency. We present the results of immunological analyses in one infant with transient zinc deficiency due to decreased zinc concentration in mother milk resulting in severe lactogenic acrodermatitis enteropathica.
Material/methods: Nine repeated examination of oxidative burst of PMNs and immunoglobulin levels using nitroblue tetrazolium dye test, chemiluminescence, flow cytometry and nephelometry were performed in the infant with severe zinc deficiency during 28 months period.
Results: The unusual prolonged but transient impairment of PMNs respiratory burst accompanied with hypogammaglobulinaemia developed since the age of 2.5 months. Dramatic improvement of the skin was observed within days with total resolution of skin lesions on the 9th day of zinc therapy, but decreased PMNs respiratory burst persisted until the age of 23 months.
Conclusions: We conclude that zinc deficiency may lead to prolonged impairment of polymorphonuclear cells functions and hypogammaglobulinaemia.