Serum zinc response in thermal injury.

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Abstract
Zinc is an essential trace element required for RNA and DNA synthesis and the function of over 200 zinc metalloenzymes. After surgery or trauma, the serum zinc concentration usually decreases. The magnitude and duration of this hypozincemia after thermal injury are unclear, as are mechanisms for this hypozincemia. In this study we evaluated, over the duration of their hospital course, serum zinc concentrations in 23 thermal injury patients. The initial mean serum zinc concentration was significantly depressed (42 +/− micrograms/dl; normal 66-110 micrograms/dl). By the second week of hospitalization, serum zinc concentrations gradually increased into the normal range in the majority of patients. Mechanisms for this hypozincemia were evaluated. Decreases in the serum zinc concentration did not correlate with increased urinary zinc excretion; thus increased urinary zinc excretion was an unlikely mechanism for the observed hypozincemia. Values for albumin, the major zinc binding protein in serum, generally were inversely correlated with the serum zinc concentration. Thus, hypoalbuminemia could not explain the decreased serum zinc concentration. Certain cytokines such as interleukin-1 are known to cause a decrease in the serum zinc concentration as part of the acute phase response. Therefore, we measured serum C reactive protein concentrations as an indicator of the acute phase response. Thermally injured patients initially had markedly elevated C-reactive protein levels which gradually decreased during hospitalization. We suggest that the initial hypozincemia observed in thermally injured patients may be a reflection of interleukin-1 mediated acute phase response. Whether one should vigorously attempt to correct this initial marked hypozincemia requires further investigation.