Fecal calprotectin correlates closely with the best invasive measures of colonic and small bowel inflammation in childhood inflammatory bowel disease. As a sensitive objective measure of bowel inflammation that is risk-free and noninvasive, fecal calprotectin lends itself particularly to the monitoring of and assessment of therapeutic interventions in children with inflammatory bowel disease.

The S-100 Ca2+ binding protein, calprotectin, isolated from neutrophil lysates, has been reported to exhibit zinc reversible biostatic activity in vitro. We verified these findings with C. albicans and investigated whether the growth inhibition resulted from zinc deprivation due to chelation by calprotectin. Calprotectin concentrations of 250 micrograms/ml significantly inhibited the growth of C. albicans. This was reversed by supplementing culture medium with 10 microM ZnSO4. Incubation of calprotectin in culture medium for 24 h prior to inoculation significantly reduced the minimum inhibitory concentration. When this latter medium was ultrafiltered to remove the calprotectin and then inoculated with C. albicans, significant growth inhibition was still present: again it was reversed by zinc. These findings implicate zinc chelation as a novel, potentially important host defence function of an abundant neutrophil protein.

Fecal calprotectin seems to reflect bowel inflammation in children with IBD. As a simple, safe, noninvasive test, it has the potential to reduce the number of invasive investigations performed in these children.

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Children recovering from severe malnutrition on a milk based diet have low plasma zinc concentrations: children recovering on a soya based diet have much lower plasma zinc concentrations, lower rates of weight gain, and higher energy costs of tissue deposition. However, they do not demonstrate the clinical features of anorexia, diarrhea, and skin lesions usually associated with zinc deficiency. We therefore supplemented 16 children with zinc acetate on the basis that a therapeutic response to zinc constitutes the best evidence of a preexisting zinc deficiency. Fourteen of the 16 children had an immediate and definite increase in their rate of weight gain with zinc supplementation. This was associated with a decrease in the energy cost of tissue deposition, regrowth of the thymus, and activation of the sodium pump. We conclude that the children were indeed zinc deficient. We suggest that the anorexia of zinc deficiency is related to an inability to metabolize nitrogen in the zinc deficient state, and that our children did not show an appetitive response because of the relatively low protein content of the diets we used. Based on the premise that the abnormalities seen in our children may have been secondary to mild zinc deficiency, we suggest that limitation of lean tissue synthesis, with resultant obesity, and a propensity to infection are the major features of a mild zinc deficiency. Children undergoing a period of "catch up" weight gain or growth should have supplemental zinc, particularly if they have had diarrhea or if the use of a soya based formula is contemplated.

Calprotectin is an abundant neutrophil cytosolic protein released during neutrophil activation or death.

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