Serum interleukin-1 and granulocyte-macrophage colony-stimulating factor levels in protein malnourished patients during acute infection.

OBJECTIVE

To investigate the response of serum interleukin-1 (IL-1) and granulocyte-macrophage colony-stimulating factor (GM-CSF) to infection of malnourished patients.

DESIGN

Prospective observational study.

SETTING

Paediatric clinics of Karadeniz Technical University, Faculty of Medicine, Trabzon, Turkey.

SUBJECTS: 13 protein-depleted (kwashiorkor marasmic kwashiorkor), 15 marasmic nutritionally repleted kwashiorkor (NRK), and 12 well-nourished control subjects.

INTERVENTIONS: Clinical and laboratory data, and serum IL-1 and GM-CSF levels during acute infections were examined.

MAIN OUTCOME MEASURES: White blood cell count, pc of circulating neutrophils (%PNL), serum total protein, albumin (ALB), IL-1 and GM-CSF levels.

RESULTS

Fever, pcPNL, serum IL-1 and GM-CSF levels of kwashiorkor patients were lower than those of marasmic and control patients (p < 0.005). Fever, neutrophil pc(PNLpc), serum IL-1 and GM-CSF levels of NRK patients during further acute infection were not significantly different from those of marasmic and control patients, but higher than those of the kwashiorkor patients. Although there were positive correlations between serum IL-1 and ALB levels (r = 0.922, p < 0.001), and between serum GM-CSF and ALB levels (r0.730, p = 0.005) in the kwashiorkor group, there were not significant correlations between the same parameters in the other groups (r < 0.5, p > 0.05). And also, although there was not significant correlations between PNL% and IL-1 levels in the kwashiorkor group (r0.312, p = 0.299), there were significant positive correlations between the same parameters in the other groups (r < 0.5, p > 0.05). However, significant positive correlations were found between fever and IL-1 levels, and between IL-1 and GM-CSF levels in all groups (r > 0.5, p < 0.05).

CONCLUSION

The responses of serum IL-1 and GM-CSF to acute infection of kwashiorkor patients are defective, and nutritional-repletion therapies restore the production of these cytokines.