| Objective: Infectious illnesses was a kind of important illnesses that do harm to children health. When a child was caught by this illness, his body would manifest a high catabolic state, such as, protein was acceleratly degraded, energy was heavily consumed, and sugar metabolism was disordered, so that negative nitrogen balance was formed. The serious infection would do harm to some parenchymal organs, and cause such as muscle wasting and body weight loss, evencachexia. The result is resistance of patient was cut down, and recovery was delayed. Growth retardation has been described in children suffering from chronic infectious illnesses. In order to explore mechanism which caused these alteration, people had done many researches, and found that reduced caloric intake couldn't solely explain negative nitrogen balance. Alteration of IGF axis had participated in metabolic mediation in infectious state, and there were GH resistance and IGF inhibition existed in infectiousperiod. Several lines of evidence support the role of proinflammatory medium, such as, tumor necrosisfactor(TNF-a ) etc, as putative mediators in many of the metabolic manifestations observed during infectiousillnesses. Endotoxemia and inflammation have been demonstrated to increase circulating concentration and/or to enhance expression of these inflammation cytokines, and through which activated thehypothalamic-pituitary-adrenal axis and increasedglucocorticoid secretion. These factors all participated in the inhibition of IGF axis. There was no report about alteration of IGF axis in different periods of children infectious illnesses, we had designed this experiment whose purpose was to explain alteration of IGF axis in children infectious illnesses.Methods: Serum levels of IGF-I and IGFBP-3 were respectively determined by radioimmunoassay and immunoradiometric assay. Infectious group included 30 cases ?of acute phase and 10 cases of convalescent, control group included 30 cases. Serum levels of TNF- a was determined by immunoenzymometric assay. Infectious group included 24 cases of acute phase, the others were the same as what were determined in IGF-K IGFBP-3.Results: concerning infectious group, serum levels of IGF-I(44.975+14.809) u g/ml in acute phase of infection were markedly decreased, there were significantly different compared with that of convalescent (150.097+ 98.696 n g/ml)(P<0.05) and control group(175.801+76.645 u g/ml) ( P<0.001 ) .But serum level of IGF-I inconvalescent had already returned to normal, there were no significant difference compared with that ofcontrol (P=0.848 p>0.05) .In acute phase of infection, serum levels of IGFBP-3 (1285.887 + 608.030) g/ml also markedly decreased, there were significantly different compared with that of convalescent (3247.323+1089.079 u g/ml)(P=0.001) and control group(3723.692+862.357 u g/ml)( P<0.001 ) .And in convalescent, serum levels of IGFBP-3 also had returned to normal, there were no significant difference compared with that of control group ( P=0.544 p>0.05 ) .Furthermore, either in acute phase( r=0.526 p<0.01 ) or in convalescent ( r=0.641 p<0.05 ) ,there were both significant positive correlation between serum levels of IGF-I and IGFBP-3. Serum levels of TNF- a (32.912+6.664pg/ml) in acute phase had obviously elevated, there was significantly different compared with that of convalescent(14.595+3.533pg/ml)(P<0.001) and control (11.674+5.419 pg/ml) ( P<0.001) .But serum levels in convalescent had almost returned to normal, there was no significant difference compared with that of control. Neither in acute phase nor in convalescent, there were correlations among serumlevels of TNF-a and IGF-I, IGFBP-3.Conclusion: (1) In acute phase of children serious bacterial infection, serum levels of IGF-I and IGF... |
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