[Changes and significance of soluble CD 163 in sepsis and severe sepsis in children].

OBJECTIVE: To investigate the changes of serum soluble CD 163 (sCD 163) level, to assess the severity of critical illness and to evaluate the immune status of sepsis or severe sepsis in children. METHOD: A prospective study was conducted. The sCD 163 was determined in 50 cases with sepsis or severe sepsis in pediatric intensive care unit (PICU) and 23 cases of age- and gender-matched healthy children were enrolled as control during the period from April 2010 to March 2011. Double-antibody sandwich ELISA was used for sCD 163 measurement. The relationship with sCD 163 level and disease severity score (pediatric critical illness score, PCIS; and pediatric risk of mortality III, PRISM III), lymphocyte subsets, C-reactive protein (CRP), tumor necrosis factor α (TNFα) were analyzed. RESULT: The sCD 163 in sepsis/severe sepsis groups (171.04 ± 177.85) mg/L was significantly higher than that in control group (44.19 ± 86.48) mg/L (P < 0.01).sCD 163 in sepsis group [(105.32 ± 145.87) mg/L] was significantly lower than that of severe sepsis group [(233.32 ± 171.78) mg/L] (P < 0.05). sCD 163 level was significantly higher in lower PCIS score patients. (P < 0.01). The sCD 163 levels was higher in PRISM III ≥ 10 than the PRISM III < 10 group. The sCD 163 levels were higher in death group than the survival group. The sCD 163 was negatively correlated with CD4 +, CD4 +/CD8 + (R = -0.820, P < 0.05; R = -0.839, P < 0.01). CONCLUSION: Detection of sCD 163 was helpful in predicting the severity of sepsis and severe sepsis, and sCD 163 may reflect the immune status of critically ill children with sepsis.

[Efficacy of continuous blood purification on rescue therapy of the critically ill children with acute lung injury and acute respiratory distress syndrome].

OBJECTIVE: To investigate the efficacy of continuous blood purification(CBP) in the treatment of acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in children. METHODS: One hundred and forty seven cases of ALI/ARDS were hospitalized to our pediatric intensive care unit, and 32 cases were treated with continuous blood purification (CBP) from June, 2006 to May, 2011. The model for CBP was continuous veno-venous hemofiltration dialysis (CVVHDF). CBP treatment persisted for at least 8 hours and replacement + dialysis fluid dose was 35 - 100 ml/(kg·h). The clinical outcome measures included the mortality rate at 28th day, respiratory index (FiO2/PO2), dynamic lung compliance (Cdyn), arterial partial pressure of oxygen (PaO2), arterial partial pressure of carbon dioxide (PaCO2), mechanical ventilation parameters, vasoactive drug dose and lung X-ray changes. RESULTS: In totally 147 cases of ALI/ARDS, 89 cases (60.5%) were male and 58 (39.5%) were female, mean age was (43.4 ± 36.7) months. Death occurred in 54 cases, the total mortality was 36.7%. The cause of ALI/ARDS was mainly severe pneumonia, severe sepsis, and leukemia or tumor diseases. There were significant differences in severity of illness between the CBP treatment group and non-CBP treatment group on Pediatric risk of score mortality (PRISM) III score (15.3 vs. 12.7, P < 0.05) and pediatric critical illness score (66.8 ± 19.3 vs. 74.6 ± 17.7, P < 0.05). The average duration of CBP treatment was 52 hours (12 hours to 232 hours). PaO2/FiO2 and Cdyn were improved after 2 hours CBP treatment compared with those before CBP treatment (P < 0.05), mechanical ventilation parameters including fraction of inspired oxygen (FiO2), peak inspiratory pressure (PiP) and positive end expiratory pressure (PEEP) were reduced. The use of vasoactive drugs in patients with MODS and shock gradually declined. The average ventilator-free days of the two groups did not show significant difference (P > 0.05). The mortality on CBP treatment group and non-treatment group were 37.5% and 36.5%, respectively, the difference was not significant (P > 0.05). CONCLUSION: CBP adjuvant treatment for ALI/ ARDS could reduce pulmonary edema, improve PaO2/FiO2 and Cdyn, and improve mechanical ventilation parameters. CBP may be a very promising treatment for ALI/ARDS in children.

Glucocorticoid receptor expression on acute lung injury induced by endotoxin in rats.

BACKGROUND: In cases of severe sepsis and septic shock, a series of pathophysiological changes lead to multiple organ dysfunction syndrome. This study aimed to investigate the expression of glucocorticoid receptor mRNA in the rat lung following endotoxin (LPS) induced shock. METHODS: Totally 56 SD rats were randomly divided into 4 groups: LPS shock group (n=16), LPS+vasoactive intestinal peptide group(VIP) group, (n=16), LPS+VIP+ glucocorticoid (GC) group, (n=16),and control group (n=8). LPS shock was induced by intravenous injection of LPS (10 mg/kg) in rats. Within 15 minutes after LPS injection, rats in the treatment groups received VIP (5 nmol/kg) or VIP and methylprednisolone (3 mg/kg). The control group was given normal saline instead of LPS. The rats of the four groups were sacrificed at 6 hours,24 hours after injection respectively, and the lung tissues were collected. Pathological changes of the lungs were examined by light microscopy and electron microscopy. GRmRNA expression in the lung tissues was evaluated by RT-PCR. RESULTS: In the LPS shock group, lung histopathology demonstrated destruction of the alveolar space,widening of the inter-alveolar space, inflammatory cell infiltration and interstitial edema. However,pathological changes in the LPS+ VIP group and LPS+ VIP+GC group were milder than those in the LPS shock group. Six hours after LPS injection, GR mRNA expression was down-regulated in the LPS group (0.72± 0.24) and LPS+ VIP group (0.88±0.27) (P<0.05) as compared with the control group (1.17±0.22). The LPS shock group showed a more significant down-regualtion than the LPS+VIP group, but the difference was not statistically significant (P>0.05). In contrast, GRmRNA expression in the LPS+ VIP+GC group was significantly up-regulated at 6 hours and further at 24 hours (1.45±0.32 and 1.91±0.46 respectively) (P<0.05). CONCLUSION: GrmRNA expression decreased in LPS induced lung injury in rats. Combined treatment with VIP and GC mitigated lung injury ang inflammation. The mechanism may be related to up-regulation of GR mRNA expression.