ABSTRACT
Objective To explore the expression and its clinical significance of serum procalcitonin (PCT)level in ventilator-associated pneumonia( VAP)in newborns. Methods One hundred and fifty-five children with suspected VAP in Shajing Hospital of Shenzhen Affiliated to Medical University of Guangzhou from June 2013 to December 2014 who were in intensive care kiunit(NICU)were selected as our subjects. According to whether they had VAP or not could be divided into VAP group(80 cases)and non-VAP group(75 cases). Immunoluminometric method was used to detect PCT level at 1st day. According to the different medicine,VAP group was divided into 40 cases of two groups. The control group was according to the situation of children which was used empirical antibiotic by clinicians. The observation group was given antibiotics according to the level of PCT(the antibiotics were used when PCT > 0. 25 μg/ L). After treatment,if PCT did not decrease,the antibiotics was replaced. If PCT decreased,the antibiotics was continued to use the same kind of antibiotics. While the PCT< 0. 25 μg/ L,the antibiotics were stopped using. The change of the PCT level at 1st,4th,7th,10th day of two groups were observed. Results Serum PCT level of VAP group was(1. 68 ± 0. 83)μg/ L,significantly higher than that of non-VAP((0. 10 ± 0. 02)μg/ L),and there was statistically significant difference( t = 52. 614,P< 0. 05). Clinical effective rate of observation group was 87. 5%(35 / 40),which was higher than that of the control group(80. 0%(32 / 40),P = 2. 067). At 4th,7th and 10th day after treatment,PCT expressions of the observation group were all significantly lower than those of the control group. The medical costs and antibiotic using time were significantly lower than those of the control group((3 525. 8 ± 1 162. 9)yuan vs.(4 706. 7 ± 803. 4),(10. 3 ± 2. 7)d vs.(13. 5 ± 1. 4)d;t = 5. 28,6. 65;P < 0. 05). Conclusion The serum PCT levels of newborns of VAP significantly increase,and monitoring the PCT can guide reasonably the use of antibiotics in clinic.
ABSTRACT
Objective To explore the effect of keratinocyte growth factor(KGF)on the lung tissue and expres-sion of transforming growth factor - β1(TGF - β1 )in newborn rats with hyperoxia. Methods The 108 newborn SD rats were randomly divided into air group,hyperoxia group and KGF intervention group,and each group had 36 rats. The rats in every group were randomly divided into the 3,7,14 days subgroups,and each group had 12 rats. The rats in the hy-peroxia group and KGF intervention group were continually exposed to more than 950 mL/ L of oxygen box until the end of the experiment. KGF intervention group simultaneously undertook oxygen inhalation,hypodermic injection of 1 mg/ d recombinant human KGF(rhKGF)on the back on the first 3 days and 0. 5 mg/ d 3 days later till the end of the experi-ment. Air group and hyperoxia group were offered equivalent 9 g/ L saline. The rats in the air group took air. The sub -groups of the 3,7 and 14 days were cut for lung tissue in the corresponding time,observing lung tissue by light micro-scope for pathological changes and TGF - β1 protein expressed in the lungs was determined by immunohistochemistry. Results Air group sprout pulmonary alveolus on the 7th day,and the alveolaration finished on the 14th day,while hy-peroxia group had alveolar growth retardation and pulmonary fibrosis,but pulmonary fibrosis was not obvious in KGF in-tervention group. There was a significant difference on 7th day and 14th day between hyperoxia group and air group in TGF - β1(9. 43 ± 0. 64 vs 8. 62 ± 0. 52,P ﹤ 0. 05;9. 97 ± 0. 49 vs 8. 66 ± 0. 48,P ﹤ 0. 01). There was no significant difference between KGF intervention group and air group in TGF - β1(8. 67 ± 0. 55 vs 8. 56 ± 0. 43,8. 77 ± 0. 52 vs 8. 62 ± 0. 52,8. 81 ± 0. 47 vs 8. 66 ± 0. 48,all P ﹥ 0. 05). There's a significant difference on 7th day and 14th day be-tween hyperoxia group and KGF intervention group in TGF - β1(all P ﹤ 0. 05). Conclusions KGF can inhibit the pro-tein expression of TGF - β1 ,and this may be one of the possible mechanism underlying the protective effect of KGF a-gainst lung injury.