Clinical characteristics of refractory Mycoplasma pneumoniae pneumonia in children / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To provide a basis for early diagnosis and treatment of refractory Mycoplasma pneumoniae pneumonia (RMPP) in children by comparing the clinical characteristics of RMPP and general Mycoplasma pneumoniae pneumonia (MPP).</p><p><b>METHODS</b>Children with MPP hospitalized between October 2015 and December 2016 were selected as study subjects. According to the diagnostic criteria, children were divided into RMPP group (n=152) and MPP group (n=551). The differences between the two groups in the basic situation, clinical manifestations, infection parameters and myocardial enzymes were compared.</p><p><b>RESULTS</b>There were no significant differences in gender and age between the RMPP and MPP groups (P>0.05). The peak temperature in the RMPP group was significantly higher than that in the MPP group on the first day of admission (P<0.01). The percentage of children with augmentation in the RMPP group was lower than that in the MPP group (P=0.009). The percentage of neutrophils [Ne(%)] and serum procalcitonin (PCT) levels in the RMPP group were both higher than those in the MPP group (P<0.05), while the percentage of lymphocytes was significantly lower in the RMPP group (P<0.05). The serum levels of aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) in the RMPP group were also higher than those in the MPP group (P<0.05). Binary logistic regression analysis showed that the peak temperature and LDH were closely related to RMPP in children (P<0.05). Receiver operating characteristic (ROC) curve analysis showed that the area under the curve (AUC) of the peak temperature and LDH for the diagnosis of RMPP was 0.647 and 0.637 respectively. In children ≤2 years old, when the threshold value of LDH was 400 U/L, the diagnostic sensitivity was 52.63% and the specificity was 54.84%. In children above 2 years old, when the threshold value of LDH was 335 U/L, the diagnostic sensitivity was 69.92% and the specificity was 51.55%.</p><p><b>CONCLUSIONS</b>The children with RMPP have a high fever in the early stage. Meanwhile there are abnormal laboratory test results in these children. Elevated serum LDH levels have a high clinical value of early diagnosis of RMPP, especially in children above 2 years.</p>

Relationship between serum 25-hydroxyl-vitamin D3 levels and galectin-3 levels in serum and bronchoalveolar lavage fluid in children with asthma / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the changes of the levels of galectin-3 (Gal-3) in serum and bronchoalveolar lavage fluid (BALF) of children with asthma whose have different serum levels of 25-hydroxyl-vitamin D₃[25(OH)D₃].</p><p><b>METHODS</b>Fifty children with asthma between January 2013 and December 2014 were enrolled as the asthma group, and they were classified into 25(OH)D₃sufficient (n=7), insufficient (n=12) and deficient subgroups (n=31) according to the serum levels of 25(OH)D₃. Twenty children with abnormal airway or tracheal foreign bodies served as the control group. The levels of 25(OH)D₃, Gal-3 and total IgE in serum and Gal-3 levels in BALF were measured using ELISA.</p><p><b>RESULT</b>The serum levels of 25(OH)D₃in the asthma group were lower than in the control group (P<0.05). The 25(OH)D₃deficient subgroup displayed the highest percentages of neutrophils, eosinophils and epithelial cells in BALF, followed by the 25(OH)D₃insufficient subgroup and the 25(OH)D₃sufficient subgroup (P<0.05). The percentages of neutrophils, eosinophils and epithelial cells in BALF in the three subgroups were all higher than in the control group (P<0.05). In children with asthma, serum levels of 25(OH)D₃were negatively correlated with the percentages of neutrophils, eosinophils and epithelial cells in BALF (r=-0.683, -0.795 and -0.670 respectively; P<0.05); and a negative correlation was also seen between serum 25(OH)D₃levels and serum Gal-3 and total IgE levels (r=-0.759 and -0.875 respectively; P<0.05).</p><p><b>CONCLUSIONS</b>The children with asthma have low serum levels of 25(OH)D₃. 25(OH)D₃and Gal-3 may be involved in the airway inflammation and the development of asthma.</p>

Distribution of pathogenic microorganisms and its relationship with clinical features in children with community-acquired pneumonia / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the distribution of pathogenic microorganisms in different genders, age groups and seasons in children with community-acquired pneumonia (CAP) and the relationship between the distribution of pathogenic microorganisms and clinical features.</p><p><b>METHODS</b>A total of 1,155 children with CAP were enrolled, among whom there were 670 boys and 485 girls, with a mean age of 3.1±2.8 years (range: one month to 14 years). Indirect immunofluorescence assay, particle agglutination test, enzyme-linked immunosorbent assay, colloidal gold method. and bacterial culture were applied to determine common respiratory pathogenic microorganisms in sputum, throat swabs, blood samples, bronchoalveolar lavage fluid, and urine.</p><p><b>RESULTS</b>A total of 758 specimens (65.63%) were tested positive by pathogen detection. The top three dominant pathogens were Mycoplasma pneumoniae (MP, 43.64%), bacteria (15.12%), and respiratory syncytial virus (RSV, 9.26%), and the rate of mixed infection was 16.02%. The rates of MP infection between boys and girls with CAP were different (40.8% vs 47.6%; P<0.05). The MP detection rate was the highest in the age group of 6-14 years (77.4%) and the lowest in children younger than 1 year (11.2%), while the detection rates of bacteria and RSV were the highest in children younger than 1 year (21.2% and 17.2%, respectively). The MP detection rate was significantly higher in summer and autumn than in winter and spring, while the detection rates of bacteria and RSV in summer and autumn were significantly lower than those in winter and spring. Among children who were MP positive, fever, chills, cough, crackles were more likely to appear; children with RSV infection were more likely to have wheezes; children with bacterial infection were less likely to have cough. Serum levels of C-reactive protein and procalcitonin were associated with bacterial infection (OR=1.747 and 1.418, respectively; both P<0.05).</p><p><b>CONCLUSIONS</b>MP plays a more and more important role in the pathogenic microorganisms of CAP in children. Prevalence and outbreaks of MP infection among children should be alerted in summer and autumn. There are differences in the detection rate of various pathogenic microorganisms in CAP children with various age groups. The clinical features of children with CAP caused by different pathogenic microorganisms are different.</p>

Alterations of SP-A, SP-D and KL-6 in serum and bronchoalveolar lavage fluid in children with Mycoplasma pneumoniae pneumonia / 中华儿科杂志

<p><b>OBJECTIVE</b>To study the alterations and relationship of surfactant protein (SP)-A, SP-D and KL-6 in serum and bronchoalveolar lavage fluids (BALF) in children with Mycoplasma pneumoniae pneumonia (MPP).</p><p><b>METHOD</b>Self-control method was used for the study on SP-A, SP-D and KL-6 in serum, infected and non-infected BALFs in 32 MMP children with only one side of MPP.</p><p><b>RESULT</b>The contents of SP-A, SP-D and KL-6 in infected BALF were [mg/L;M (IQR) ]: 243 (90-468) , 187 (43-333) , 148 (47-426) ;104 (37-257) , 56 (25-131) , 35 (12-147) in non-infected BALF; 35 (25-69) , 33 (9-149) and 24 (15-62) in serum. The correlation coefficient of KL-6 between serum and infected BALF were -0.534 and -0.378 (P < 0.05).</p><p><b>CONCLUSION</b>There were significant correlation between the alterations of SP-A, SP-D and KL-6 in serum and lung infection in children with CAP. KL-6 in serum may be more sensitive than SP-A and SP-D.</p>

Changes to surfactant proteins in the bronchoalveolar lavage fluid and serum of children with Mycoplasma pneumoniae pneumonia / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the changes to surfactant proteins in the serum and bronchoalveolar lavage fluids (BALF) of children with Mycoplasma pneumoniae pneumonia (MPP) and their significance.</p><p><b>METHODS</b>Self-control method was used in the study. Forty-seven MPP children were divided into single lung infected (n=32) and bilateral lung infected groups (n=15) according to lung CT results. Surfactant proteins SP-A, B, C and D were measured using ELISA in the serum and BALF in the two groups. The correlations between SP-A, B, C and D content in the serum and BALF were evaluated by Spearman correlation analysis.</p><p><b>RESULTS</b>SP-A, B, C and D content in BALF from the majorly infected or infected lung were significantly higher than from the opposite lung and serum (P<0.01). SP-A, B and C content in serum was significantly lower than in BALF from the non-infected lung in the single-side infected lung group (P<0.01 or 0.05), but there was no significant difference between serum SP-D content and BALF SP-D content from the non-infected lung. There were no significant differences in SP-A, B, C and D content in serum and BALF from the minorly infected lung in the bilateral lung infected group. Serum SP-D content was positively correlated with BALF SP-D content from the majorly infected lung in the bilateral lung infected group (P<0.01).</p><p><b>CONCLUSIONS</b>Serum SP-D content may serve as a biomarker for evaluating the severity of pulmonary infection in children with community-acquired pneumonia.</p>

Effects of Streptococcus pneumoniae on the ultrastructure of alveolar epithelial cells type Ⅱ in the lung tissues of mice and children / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the possible mechanisms of lung necrosis by examining the effects of Streptoccus pneumoniae (S.p) on the ultrastructure of alveolar epithelial cells type Ⅱ(AEC-Ⅱ) in the lung tissues of mice and children.</p><p><b>METHODS</b>The suspended solutions of S.p strains cultured from the blood of a child with pneumococcal necrotizing pneumonia (PNP) (0.3 mL, CFU: 1×108/L) were instilled into the trachea of pathogen-free mice to prepare PNP model. The same amount of normal saline was given for the control group (10 mice). The samples (1 mm3) from the lower lobe of right lung of the mice were obtained 92 hrs later and fixed in 2.5% glutaraldehyde. Normal and abnormal lung tissues (1 mm3) were obtained while operation for the left lower lobe pulmonary cavity excision in the child with PNP. The specimens were fixed in 2.5% glutaraldehyde and stored at 4℃. A transmission electron microscope was employed for the examination of the ultrastructure of AEC-Ⅱ in the lung tissues.</p><p><b>RESULTS</b>Quantitative reduction and exfoliation of microvilli in S.p-infected AEC-Ⅱ were observed in both mice and this child compared with the control. Enlarged size, enhanced evacuation and reduced density of the lamellar bodies were also presented. The number of mitochondria was obviously reduced. The nucleolus chromatin concentrated and showed an inhomogeneous distribution.</p><p><b>CONCLUSIONS</b>S.p infection results in comparable damage to the ultrastructure of AEC-Ⅱ in mice and children that may represent one of the primary causes responsible for S.p-induced lung tissue necrosis.</p>

Changes of pulmonary surfactant protein A in young rats with acute lung injury induced by lipopolysaccharide / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Pulmonary surfactant protein A (SP-A) plays an important role in the maintenance of pulmonary surfactant function and innative immune defence. This study aimed to explore the changes of SP-A concentration in the lungs of young rats with acute lung injury.</p><p><b>METHODS</b>Sprague-Dawley rats were randomly assigned to control and lung injury groups. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the lung injury group. The same amount of normal saline was given for the control group. The two groups were subdivided into 6 groups sacrificed at 6, 12, 24, 36, 48 and 72 hrs of injection (n=8 each). Western blot was employed to detect SP-A concentration in the lung tissues.</p><p><b>RESULTS</b>SP-A concentration in the lung injury group was not different from the the control group within 12 hrs after LPS injection. SP-A concentration in the lung injury group was elevated significantly during 24-48 hrs after LPS injection, peaking at 36 hrs (6.94+/-0.80 vs 5.01+/-0.36; P< 0.01), compared with the controls. However, SP-A concentration in the lung injury group was significantly reduced 72 hrs after LPS injection compared with the controls (P< 0.01).</p><p><b>CONCLUSIONS</b>The changes of lung SP-A concentration in rats following acute lung injury were time-dependent. The transient elevation of SP-A concentration in the lungs indicated a strong compensation ability of SP-A in the host defence against acute lung injury.</p>

Relationship between alveolar epithelial type II cells and pulmonary surfactant protein A levels in young rats with acute lung injury / 中国当代儿科杂志

<p><b>OBJECTIVE</b>This study examined the relationship between the ultrastructural alterations of alveolar epithelial cells type II (AEC-II) and pulmonary surfactant protein A (SP-A) levels in the lung tissue of young rats with acute lung injury (ALI) in order to explore the possible mechanism of ALI.</p><p><b>METHODS</b>Forty-eight young Sprague-Dawley rats were randomly divided into control and ALI groups. The rats in the ALI group were intraperitoneally injected with 4 mg/kg of lipopolysaccharide (LPS) in order to induce ALI. The control subjects were injected with the same volume of normal saline. Rats were sacrificed at 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of the left lung and fixed with 2.5% glutaraldehyde for transmission electron microscope examination and for Western blot test of SP-A.</p><p><b>RESULTS</b>The microvilli of AEC-II disappeared 24 hrs after LPS injection. After 24 and 48 hrs of LPS injection, lamellar body (Lb) increased in number, enlarged in size and reduced in density, and the ring-like arrangement of Lb was present. By 48 hrs after LPS injection, giant Lb with vacuole-like deformity appeared. The contents of lung SP-A in the ALI group 24 hrs (6.52+/-0.62 vs 5.02+/-0.35; P<0.01) and 48 hrs (6.65+/-0.62 vs 5.01+/-0.36; P<0.01) after LPS injection were significantly higher than those in the control group. By 72 hrs after LPS injection, Lbs ruptured and were reduced in number. The shape of the nuclei was irregular and the border was blurred. The content of lung SP-A was greatly reduced in the ALI group 72 hrs after LPS injection compared with that in the control group (3.87+/-0.50 vs 5.22+/-0.36; P<0.01).</p><p><b>CONCLUSIONS</b>The alterations of AEC-II and lung SP-A were time-dependent in young rats with ALI induced by LPS. In the early stage of ALI, the lung SP-A content showed a compensatory increase. With the increasing injury of AEC-II cells, the secretion of SP-A presented with a decompensation and the lung SP-A content decreased. This may be one possible mechanism for the development of ARD.</p>

Effects of dexamethasone on the ultrastructure of alveolar type II cells in young rats with lipopolysaccharide-induced acute lung injury / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Alveolar type II (AT II) cells play a crucial role in the maintenance of pulmonary surfactant homeostasis and pulmonary immunity. The effects of dexamethasone (Dex) on the ultrastructure of AT II cells after acute lung injury remain unknown. This study focused on the ultrastructural changes caused by acute lung injury and on the effects of Dex administration on these ultrastructural changes in young rats.</p><p><b>METHODS</b>Seventy-two 21-day-old Sprague-Dawley rats were randomly divided into control, acute lung injury and Dex-treated groups. Rats in the lung injury group were intraperitoneally injected with 4 mg/kg lipopolysaccharide (LPS) in order to induce acute lung injury, while the control rats were injected with the same amount of normal saline (NS). The Dex-treated group was injected first with LPS followed 1 hr later by Dex (5 mg/kg) injection. Eight rats in each group were sacrificed 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of left lungs and fixed with 2.5% glutaraldehyde for transmission electron microscope examination.</p><p><b>RESULTS</b>Microvilli of AT II cells disappeared and the number of lamellar bodies (LBs) increased in the lung injury group 24 hrs after LPS injection. The ring-like arrangement of LBs around nuclei was present until 48 hrs after LPS injection. By 48 hrs after LPS injection, giant LBs with vacuole-like abnormalities appeared. The shape of nuclei became irregular and the border of the nuclei became blurred. By 72 hrs after LPS injection, the number of LBs was obviously reduced; nucleoli disappeared; and karyolysis occurred in some of the nuclei. In contrast, in the Dex-treated group, LBs crowded on one side of AT II cells and exocytosis appeared on the same side by 24 hrs after LPS injection. By 48 hrs, the number of LBs was reduced. The number of mitochondria increased, and some of them became swollen and enlarged. However, by 72 hrs, the number of LBs increased and the ring-like arrangement of LBs around the nucleus again appeared.</p><p><b>CONCLUSIONS</b>Ultrastructural changes of AT II cells following lung injury induced by LPS were time-dependent in young rats. Dex may ameliorate AT II cell injury and promote functional restoration of AT II cells in LPS-induced acute lung injury.</p>

Effect of dexamethasone on the content of pulmonary surfactant protein D in young rats with acute lung injury induced by lipopolysaccharide / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Pulmonary surfactant protein-D (SP-D) is regarded as a valuable biomarker in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). This study was to explore the changes of SP-D content in lung tissue following ALI and the effect of dexamethasone (Dex) on the SP-D content in young rats.</p><p><b>METHODS</b>One hundred and forty-four 21-day-old Sprague-Dawley rats were randomly assigned into control, ALI and Dex-treated groups. ALI was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the rats from the ALI and Dex-treated groups. Normal saline was given for the control group. Dex (5 mg/kg) was administered 1 hr after LPS injection in the Dex-treated group. At each time interval of 6, 12, 24, 36, 48 and 72 hrs after LPS injection, eight rats of each group were randomly chosen and sacrificed. Western blot was employed to detect the content of SP-D in lung tissues.</p><p><b>RESULTS</b>The pulmonary SP-D content decreased significantly at 36, 48 and 72 hrs after LPS administration in the ALI group, and reduced to a nadir (0.92 +/-0.11 vs 3.27 +/- 0.52) at 48 hrs compared with that of the control group (P < 0.01). The SP-D content in the Dex-treated group increased significantly at 36,48 and 72 hrs after LPS administration when compared with the ALI group (P < 0.01). A significant difference in the SP-D content between the Dex-treated and the control group was noted only at 72 hrs after LPS administration (P < 0.05).</p><p><b>CONCLUSIONS</b>The SP-D content in lung tissue was reduced following ALI in young rats at the early stage. Early administration of Dex can significantly increase the pulmonary SP-D content.</p>

Effect of glutamine on apoptosis of the small intestine in young rats with endotoxemia and its mechanism / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the effect of glutamine on intestinal epithelial apoptosis by examining changes regarding Bcl-2 and Bax mRNA expressions in the small intestine of young rats with endotoxemia and to explore the protective mechanism that glutamine may have.</p><p><b>METHODS</b>A total of 120 18-day-old rats were randomly assigned into Endotoxemia, Glutamine-treated and Control groups (n = 40 each). The endotoxemia model was established by intraperitoneal injection of endotoxin (4 mg/kg of O55B5 Escherichia coli lipopolysaccharide). Rats in the Glutamine-treated group were intraperitoneally injected with N (2)-L-alanyl-L-glutamine (2 g/kg) along with endotoxin. Rats in the Control group were intraperitoneally injected with an equal volume of normal saline. The entire ileum was collected at 2, 4, 6, 24, and 72 hrs after injection. Bcl-2 and Bax mRNA expressions were detected by semi-quantities reverse transcriptase chain reaction.</p><p><b>RESULTS</b>Bcl-2 mRNA was not expressed in the Control and the Endotoxemia groups but increased in the Glutamine-treated group at each time point. Bax mRNA expression was weak in the Control group, and significantly increased in the Endotoxemia group at each time point. The Glutamine-treated group showed noticeably reduced Bax mRNA expression at 2 hrs post-injection while other time points were similar to the Control group. The ratio of Bax and Bcl-2 mRNA expression at each time point in the Endotoxemia group was significantly higher than that in the Control group while the Glutamine-treated group demonstrated significantly lower ratio of Bax and Bcl-2 mRNA expression than both.</p><p><b>CONCLUSIONS</b>Glutamine treatment increased Bcl-2 mRNA expression and decreased Bax mRNA expression, as a result, the ratio of Bax and Bcl-2 mRNA expression decreased. The effects of glutamine resulted in a suppression of intestinal epithelial apoptosis and maintained the integrity of the gut barrier structure.</p>