Objective To investigate the factors in first-time adrenocorticotropic hormone (ACTH) therapy and their influence on spasm control time in infants with infantile spasms. Methods A total of 72 infants with infantile spasms who were admitted from January 2008 to October 2013 were enrolled. Their clinical data were collected, and the exposure factors for infantile spasms were selected. A Cox proportional-hazards regression model analysis was performed for these factors to analyze their influence on spasm control time. Results Clarification of the etiology (known or unexplained etiology), frequency of spasms before treatment, and presence or absence of combination therapy (ACTH used alone or in combination with magnesium sulfate) had a significant influence on spasm control time in infants with infantile spasms. The infants with a known etiology had a significantly shorter spasm control time than those with unexplained etiology, and the infants with a low frequency of spasms before treatment and receiving ACTH combined with magnesium sulfate early had a significantly longer spasm control time than their counterparts (P < 0.05). Conclusions For infants with infantile spasms at initial diagnosis, etiology should be clarified, which may helpful for evaluating prognosis. A combination of ACTH and magnesium sulfate should be given as soon as possible, which may improve their prognosis.
Infantile neuroaxonal dystrophy (INAD) is a rare neurodegenerative disease. Two boys aged 3 years and 4 years and 2 months respectively, were admitted to the hospital due to delayed mental and motor development. There were no abnormalities at birth, and both children had low muscle strength and tension on admission. One child was not able to stand alone and had impaired vision. Electromyography showed neurogenic damage, and head MRI revealed cerebellar atrophy. High-throughput sequencing revealed compound heterozygous mutations in the PLA2G6 gene in the two children. The mutations (IVS11-1G > T and c.1984C > G) in one child were new mutations, and immunohistochemistry showed a reduction in the protein expression of PLAG6 in the muscular tissue of this child. INAD has the main clinical manifestations of psychomotor developmental regression and cerebellar atrophy. High-throughput sequencing can help with clinical diagnosis.
Objective To investigate the infection factors associated with neurodysplasia in early and moderately preterm infants at a corrected age of 18 months. Methods The preterm infants with a gestational age of 28 weeks to < 34 weeks who were admitted to the neonatal intensive care unit and followed up at the outpatient service for high-risk preterm infants from June 2015 to December 2018 were enrolled as subjects. At a corrected age of 18 months, the revised Bayley Scales of Infant Development was used to evaluate neurodevelopment. Univariate and multivariate logistic regression analyses were used to investigate the infection factors affecting neurodevelopment. Results A total of 138 early or moderately preterm infants were enrolled, among whom 59 had neurodysplasia at a corrected age of 18 months. The univariate logistic regression analysis showed that neurodysplasia was associated with late-onset infection, positive blood culture, and other systemic infections (P < 0.05). The multivariate logistic regression analysis showed that late-onset infection was an independent risk factor for neurodysplasia (OR=1.510, 95%CI:1.133-3.600, P < 0.05). Conclusions Late-onset infection can increase the risk of neurodysplasia in early and moderately preterm infants.
Objective To examine the levels of airway inflammatory mediators in peripheral blood in infants and young children with wheezing and to study the possible pathogenesis of wheezing from the aspects of T helper cell 1 (Th1)/T helper cell 2 (Th2) imbalance and airway inflammation. Methods A total of 50 children aged 1 month to 3 years with an acute wheezing episode were enrolled as the wheezing group, and 25 age-matched healthy infants were enrolled as the healthy control group. According to the number of wheezing episodes, the wheezing group was divided into a first-episode group (n=25) and a recurrent wheezing (number of episodes ≥ 2) group (n=25). According to the presence or absence of high-risk factors for asthma, the wheezing group was divided into a high-risk factor group (n=22) and a non-high-risk factor group (n=28). According to the results of pathogen detection, the wheezing group was divided into a positive pathogen group (n=23) and a negative pathogen group (n=27). Levels of interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-13 (IL-13), transforming growth factor-β1 (TGF-β1), and total IgE (TIgE) in peripheral blood were measured for each group. For children with wheezing, eosinophil (EOS) count in peripheral blood was measured, and related samples were collected for respiratory pathogen detection. Results The wheezing group had significantly higher levels of IL-4, IL-5, IL-13, TGF-β1, and TIgE in peripheral blood than the healthy control group (P < 0.05). There were no significant differences in the levels of IL-2, IL-4, IL-5, IL-13, TGF-β1, and TIgE in peripheral blood between the first-episode and recurrent wheezing groups, between the high-risk factor and non-high-risk factor groups, and between the positive pathogen and negative pathogen groups (P > 0.05). The correlation analysis showed that in children with wheezing, EOS count was positively correlated with IL-4 level (P < 0.01), IL-4 level was positively correlated with IL-5 and IL-13 levels (P < 0.01), IL-5 level was positively correlated with IL-13 level (P < 0.01), and IL-2 level was positively correlated with TGF-β1 level (P < 0.05). Conclusions Th1/Th2 imbalance with a predominance of Th2 is observed in infants and young children with wheezing. IL-4, IL-5, IL-13, TGF-β1, and IgE are involved in the pathogenesis of wheezing in these children. Airway inflammation is also observed in these children with wheezing, but it is not associated with the number of wheezing episodes, presence or absence of high-risk factors for asthma, or results of pathogen detection.
Objective To study the significance of plasma neutrophil extracellular trap (NET) and its markers in the diagnosis of community-acquired pneumonia (CAP) in children. Methods A total of 160 children with CAP were enrolled as the CAP group, and 50 healthy children were enrolled the control group. According to disease severity, the CAP group was further divided into a mild CAP subgroup with 137 children and a severe CAP subgroup with 23 children. According to the pathogen, the CAP group was further divided into a bacterial pneumonia subgroup with 78 children, a Mycoplasma pneumonia subgroup with 35 children, and a viral pneumonia subgroup with 47 children. The levels of plasma NET and its markers[antibacterial peptide (LL-37), extracellular free DNA (cfDNA), and deoxyribonuclease I (DNase I)] were measured. Receiver operating characteristic (ROC) curve was used to analyze the value of each index in diagnosing CAP and assessing its severity. Results Compared with the control group, the CAP group had significant increases in the levels of NET, LL-37, and cfDNA and a significant reduction in the activity of DNase I (P < 0.05). Compared with the mild CAP subgroup, the severe CAP subgroup had significantly higher levels of NET, LL-37 and cfDNA and a significantly lower activity of DNase I (P < 0.05). There were no significant differences in the levels of NET, LL-37, and cfDNA and the activity of DNase I among the bacterial pneumonia, Mycoplasma pneumonia, and viral pneumonia subgroups (P > 0.05). In the CAP group, plasma NET levels were positively correlated with white blood cell count (WBC), percentage of neutrophils, and serum levels of C-reactive protein (CRP), procalcitonin and tumor necrosis factor-α (r=0.166, 0.168, 0.275, 0.181 and 0.173 respectively, P < 0.05); LL-37 and cfDNA levels were positively correlated with WBC (r=0.186 and 0.338 respectively, P < 0.05) and CRP levels (r=0.309 and 0.274 respectively, P < 0.05); the activity of DNase I was negatively correlated with CRP levels (r=-0.482, P < 0.05). The ROC curve analysis showed that NET, LL-37, cfDNA, and DNase I had an area under the ROC curve (AUC) of 0.844, 0.648, 0.727, and 0.913 respectively in the diagnosis of CAP, with optimal cut-off values of 182.89, 46.26 ng/mL, 233.13 ng/mL, and 0.39 U/mL respectively, sensitivities of 88.12%, 35.63%, 54.37%, and 91.25% respectively, and specificities of 74.00%, 92.00%, 86.00%, and 76.00% respectively. In the assessment of the severity of CAP, NET, LL-37, cfDNA, and DNase I had an AUC of 0.873, 0.924, 0.820, and 0.778 respectively, with optimal cut-off values of 257.7, 49.11 ng/mL, 252.54 ng/mL, and 0.29 U/mL respectively, sensitivities of 83.21%, 86.96%, 78.26%, and 95.65% respectively, and specificities of 78.26%, 83.94%, 76.64%, and 56.93% respectively. Conclusions Plasma NET and its related markers have a certain value in diagnosing CAP and assessing its severity in children.
Objective To study the correlation of Mycoplasma pneumoniae DNA (MP-DNA) replication level in throat swab and bronchoalveolar lavage fluid (BALF) with disease severity in children with severe Mycoplasma pneumoniae pneumonia (SMPP). Methods A total of 44 children with SMPP who underwent bronchoalveolar lavage were enrolled as subjects. The serum levels of cytokines and MP-DNA replication times in throat swab were measured in the acute stage and the recovery stage, and the levels of interleukin (IL)-8 and MP-DNA replication times in BALF were measured in the acute stage. According to whether mechanical ventilation was needed for respiratory failure, the children were divided into a mechanical ventilation group (n=19) and a non-mechanical ventilation group (n=25), and the two groups were compared in MP-DNA replication times in BALF. Results For the children with SMPP, serum levels of C-reactive protein, erythrocyte sedimentation rate, lactate dehydrogenase, IL-1, IL-6, IL-8, and IL-18 in the acute stage were significantly higher than those in the recovery stage (P < 0.05). In the acute stage, MP-DNA replication times in throat swab were positively correlated with those in BALF (r=0.613, P < 0.05), and MP-DNA replication times in BALF were positively correlated with IL-18 levels in peripheral blood and BALF (r=0.613 and 0.41 respectively, P < 0.05). Compared with the non-mechanical ventilation group, the mechanical ventilation group had significantly higher MP-DNA replication times in BALF, a significantly longer duration of systemic hormone treatment, significantly higher serum levels of lactate dehydrogenase and IL-18, and significantly higher white blood cell count and IL-18 level in BALF (P < 0.05). Conclusions In children with SMPP, MP-DNA replication level in throat swab and BALF can be used as a reference index for the assessment of disease severity.
No abstract available
Diffuse alveolar hemorrhage (DAH) is a clinical syndrome with major clinical manifestations of hemoptysis, anemia, and diffuse infiltration in the lung. DAH has a high mortality rate in the acute stage and is a life-threatening emergency in clinical practice. Compared with adult DHA, childhood DHA tends to have a specific spectrum of underlying diseases. It has long been believed that idiopathic pulmonary hemosiderosis (IPH) is the main cause of childhood DAH; however, with the increase in reports of childhood DAH cases, the etiology spectrum of childhood DAH is expanding. The treatment and prognosis of DAH with different etiologies are different. This review article gives a general outline of childhood DAH, with focuses on DAH caused by IPH, systemic lupus erythematosus, anti-neutrophil cytoplasmic antibody-related vasculitis, COPA syndrome, or IgA vasculitis.
