中国当代儿科杂志最新文献

{"title":"[Clinical features and prognosis of children with influenza-associated encephalopathy: an analysis of 23 cases].","authors":"Dan Wang, Hu Guo, Chun-Feng Wu, Gang Zhang, Min Xu","doi":"10.7499/j.issn.1008-8830.2412117","DOIUrl":"10.7499/j.issn.1008-8830.2412117","url":null,"abstract":"<p><strong>Objectives: </strong>To study the clinical and imaging features of children with influenza-associated encephalopathy (IAE), and to investigate the influencing factors for prognosis.</p><p><strong>Methods: </strong>A retrospective analysis was conducted on the medical data (clinical data, laboratory examinations, imaging data, and prognosis) of 23 children with IAE who were diagnosed and treated in Children's Hospital of Nanjing Medical University from May 2022 to April 2023.</p><p><strong>Results: </strong>Among the 23 patients, 18 (78%) had influenza A and 5 (22%) had influenza B. All patients had fever and encephalopathy, and 20 patients (87%) had seizures, while 11 patients (48%) had persistent convulsions. There were 10 patients (43%) with an increase in alanine aminotransferase, 14 (61%) with an increase in aspartate aminotransferase, and 18 (78%) with an increase in lactate dehydrogenase. Abnormal imaging findings were observed in 20 patients (87%), among whom 10 (43%) had acute necrotizing encephalopathy. All 23 patients received peramivir or oseltamivir. Of all patients, 12 (52%) achieved complete recovery, 5 (22%) had varying degrees of neurological dysfunction, and 6 (26%) died. Compared with the good prognosis group, the poor prognosis group had significantly higher levels of alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase (<i>P</i><0.05).</p><p><strong>Conclusions: </strong>Fever and convulsions are the most common symptoms of children with IAE, and acute necrotizing encephalopathy is the most common clinical imaging syndrome. Increases in alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase have a certain value in predicting poor prognosis.</p>","PeriodicalId":39792,"journal":{"name":"中国当代儿科杂志","volume":"27 7","pages":"829-833"},"PeriodicalIF":0.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12291560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144691832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Role and mechanism of copper overload-mediated endoplasmic reticulum stress in vascular endothelial injury in Kawasaki disease].","authors":"Shi-Fang Wen, Zhi-Yuan Tang, Xian-Juan Shen, Tao Chen, Jian-Mei Zhao","doi":"10.7499/j.issn.1008-8830.2412085","DOIUrl":"10.7499/j.issn.1008-8830.2412085","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the role and mechanism of copper overload-mediated endoplasmic reticulum stress (ERS) in vascular endothelial injury in Kawasaki disease (KD).</p><p><strong>Methods: </strong>Four-week-old male C57BL/6 mice were randomly divided into four groups: control, KD, KD plus copper chelator tetrathiomolybdate (TTM), and KD plus ERS inhibitor AMG PERK 44 (AMG) (<i>n</i>=20 per group). A KD mouse model was established using Candida albicans extract. Human umbilical vein endothelial cells (HUVECs) were divided into control (intervention with healthy children's serum), KD (intervention with KD patients' serum), and KD+TTM (intervention with KD patients' serum plus 20 µmol/L TTM). Copper deposition in mouse heart tissue was assessed using rubeanic acid staining. Vascular pathological changes were observed using hematoxylin-eosin staining and measurement of abdominal aortic diameter and area. ERS activation was detected by transmission electron microscopy and immunofluorescence. HUVEC viability, apoptosis, and functional changes were evaluated using CCK8, flow cytometry, cell scratch assay, and angiogenesis experiments. ERS marker protein expression levels were measured by Western blot.</p><p><strong>Results: </strong>Compared to the KD group, the KD+TTM and KD+AMG groups showed reduced copper deposition in the vascular wall, decreased swelling of coronary endothelial cells and endoplasmic reticulum, reduced inflammatory cell infiltration, and less abdominal aortic lesion expansion. The abdominal aortic diameter and area, and the fluorescence intensity of ERS marker proteins (GRP78 and CHOP) were significantly lower (<i>P</i><0.05). Compared to the KD group, the KD+TTM group exhibited increased cell viability, tube number, and scratch healing rate, along with decreased apoptosis rate and expression of ERS marker proteins (GRP78, CHOP, ATF6, and p-PERK) (<i>P</i><0.05).</p><p><strong>Conclusions: </strong>Copper overload aggravates vascular endothelial injury in KD by activating the ERS pathway. TTM can exert protective effects on the endothelium by regulating copper metabolism and inhibiting the ERS pathway.</p>","PeriodicalId":39792,"journal":{"name":"中国当代儿科杂志","volume":"27 7","pages":"842-849"},"PeriodicalIF":0.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12291571/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144691855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[How I treat pediatric chronic myeloid leukemia].","authors":"Wen-Bin An, Wen-Yu Yang","doi":"10.7499/j.issn.1008-8830.2503021","DOIUrl":"10.7499/j.issn.1008-8830.2503021","url":null,"abstract":"<p><p>Pediatric chronic myeloid leukemia (CML) is more aggressive than adult CML, with unique molecular characteristics and a higher propensity for lymphoid blast crisis. The application of tyrosine kinase inhibitors (TKIs) has significantly improved the prognosis of pediatric CML. Based on international consensus and clinical experience, this article proposes standardized diagnosis and treatment recommendations for pediatric CML, covering initial therapy selection, efficacy evaluation, drug switching, and management of adverse effects. Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is recommended only for patients with disease progression or failure of multiple lines of TKI therapy. For children newly diagnosed with CML in accelerated phase, high-dose imatinib or second-generation TKIs are recommended as first-line therapy. Those achieving optimal responses should continue maintenance therapy, while non-responders require switching to alternative TKIs and consider allo-HSCT. For blast-phase CML, induction therapy requires a combination of TKIs and chemotherapy, with allo-HSCT serving as the core curative intervention. This article highlights common but challenging problems (poor response, drug intolerance, and disease progression) in pediatric CML treatment using three typical cases, aiming to optimize treatment strategies. Furthermore, the goal of achieving treatment-free remission needs to be further addressed through multi-center clinical studies.</p>","PeriodicalId":39792,"journal":{"name":"中国当代儿科杂志","volume":"27 7","pages":"792-801"},"PeriodicalIF":0.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12291566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144691839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Sequential therapy with carglumic acid in three cases of organic acidemia crisis].","authors":"Yan-Yan Chen, Ting-Ting Cheng, Jie Yao, Long-Guang Huang, Xiu-Zhen Li, Wen Zhang, Hong Liang","doi":"10.7499/j.issn.1008-8830.2412043","DOIUrl":"10.7499/j.issn.1008-8830.2412043","url":null,"abstract":"<p><p>Case 1: A 19-day-old male infant presented with poor feeding and decreased activity for 2 weeks, worsening with poor responsiveness for 3 days. At 5 days old, he developed poor feeding and poor responsiveness, was hospitalized, and was found to have elevated blood ammonia and thrombocytopenia. Whole-genome genetic analysis revealed a pathogenic homozygous mutation in the <i>PCCA</i> gene, NM-000282.4: c.1834-1835del (p.Arg612AspfsTer44), leading to a diagnosis of propionic acidemia. Case 2: A 4-day-old male infant presented with poor responsiveness and feeding difficulties since birth, with elevated blood ammonia for 1 day. He showed weak sucking and deteriorating responsiveness, with blood ammonia >200 µmol/L. Genetic testing identified two heterozygous mutations in the <i>MMUT</i> gene: NM_000255.4: c.1677-1G>A and NM_000255.4: ex.5del, confirming methylmalonic acidemia. Case 3: A 20-day-old male infant presented with poor feeding for 15 days and skin petechiae for 8 days. He developed feeding difficulties at 5 days old and lower limb petechiae at 12 days old, with blood ammonia measured at 551.6 µmol/L. Genetic analysis found two heterozygous mutations in the <i>PCCA</i> gene: NM_000282.4: c.1118T>A (p.Met373Lys) and NM_000282.4: ex.16-18del, confirming propionic acidemia. In the first two cases, continuous hemodiafiltration was performed for 30 hours and 20 hours, respectively, before administering carglumic acid. In the third case, carglumic acid was administered orally without continuous hemodiafiltration, resulting in a decrease in blood ammonia from 551.6 µmol/L to 72.0 µmol/L within 6 hours, with a reduction rate of approximately 20-25 µmol/(kg·h), similar to the first two cases. Carglumic acid was effective in all three cases, suggesting it may help optimize future treatment protocols for organic acidemia.</p>","PeriodicalId":39792,"journal":{"name":"中国当代儿科杂志","volume":"27 7","pages":"850-853"},"PeriodicalIF":0.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12291575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144691856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[The causal association between circulating zinc, magnesium, and other minerals with autism spectrum disorder: a Mendelian randomization study].","authors":"Bing-Quan Zhu, Sai-Jing Chen, Tian-Miao Gu, Si-Run Jin, Dan Yao, Shuang-Shuang Zheng, Jie Shao","doi":"10.7499/j.issn.1008-8830.2506025","DOIUrl":"10.7499/j.issn.1008-8830.2506025","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the causal association between circulating levels of zinc, magnesium, and other minerals and autism spectrum disorder (ASD).</p><p><strong>Methods: </strong>A two-sample Mendelian randomization (MR) analysis was performed using summary statistics from large-scale genome-wide association studies of European populations, including 18 382 ASD cases and 27 969 controls. Genetic data for iron, calcium, and magnesium were obtained from the UK Biobank, and data for zinc and selenium were sourced from an Australian-British cohort. A total of 351 genetic instrumental variables were selected. Causal inference was performed using inverse-variance weighting as the primary analysis method. Sensitivity analyses were performed by Cochran's <i>Q</i> test and MR-PRESSO global test to assess the robustness of the findings.</p><p><strong>Results: </strong>No statistically significant causal effect was observed for circulating zinc, magnesium, calcium, selenium, or iron levels on ASD risk (all <i>P</i>>0.05). The odds ratios and 95% confidence intervals from the inverse-variance weighting analysis were 0.934 (0.869-1.003) for zinc, 1.315 (0.971-1.850) for magnesium, 1.055 (0.960-1.159) for calcium, 1.015 (0.953-1.080) for selenium, and 0.946 (0.687-1.303) for iron. Sensitivity analysis revealed significant heterogeneity in the causal association between circulating calcium and ASD (<i>P</i>=0.006), while the effect estimate remained stable after MR-PRESSO correction (<i>P</i>=0.487). The causal effect estimates for the remaining minerals demonstrated good robustness.</p><p><strong>Conclusions: </strong>This study did not find significant evidence supporting a causal association between circulating zinc, magnesium, calcium, selenium, or iron levels and ASD risk, providing important clues for the etiology of ASD and precision nutritional interventions.</p>","PeriodicalId":39792,"journal":{"name":"中国当代儿科杂志","volume":"27 9","pages":"1098-1104"},"PeriodicalIF":0.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[A qualitative study of sensory hypersensitivity in children with autism spectrum disorder and individuals with subclinical autistic traits].","authors":"Yan-Cheng Liu, Dan-Ling Zhu, Xin-Ru Hong, Han-Yu Zhou","doi":"10.7499/j.issn.1008-8830.2503016","DOIUrl":"10.7499/j.issn.1008-8830.2503016","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the manifestations of sensory hypersensitivity in children with autism spectrum disorder (ASD) and individuals with subclinical autistic traits.</p><p><strong>Methods: </strong>From September 2021 to April 2023, interviews were conducted on 18 college students with high levels of autistic traits and sensory hypersensitivity selected using the Adolescent/Adult Sensory Profile and the Autism Spectrum Quotient (as subclinical group). Interviews were also conducted on the parents of 11 children with ASD aged 6-13 years selected using the intensity sampling method (as clinical group). Qualitative content analysis and thematic analysis were performed on the interview texts to investigate the scenarios and impact of sensory hypersensitivity and coping strategies in the two groups.</p><p><strong>Results: </strong>The Autism Spectrum Quotient score was significantly positively correlated with sensory hypersensitivity (<i>r</i>=0.504, <i>P</i><0.001; <i>n</i>=225). Sensory modalities that triggered sensitive reactions were similar in the subclinical and clinical groups, with auditory hypersensitivity being the most prominent. Sensory hypersensitivity had significant negative impact on emotional wellbeing, cognitive ability, physical health, interpersonal relationships, and general adaptive functioning. These dimensions were interconnected, culminating in a holistic experience. Avoidance was the most commonly used coping mechanism for both groups (16 subclinical participants mentioned it 44 times; 8 clinical participants mentioned it 40 times). The clinical group required more support and help from their caregivers (18 times), while the subclinical group used more proactive coping strategies (e.g., facing sensitive scenarios, distracting attention) to alleviate the negative impact (51 times).</p><p><strong>Conclusions: </strong>Sensory hypersensitivity is a common manifestation across the broad ASD phenotype, posing negative effects on multiple aspects of their lives. There is an urgent need for social tolerance and acceptance as well as the development of effective intervention measures.</p>","PeriodicalId":39792,"journal":{"name":"中国当代儿科杂志","volume":"27 9","pages":"1082-1088"},"PeriodicalIF":0.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447937/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Progress in diagnosis and treatment of <i>RAS</i>-related autoimmune lymphoproliferative disorder].","authors":"Jia-Ning Ren, Yang Wan, Xiao-Fan Zhu","doi":"10.7499/j.issn.1008-8830.2502103","DOIUrl":"10.7499/j.issn.1008-8830.2502103","url":null,"abstract":"<p><p><i>RAS</i>-associated autoimmune lymphoproliferative disorder (RALD) is a rare congenital immunodeficiency disorder caused by somatic mutations in <i>NRAS</i> or <i>KRAS</i>. Its main pathological feature is immune dysregulation-induced hematologic destruction, presenting with symptoms resembling autoimmune diseases. RALD exhibits significant clinical heterogeneity, with manifestations including autoimmune phenomena, hepatosplenomegaly, lymphadenopathy, monocytosis, and increased susceptibility to infections. Owing to its rarity and its unclear nature, a standardized therapeutic regimen for RALD is currently lacking. This review summarizes the latest advances in the pathogenesis, clinical manifestations, differential diagnosis, and treatment of RALD, aiming to provide new insights and reference for the understanding and management of this disorder.</p>","PeriodicalId":39792,"journal":{"name":"中国当代儿科杂志","volume":"27 9","pages":"1149-1155"},"PeriodicalIF":0.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12447939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Guideline for the diagnosis and treatment of common neonatal diseases in primary healthcare institutions: neonatal pertussis (2025)].","authors":"","doi":"10.7499/j.issn.1008-8830.2412132","DOIUrl":"10.7499/j.issn.1008-8830.2412132","url":null,"abstract":"<p><p>In order to effectively assist primary healthcare providers in promptly identifying neonatal pertussis and administering effective treatment to reduce the incidence of severe neonatal pertussis, the Subspecialty Group of Neonatology, Society of Pediatrics, Chinese Medical Association organized a panel of experts to develop the \"Guideline for the diagnosis and treatment of common neonatal diseases in primary healthcare institutions: neonatal pertussis (2025)\", based on the latest clinical evidence and expert consensus. This guideline provides primary healthcare providers with 14 recommendations addressing nine common clinical questions in neonatal pertussis.</p>","PeriodicalId":39792,"journal":{"name":"中国当代儿科杂志","volume":"27 6","pages":"629-637"},"PeriodicalIF":0.0,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12234140/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144530209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Cohen syndrome in a child caused by compound heterozygous variants in <i>VPS13B</i> gene].","authors":"Xin Mei, Xiao-Liang He, Wei-Na Gao, Meng-Yao Wang, Jing-Wen Shen, Jing Wei, Yun Xue","doi":"10.7499/j.issn.1008-8830.2412119","DOIUrl":"10.7499/j.issn.1008-8830.2412119","url":null,"abstract":"<p><p>A 7-year-old girl was admitted to the hospital with rapidly progressive vision loss. Since 1 year of age, she had exhibited developmental delay accompanied by visual impairment and neutropenia. Combined with genetic testing and molecular pathogenicity analysis, she was diagnosed with Cohen syndrome (CS) caused by compound heterozygous variants in <i>VPS13B</i> (c.6940+1G>T and c.2911C>T). The c.6940+1G>T variant resulted in exon 38 skipping, leading to a frameshift and premature termination. Reverse transcription quantitative polymerase chain reaction revealed significantly reduced <i>VPS13B</i> gene expression (<i>P</i><0.05). Bioinformatic analysis suggested that both variants likely produce truncated proteins. This case highlights that integrating clinical features with molecular pathogenicity assessment (DNA, RNA, and protein analysis) can improve early diagnostic accuracy for CS.</p>","PeriodicalId":39792,"journal":{"name":"中国当代儿科杂志","volume":"27 6","pages":"740-745"},"PeriodicalIF":0.0,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12234146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144530206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Genetic screening and follow-up results in 3 001 newborns in the Yunnan region].","authors":"Ao-Yu Li, Bao-Sheng Zhu, Jin-Man Zhang, Ying Chan, Jun-Yue Lin, Jie Zhang, Xiao-Yan Zhou, Hong Chen, Su-Yun Li, Na Feng, Yin-Hong Zhang","doi":"10.7499/j.issn.1008-8830.2412134","DOIUrl":"10.7499/j.issn.1008-8830.2412134","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the application value of genetic newborn screening (gNBS) in the Yunnan region.</p><p><strong>Methods: </strong>A prospective study was conducted with a random selection of 3 001 newborns born in the Yunnan region from February to December 2021. Traditional newborn screening (tNBS) was used to test biochemical indicators, and targeted next-generation sequencing was employed to screen 159 genes related to 156 diseases. Positive-screened newborns underwent validation and confirmation tests, and confirmed cases received standardized treatment and long-term follow-up.</p><p><strong>Results: </strong>Among the 3 001 newborns, 166 (5.53%) were initially positive for genetic screening, and 1 435 (47.82%) were genetic carriers. The top ten genes with the highest variation frequency were <i>GJB2</i> (21.29%), <i>DUOX2</i> (7.27%), <i>HBA</i> (6.14%), <i>GALC</i> (3.63%), <i>SLC12A3</i> (3.33%), <i>HBB</i> (3.03%), <i>G6PD</i> (2.94%), <i>SLC25A13</i> (2.90%), <i>PAH</i> (2.73%), and <i>UNC13D</i> (2.68%). Among the initially positive newborns from tNBS and gNBS, 33 (1.10%) and 47 (1.57%) cases were confirmed, respectively. A total of 48 (1.60%) cases were confirmed using gNBS+tNBS. The receiver operating characteristic curve analysis demonstrated that the areas under the curve for tNBS, gNBS, and gNBS+tNBS in diagnosing diseases were 0.866, 0.982, and 0.968, respectively (<i>P</i><0.05). DeLong's test showed that the area under the curve for gNBS and gNBS+tNBS was higher than that for tNBS (<i>P</i><0.05).</p><p><strong>Conclusions: </strong>gNBS can expand the range of disease detection, and its combined use with tNBS can significantly shorten diagnosis time, enabling early intervention and treatment.</p>","PeriodicalId":39792,"journal":{"name":"中国当代儿科杂志","volume":"27 6","pages":"654-660"},"PeriodicalIF":0.0,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12234138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144530208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}