Bordetella pertussis (BP) infection has risen rapidly in pediatrics recently, and next-generation sequencing has significantly improved pertussis’ early diagnosis. High detection rates raise the concern of pertussis re-emergence. We used tNGS to analyze respiratory secretions from children with lower respiratory tract infections, aiming to assess the significance of BP co-detected. This study included pediatric patients aged 1 month to 14 years who were hospitalized for lower respiratory tract infections from April 2023 to March 2024. Respiratory secretions were collected and analyzed using tNGS sequencing. Clinical data were collected, including clinical symptoms and laboratory markers. According to tNGS read per ten million (RPTM), pertussis patients were divided into three groups: low RPTM group (< 10,000), medium RPTM group (10,000–25,000), and high RPTM group (> 25,000). The association between pertussis RPTM and clinical characteristics was evaluated. Among the 865 pediatric lower respiratory tract infections, 56 cases (6.47

Alveolar macrophages (AMs) are crucial for defending against respiratory syncytial virus (RSV) and regulating lung inflammation. Notch signaling is essential for macrophage polarization and its functional diversity.However, the role of macrophages Notch1 in RSV-induced lung injury and its underlying mechanisms remain incompletely understood. This study used macrophage-specific Notch1 knockout (MKO) mice to investigate the lung lesions and inflammation in RSV-infected mice. The effects of various interventions, including JAG1, Nr1d1 inhibitor, and Bnip3 gene manipulation, were assessed in RSV-infected mice. Western blot (WB) was used to measure the expression of inflammasome-related proteins, such as NLR family, pyrin domain containing 3 (Nlrp3), Asc, Cleaved-caspase1, and nuclear receptor subfamily 1, group D, member 1 (Nr1d1), BCL2/adenovirus E1B 19 kDa interacting protein 3 ‌(Bnip3) in lung or macrophages. Additionally, RNA sequencing (RNA-seq) of macrophages from RSV-infected mice was performed to identify differential gene expression between MKO and wild-type (Flox) mice. Confocal microscopy visualized the localization of autophagy complexes in cellular mitochondria. ELISA assays measured LDH, IL-1β and IL-18 levels in bronchoalveolar lavage fluid (BALF). Compared to Flox mice, MKO mice showed milder lung lesions, increased Nr1d1 and Bnip3 expression, and decreased Nlrp3 inflammasome activity in RSV-exposed mice. Moreover, Nr1d1 inhibitor reduced Bnip3 expression, increased IL-1β and IL-18 release, and exacerbated pulmonary inflammation. Inhibiting Bnip3 exacerbated RSV-induced lung injury by enhancing Nlrp3 inflammasome activity and impairing mitophagy. These results suggest that Notch signaling regulates Nr1d1/Bnip3-induced mitophagy, influencing the Nlrp3 inflammasome and the inflammatory response during RSV infection.

ObjectiveTo explore the characteristics of gut microbiota in children with Language Developmental Delay (LDD).MethodsChildren aged 0–6 years diagnosed with LDD at the Pediatric Outpatient Department of Zhongnan Hospital of Wuhan University, and healthy children undergoing physical examinations during the same period (June 2023 to June 2024) were enrolled as study subjects. Fecal samples were collected, and the characteristics of gut microbiota were assessed using 16S rDNA high-throughput sequencing.ResultsA total of 50 children were enrolled, including 24 in the LDD group average age (4.1 ± 1.7) years and 26 in the control group average age (4.0 ± 1.5) years, with no significant demographic differences (P > 0.05). The Gesell developmental score in the LDD group (60 ± 12) was significantly lower than that in the control group (102 ± 15) (P < 0.05). At the phylum level, the dominant phyla were Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria, with no significant difference in abundance between groups (P > 0.05). Alpha diversity indices, including Observed species, Chao1 index, Shannon index, and Simpson index, showed no significant difference (P > 0.05). Beta diversity analysis (PCoA) revealed no significant difference in microbial community structure between the two groups. Linear discriminant analysis Effect Size (LEfSe) analysis (LDA score > 2) indicated that the LDD group lacked certain bacterial taxa compared to the control group, including Mycobacteriaceae, Sphingobacteriaceae, Sphingobacteriales, Sphingobacteriia, Caulobacteriaceae, Caulobacterales, Erythrobacteraceae, Sphingomonadaceae, and Sphingomonadales.ConclusionChildren with Language Developmental Delay exhibited gut microbial dysbiosis, but no specific gut microbial composition was identified.

A congenital portosystemic shunt (CPSS), a rare developmental malformation of the portal venous system, often presents with atypical clinical manifestations in the neonatal period that are prone to be missed or misdiagnosed. Herein, we report two neonatal CPSS cases. Case 1 initially manifested as respiratory distress, diffuse ecchymosis, and petechial hemorrhages and later caused progressive liver dysfunction, disseminated intravascular coagulation (DIC), and patent ductus arteriosus. Case 2 initially exhibited respiratory distress and multiple cutaneous hemangiomas, subsequently leading to progressive liver dysfunction, an increase in the number and size of hemangiomas, and severe pulmonary hypertension. Alongside our two neonatal CPSS cases, this article reviews 34 other neonatal cases reported in the literature over the past decade, aiming to enhance clinical recognition by summarizing the disease's clinical characteristics, diagnosis, treatment, and prognostic features during the neonatal period. Particularly, the early onset of idiopathic DIC, multiple cutaneous hemangiomas, progressive liver dysfunction, and pulmonary hypertension in neonates may be suggestive of CPSS. Furthermore, it underscores the critical importance of prenatal ultrasound screening, comprehensive multisystem assessment, and multidisciplinary care for the early diagnosis, individualized treatment, and improved prognosis of neonatal CPSS.

Background: As pivotal immunoregulatory sentinels in pulmonary defense systems, alveolar macrophages (AMs) play dual roles in mediating inflammatory responses and tissue repair processes during various phases of inflammatory cascades. The present investigation focuses on elucidating the regulatory influence of Notch pathway activation within AM populations on the pathophysiological mechanisms underlying acute lung injury (ALI) development. Methods: To investigate the regulatory roles of Notch intracellular domain (NICD) and C-C chemokine receptor type 5 (CCR5) in pulmonary inflammation, an ALI model was established through lipopolysaccharide (LPS) administration. Complementary studies used macrophage-specific Notch1 knockout mice and immortalized bone marrow-derived macrophages (iBMDMs). Molecular profiling of CCR5 and inflammatory mediators was performed through real-time quantitative reverse transcription PCR (qRT-PCR) and immunofluorescence staining. Functional assessments of macrophage migration were carried out using scratch wound healing assays and transwell migration assays. Results: In the LPS-induced ALI model, pulmonary tissues exhibited elevated expression of both NICD and CCR5. Conversely, Notch1 knockout mice attenuated CCR5 expression, reduced macrophage infiltration and downregulated transcription of pro-inflammatory mediators compared to wild-type controls (p < 0.05). Lung injury was milder in the Notch1-deficient mice model compared to wild mice (p < 0.05). In vitro experiments demonstrated that inhibiting the Notch pathway in macrophages reduced CCR5 expression and attenuated CCL5-induced macrophage migration. Conclusion: Notch signaling regulates macrophage infiltration and the inflammatory response by modulating CCR5 expression in ALI induced by LPS.

BACKGROUND:To characterize the epidemiology of pathogens in children with lower respiratory tract infections (LRTI) using targeted next-generation sequencing (tNGS), assess the correlation between reads per ten million (RPTM) of co-detected pathogens, identify common co-detection patterns, and explore their clinical significance. METHODS:Children aged 29 days to 14 years hospitalized for LRTI at the Department of Pediatrics, Zhongnan Hospital of Wuhan University, from April 2023 to August 2024 were included. Bronchoalveolar lavage fluid (BALF) or nasopharyngeal swab (NS) samples were tested for pathogens using tNGS, and clinical data were collected. The data and RPTM were statistically analyzed based on lung X-ray and CT scan results, classifying cases as pneumonia or lung consolidation/pulmonary atelectasis (LC/PA). RESULTS:Among 1118 children, the highest pathogen detection rate was Mycoplasma pneumoniae (MP) at 60.20%, followed by Haemophilus influenzae (HI) at 42.40% and Streptococcus pneumoniae (SP) at 35.42%. In children under 4 years old, common pathogens were HI, Rhinovirus (RhV), and Respiratory syncytial virus (RSV). For those over 4 years old, MP and HI were predominant. In common pneumonia cases, MP, HI, and RhV were frequent, with MP being the primary pathogen in LC/PA. 80.70% of respiratory samples detected two or more pathogens, and viruses were more frequently detected in NS than in BALF. Correlation analysis showed that MP RPTM was negatively correlated with other co-detected pathogens' RPTM, SP was negatively correlated with RSV but positively correlated with Influenza virus (flu virus), HI was positively correlated with Adenovirus (ADV) and flu virus, RhV was negatively correlated with flu virus. Clinical characteristics of co-detected pathogens showed no significant differences in acute LRTI symptoms among different combinations. CONCLUSION:Co-detection of pathogens in children's LRTI using tNGS was common, with MP and bacterial infections being predominant. There were synergistic and competitive relationships between the RPTM of co-detected pathogens.

BACKGROUND:Fine particulate matter (PM2.5)-induced airway epithelial damage plays a pivotal role in driving the development of airway inflammation. Although pyroptosis is recognized for its highly proinflammatory nature, its precise role in PM2.5-associated airway inflammation, particularly in asthmatic condition, remains to be fully elucidated. METHODS:In ovalbumin (OVA)-sensitized asthmatic mice, we assessed pulmonary histopathology, inflammatory cell counts and Th2 cytokine levels (IL-4, IL-5, and IL-13) in bronchoalveolar lavage fluid (BALF), airway hyperresponsiveness (AHR), and airway epithelial pyroptosis. To investigate the effects of PM2.5 on airway epithelial cells, BEAS-2B cells were exposed to PM2.5. Cell viability was evaluated using the CCK-8 assay, while pyroptosis-related protein levels and inflammatory cytokine release were analyzed by Western blot and ELISA, respectively. Additionally, transmission electron microscopy (TEM) was employed to examine PM2.5-induced ultrastructural changes in BEAS-2B cells. To further elucidate the underlying mechanism, we administered the NLRP3 inhibitor MCC950 and the Caspase-1 inhibitor Ac-YVAD-cmk to verify the involvement of NLRP3 inflammasome activation and pyroptosis in PM2.5-exposed asthmatic mice. RESULTS:PM2.5 exposure significantly aggravated airway inflammation in asthmatic mice, as demonstrated by elevated histopathological inflammatory scores in lung tissues and increased pro-inflammatory cytokine levels in BALF. Furthermore, PM2.5 upregulated the abundance of pyroptosis-related markers, namely NLRP3, Caspase-1, GSDMD, and IL-1β, in the lung tissues of asthmatic mice. In BEAS-2B cells, PM2.5 exposure led to a dose-dependent reduction in cell viability and promoted the activation of NLRP3 inflammasome, subsequently leading to Caspase-1-mediated GSDMD cleavage and IL-1β secretion. TEM further confirmed pyroptosis, revealing characteristic morphological alterations such as cytoplasmic vacuolation, mitochondrial swelling, and plasma membrane pore formation in BEAS-2B cells exposed to PM2.5. Critically, inhibition of NLRP3 (MCC950) or Caspase-1 (Ac-YVAD-cmk) markedly attenuated PM2.5-induced pyroptosis and ameliorated airway inflammation in asthmatic mice, underscoring the pivotal role of the NLRP3/Caspase-1/GSDMD axis in this pathogenic process. CONCLUSION:Our findings demonstrate that PM2.5 exposure induces airway epithelial pyroptosis through NLRP3 inflammasome activation, thereby exacerbating airway inflammation in asthmatic mice.

BackgroundPremature delivery interrupts the natural growth of the fetus. The postnatal healthy management of preterm infants still follows term standards after a postmenstrual age (PMA) of 40 weeks and there is a lack of research on the longitudinal dynamic postnatal growth tracks of preterm infants.MethodsBased on the database established by the Wuhan University Internet+ Early Childhood Development Alliance in China, information on preterm infants, including birth registration and health follow-ups from 2016 to 2022, was incorporated into the health management system. Standardized anthropometric measurements of preterm infants were recorded from birth to a corrected age (CA) of 36 months. A generalized additive model based on location, scale, and shape was used to establish the percentile values and growth curves.ResultsIn total, 79,514 preterm infants were included in this study, and the birth weights at each gestational age (GA) were similar to Chinese standards. When evaluated by term birth weight, we found that the proportions of extrauterine growth retardation at a PMA of 40 weeks were all above 10% in the GA ≤34-week groups and reached between 17.19% and 55.56% in very preterm infants (VPIs). There was a high incidence of preterm infants with a weight below the third percentile in VPIs when referring to term standards at CAs of 0, 6, 12, 24, and 36 months (p < 0.001). We established natural growth curves of the preterm population with different GAs between CAs of 0 and 36 months, which indicated that the weight/length of late preterm infants was close to term standards while the growth trajectory of VPIs consistently lagged behind (p < 0.001).ConclusionOur study revealed the different growth trajectories of preterm infants with different GAs. A set of growth curves and percentile values for preterm infants of different GAs between CAs of 0 and 36 months were established, offering an optional method for growth assessment of this special population.

ObjectiveCardiac biomarkers are widely used to evaluate postoperative myocardial injury, but studies on their relationship with cardiac function in pediatrics are limited. This study aimed to characterize the dynamic changes of cardiac biomarkers after congenital heart disease (CHD) surgery in patients aged 0–3 years and assess their correlation with cardiac function.MethodsWe retrospectively enrolled 63 pediatric patients (0–3 years) who underwent CHD surgery at Zhongnan Hospital between January 2021 and June 2024. Biomarkers and left ventricular ejection fraction (LVEF) were measured preoperatively and postoperatively within 1 week. The associations between the biomarkers and LVEF were analyzed. Receiver operating characteristic (ROC) curves were used to assess the predictive accuracy of the biomarkers for cardiac dysfunction, composite complications, and early mortality.ResultsBiomarker levels peaked on postoperative day (POD) 1 and declined to near-baseline levels within 1 week. LVEF decreased initially and then gradually recovered to near preoperative levels by POD 4–7. LVEF on POD 1 negatively correlated with the peak high-sensitivity troponin I (hs-TnI) and creatine kinase–MB (CK-MB) levels. The ROC analysis showed that hs-TnI and CK-MB had good predictive power for cardiac dysfunction (AUC = 0.818 and 0.828) and composite complications (AUC = 0.736 and 0.745), but limited value for early mortality (AUC = 0.665).ConclusionHs-TnI and CK-MB are key biomarkers that reflect the relationship between myocardial injury and cardiac function recovery after CHD surgery in pediatric patients aged 0–3 years. Their peak postoperative levels can predict cardiac function recovery and composite complications.

Sepsis-induced acute lung injury (ALI) is a critical condition characterized by excessive inflammation, with macrophage polarization playing a pivotal role in its pathogenesis. In this study, we constructed myeloid-specific Notch1 knockout mice, overexpressed the Notch intracellular domain (NICD), and inhibited β-catenin using XAV939 to investigate the impact and mechanisms of Notch1 regulation in macrophage polarization and inflammatory responses in cecal ligation and puncture (CLP)-induced septic mice. The results demonstrated that Notch1 knockout significantly reduced M1 macrophage polarization, alleviated systemic inflammation, mitigated lung injury, and improved survival in septic mice. In sepsis, Notch1 enhances β-catenin expression, which synergizes with the NF-κB pathway to promote M1 polarization and pro-inflammatory cytokine production. Specifically, NICD interacts with β-catenin in macrophages, amplifying NF-κB activation and its nuclear translocation. These results demonstrate that the Notch1 signaling pathway plays a pivotal role in regulating macrophage phenotypic switching, highlighting its potential as a therapeutic target for attenuating sepsis-associated ALI through immune homeostasis restoration.

Neutrophilic asthma (NA) is a common subtype of non-eosinophilic asthma, characterized by the infiltration of neutrophils. Basic leucine zipper transcription factor ATF-like (BATF) is the nuclear transcription factor that initiates lymphocyte differentiation. The mechanism by which BATF affects T cell differentiation leading to neutrophil accumulation in NA lung tissue remains unclear. In this study, we established murine models of NA through sensitization with ovalbumin (OVA) /complete Freund's adjuvant and subsequent challenge with OVA/lipopolysaccharide. Using these models, we systematically investigated pathological alterations, inflammatory cell infiltration patterns, and cytokine expression profiles in murine lung tissues. The impact of glucocorticoid intervention on the pathology of airway inflammation in NA mice was assessed, and the markers associated with lymphocyte differentiation RORγt and FoxP3 were detected. Furthermore, on the basis of BATF knockdown, the distribution of lymphocyte subtypes and the effect on neutrophil activity in the lung tissues of NA mice were observed. Our results revealed that both BATF and IL-17A showed high expression in NA lung tissue, and neutrophils were predominant in bronchoalveolar lavage fluid (BALF). Glucocorticoid treatment failed to alleviate lung histopathological lesion and exacerbated neutrophil accumulation in NA. Inhibiting BATF could significantly reduce neutrophil accumulation, as well as downregulate IL-17A expression, thus alleviating lung histopathological injury in NA. BATF was involved in mainly regulating naïve lymphocyte differentiation to T helper cell 17 (Th17) rather than regulatory T cells (Tregs). Our results demonstrate that BATF plays an important proinflammatory role in neutrophil asthma, and the inhibition of BATF could reduce lung inflammation by reducing IL-17A, acting as a potential therapeutic target.

PIM1, the proviral integration site for Moloney murine leukemia virus, is a member of the serine/threonine protein kinase family. It is involved in many biological events, such as cell survival, cell cycle progression, cell proliferation, and cell migration, and has been widely studied in malignant diseases. However, recent studies have shown that PIM1 plays a prominent role in immunoinflammatory diseases, including autoimmune uveitis, inflammatory bowel disease, asthma, and rheumatoid arthritis. PIM1 can function in inflammatory signal transduction by phosphorylating multiple inflammatory protein substrates and mediating macrophage activation and T lymphocyte cell specification, thus participating in the development of multiple immunoinflammatory diseases. Moreover, the inhibition of PIM1 has been demonstrated to ameliorate certain immunoinflammatory disorders. Based on these studies, we suggest PIM1 as a potential therapeutic target for immunoinflammatory diseases and a valid candidate for future research. Herein, for the first time, we provide a detailed review that focuses on the roles of PIM1 in the pathogenesis of immunoinflammatory diseases.

Prenatal dexamethasone exposure (PDE) can lead to increased susceptibility to various diseases in adult offspring, but its effect on gut microbiota composition and the relationship with disease susceptibility remains unclear. In this study, we find sex-differential changes in the gut microbiota of 6-month-old infants with prenatal dexamethasone therapy (PDT) that persisted in female infants up to 2.5 years of age with altered bile acid metabolism. PDE female offspring rats show abnormal colonization and composition of gut microbiota and increased susceptibility to cholestatic liver injury. The aberrant gut microbiota colonization in the PDE offspring can be attributed to the inhibited Muc2 expression caused by decreased CDX2 expression before and after birth. Integrating animal and cell experiments, we further confirm that dexamethasone could inhibit Muc2 expression by activating GR/HDAC11 signaling and regulating CDX2 epigenetic modification. This study interprets abnormal gut microbiota and disease susceptibility in PDT offspring from intrauterine intestinal dysplasia.

Moyamoya disease (MMD) is a condition characterized by the gradual narrowing and blockage of blood vessels in the brain, specifically those in the circle of Willis and the arteries that supply it.This results in reduced blood flow and oxygen to the brain, leading to progressive symptoms and potential complications.The underlying pathophysiological mechanism remains elucidated.However, recent studies have highlighted numerous etiologic factors: abnormal immune complex responses, susceptibility genes, branched-chain amino acids, antibodies, heritable diseases, and acquired diseases, which may be the great potential triggers for the development of moyamoya disease.Its clinical presentation has varying degrees from transient asymptomatic events to significant neurological deficits.Moyamoya disease (MMD) shows different patterns in children and adults.Children with MMD are more susceptible to ischemic events due to decreased blood flow to the brain.Conversely, adults with MMD are more prone to hemorrhagic events involving brain bleeding.Children with MMD may experience a range of symptoms including motor impairments, sensory issues, seizures, headaches, dizziness, cognitive delays, or ongoing neurological problems.Although adults may present with similar clinical symptoms as children, they are more prone to experiencing sudden onset intraventricular, subarachnoid, or intracerebral hemorrhages.One of the challenges in moyamoya disease is the potential for misdiagnosis or delayed diagnosis, particularly when physicians fail to consider MMD as a possible cause in stroke patients.This review aims to provide a comprehensive overview of recent global studies on the pathophysiology of MMD, along with advancements in its management.Additionally, the review will delve into various surgical treatment options for MMD, as well as its rare *Corresponding authors.

This article presents the diagnostic and therapeutic journey of a 14-year-old male patient diagnosed with Primary Amebic Meningoencephalitis (PAM), incorporates a review of pertinent literature and a discussion on recent advancements in the study of this condition. The patient presented with symptoms of fever and headache for three days, accompanied by seizures and a half-day episode of altered consciousness. Upon admission, clinical findings included a mild coma, respiratory distress, rigidity of limbs, and negative pathological reflexes. The patient's history showed in a local outdoor pond swimming in July and August of the same year. Metagenomic Next-Generation Sequencing (mNGS) of the cerebrospinal fluid identified the presence of Naegleria fowleri. Cranial CT and MRI scans indicated signs of brain edema and meningitis. The patient was confirmed with pediatric primary amebic meningoencephalitis. A 45-day comprehensive treatment regimen was administered, encompassing anti-amebic medications, anticonvulsant therapy, management of brain edema, and intracranial pressure reduction. This case represents the longest survival period recorded for such pediatric cases in China. The purpose of this report is to heighten clinical awareness of PAM, share diagnostic and therapeutic insights, expand upon existing treatment approaches, and ultimately contribute to improving the survival rates of PAM patients.

Background Gestational diabetes mellitus (GDM), a condition characterized by high blood sugar levels during pregnancy, is increasingly prevalent globally. While resolving after delivery, GDM can have lasting implications for the developing fetus, particularly regarding neurodevelopmental outcomes. This association is garnering significant attention within the medical community, driving research into the underlying mechanisms and potential interventions. We aimed to investigate the prevalence and association between gestational diabetes mellitus (GDM) and neurodevelopmental outcomes in infants. Methods This Retrospective Single Based cohort study utilized data from 2018 to 2022 at Zhongnan Hospital of Wuhan University. A total of 1430 for gestational diabetic mothers and 1430 infants aged 0 to 12months were recruited in the study. Inclusion criteria: Mothers with confirmed diagnosis of Gestational Diabetes Mellitus, no pre-gestational diabetes mellitus. Infants aged 0 to 12months, born from gestational diabetic mothers. Results A total of 1430 infants, male 832(58.18%); Female 598(41.82%). Prevalence of gestational diabetes mellitus was 75.61%. The overall Denver II Developmental Screening Test Results were; Normal 1370(95.80%), Abnormal 8(0.56%), Suspicious 44(3.10%) and Unable to Judge 8(0.56%). The probability of finding abnormal findings on DDST was higher on primiparity, p < 0.001; on normal head circumference, p = 0.002; on earliest infants’ age less than six months, p = 0.043; and on normal anterior fontanelle, p < 0.001. Mental response; infants with [(normal head circumference and microcephaly showed poor mental responses compared to macrocephaly infants p < 0.001); infants with low weight level, birth weights between 1-1.5k, 1.5-2.5kg and 2.5-4kg and normal anterior fontanelle showed abnormal mental responses; all p < 0.001]. Gender, maternal age, Gestational age, Delivery method, and Birth length, showed no statistically significant on mental response; p > 0.05. Conclusion The findings from this study underscore the significant impact of gestational diabetes mellitus on neurodevelopmental outcomes in exposed infants to GDM. Infants born to mothers with GDM showed varied neurodevelopmental and mental response impairments, with certain levels being more susceptible.

Objective This study is aimed to elucidate age-associated clinical and echocardiography-defined coronary artery (CA) abnormalities features and to identify independent determinants of CA dilatation in pediatric patients with complete Kawasaki disease (cKD) and incomplete KD (iKD) over 15 years in a tertiary hospital in China.Methods This study comprised 241 patients with KD hospitalized in the pediatric department between 2003 and 2018. Patients were divided into three groups according to age at diagnosis: <= 12, 13 to 35, and >= 36 months.Results A total of 167 (69.3%) patients were defined as cKD (aged 24 months, male 60.5%) and 74 (30.7%) patients as iKD (aged 18 months, male 59.5%). The prevalence of cervical lymphadenopathy significantly increased with age in both cKD and iKD patients. In iKD patients, the prevalence of rash significantly decreased with age. CA dilatation most frequently occurred in patients with cKD and iKD aged <= 12 months. The absence of conjunctivitis or oral changes and higher serum creatinine levels were independent determinants of CA dilatation in KD patients aged <= 12 months, regardless of age, sex, and the type of KD.Conclusion Present study underlines the age-stratified disease characteristics, and the factors associated with CA dilatation in cKD and iKD patients. The absence of conjunctivitis or oral changes, higher serum creatinine levels, and mycoplasma, cytomegalovirus, and adenovirus infections might be associated with an increased risk of CA dilatation in KD patients. These findings provide additional hints for pediatricians in the early diagnosis and treatment of KD, especially for individual medical care of cKD and iKD patients in different age groups.