Pediatric occipital lobe epilepsy (OLE) comprises syndromes with seizures originating from the posterior cerebral cortex. Previously “benign”, recent International League Against Epilepsy (ILAE) updates reclassified these as self-limited or structural focal epilepsies, reflecting their complex causes and morbidity potential. The 2017 ILAE guidelines shifted from syndromic recognition to an etiology-driven approach. High-resolution magnetic resonance imaging is crucial to differentiate self-limited genetic syndromes from structural OLE (e.g. , focal cortical dysplasia), as the latter often requires surgery. Self-limited epilepsy with autonomic seizures (formerly Panayiotopoulos syndrome) presents with prolonged nocturnal autonomic seizures. Childhood occipital visual epilepsy (previously Gastaut type) manifests as frequent, brief daytime visual hallucinations. Despite high seizure freedom rates with monotherapy, patients face neurocognitive challenges in visuospatial processing and academic performance. For drug-resistant structural cases, surgery offers high seizure freedom rates, though with risk of visual deficits. Accurate differentiation between idiopathic and structural OLE is essential for improving outcomes. The shift from “benign” to “self-limited” terminology emphasizes the need to monitor cognitive comorbidities and syndrome evolution. Early diagnosis is critical to avoid clinical mimics and enhance neurodevelopmental outcomes. This review examines the evolving landscape of pediatric OLE, highlighting the shift from syndromic to etiological classification and management strategies.
Autoimmune diseases in children, including type 1 diabetes, celiac disease, and juvenile arthritis, represent a growing global health challenge. This surge, too rapid to be explained by genetic shifts alone, highlights the critical role of environmental factors and underscores the urgent need for proactive prevention. This review presents an integrated, evidence-based framework for preventing pediatric autoimmune diseases across the care spectrum, from primordial to tertiary prevention. We define high-risk pediatric populations using a multidimensional approach that integrates family history, genetic data (e.g. , polygenic risk scores), and preclinical biomarkers. The review details a multi-tiered prevention strategy: Primordial prevention focuses on optimizing maternal and early-life health to establish immune tolerance in the first 1000 days; primary prevention targets at-risk children with personalized nutritional and lifestyle interventions; secondary prevention uses early screening and surveillance to identify preclinical autoimmunity, allowing for targeted immunomodulatory therapies that can delay or prevent disease onset; and tertiary prevention employs early aggressive therapy to limit long-term complications in children with established disease. By synthesizing epidemiological data, mechanistic understanding, and a comprehensive prevention framework, this article aims to inform clinical practice, guide research priorities, and support public health policies to combat the increasing incidence of pediatric autoimmunity.
BACKGROUND Kidney transplantation (KT) is essential for end-stage renal disease, significantly improving survival and quality of life. Yet, in pediatric renal disease management, minority children face poorer dialysis outcomes and reduced access to transplantation. AIM To identify and understand these differences in the pediatric population. METHODS Using ICD-10 codes, we queried the 2022 Health Care Cost and Use Project Kid’s Inpatient Database for admissions with a primary or secondary diagnosis of severe chronic kidney disease (sCKD), namely stages 4 and 5, or a KT procedure. Patient demographics, insurance types, and hospital stay metrics were assessed through statistical analyses including Wilcoxon Rank Sum, χ 2, and logistic regression. RESULTS A total of 636 hospital admissions related to KT surgery and 3733 hospital admissions with sCKD as the primary diagnosis were identified. In both the KT and sCKD cohorts, most patients were White (42.6% vs 36.6%), male (59.8% in both groups), aged 12-18 years (57.9% vs 50.3%), and insured by Medicaid (35.7% vs 43.0%). KT and sCKD hospitalizations were uncommon among infants aged 0-1 year (1.6% and 9.9%, respectively). Analysis of income quartiles based on patients’ residential zip codes demonstrated no significant differences between those who underwent KT and those with sCKD without transplant. Although mortality rates did not differ statistically between groups, a numerical difference was observed, with higher mortality in the sCKD cohort compared to the KT cohort (16 deaths vs 4 deaths). After adjusting for socioeconomic and geographic factors, Black race was independently associated with lower odds of undergoing KT (adjusted odds ratio 0.69; 95% confidence interval: 0.53-0.89). CONCLUSION Pediatric KT recipients were more likely to be male, White, and aged 12-18 years. Racial disparities persist, with ethnic minority groups-particularly Black patients-facing reduced access to KT. These findings underscore the necessity of implementing targeted interventions to promote equitable access to pediatric KT.
BACKGROUND:Previous studies have suggested a link between Helicobacter pylori (H. pylori) and metabolic complications outside the gastrointestinal tract, but the relationship with pediatric obesity remains unclear. We aim to study the correlation between H. pylori infection and components of insulin resistance (IR), inflammation [tumor necrosis factor-alpha (TNF-α)], and cardiometabolic parameters in obese children/adolescents with a metabolic syndrome (MetS) phenotype. AIM:To elucidate the association between H. pylori infection and metabolic disturbances in children with obesity and MetS, focusing on homeostasis model assessment of IR (HOMA-IR), inflammatory markers (TNF-α), and the lipid profile. METHODS:The study recruited 70 obese children/adolescents with MetS phenotype from the pediatric units of Minia University Hospital from September 2023 to October 2024. H. pylori stool antigen quantitative enzyme-linked immunosorbent assay was used to classify participants into H. pylori-negative (n = 35) and H. pylori-positive (n = 35). Assessment of fasting glucose, glycated hemoglobin (HbA1c), fasting insulin, lipid profile, liver enzymes, TNF-α, adiponectin, and leptin, as well as other parameters, was done. IR was calculated in detail using the HOMA-IR formula (fasting insulin × fasting glucose/405). Various statistical analyses, including intergroup comparisons, correlation analyses, and receiver operating characteristic curve analyses, were also performed. RESULTS:Groups were similar in age, sex, and standardized body mass index (BMI) value. Elevated blood pressure (65.7% vs 31.4%, P = 0.004) and hepatomegaly (62.9% vs 28.6%, P = 0.004) were more common in H. pylori-positive participants. The infected group had higher alanine aminotransferase and aspartate aminotransferase (AST) levels (both P < 0.001). It had higher triglycerides and low-density lipoprotein cholesterol and lower high-density lipoprotein cholesterol (HDL) levels, indicating a more unfavorable lipid profile (all P < 0.001) and more impaired glycemic/IR indices: Fasting glucose (158.5 ± 40.1 mg/dL vs 109.5 ± 22.7 mg/dL, P < 0.001), HbA1c (8.5 ± 2.2 vs 7.4 ± 1.7, P = 0.019), fasting insulin (9.4 ± 3.6 μIU/mL vs 3.9 ± 1.0 μIU/mL, P < 0.001), and HOMA-IR (3.61 ± 1.45 vs 1.06 ± 0.36, P < 0.001). TNF-α was elevated in the infected group (median 7.13 vs 6.23, P = 0.011). In H. pylori-positive participants, HOMA-IR had a strong positive correlation with standardized BMI value (r = 0.889, P < 0.001) and TNF-α (r = 0.896, P < 0.001). HOMA-IR > 1.67 had excellent sensitivity and specificity for detecting H. pylori positivity [area under the curve (AUC): 0.954; sensitivity 88.6%, specificity 97.1%], and TNF-α had moderate sensitivity (AUC: 0.677). CONCLUSION:H. pylori positivity was linked to elevated IR, TNF-α, atherogenic dyslipidemia, and a greater hepatic/clinical metabolic burden in the MetS phenotype of obesity in children and adolescents. More longitudinal studies that will help control socioeconomic and lifestyle confounding are warranted.
BACKGROUND Neonatal heart rate (HR) is an important parameter in the evaluation of newborn health and viability in the immediate postnatal period. AIM To evaluate the accuracy, reliability, and clinical applicability of emerging non-contact and artificial intelligence (AI)-assisted HR monitoring technologies in neonates compared to conventional electrocardiography (ECG)-based systems. METHODS A comprehensive literature search was conducted across PubMed, EMBASE, Google Scholar, and Cochrane databases from January 2013 through June 2025 following PRISMA guidelines. RESULTS The analysis revealed a progressive shift from contact-based ECG and pulse oximetry to camera-based photoplethysmography, thermal imaging, and AI-enhanced multimodal systems. These newer methods demonstrated a strong correlation with ECG readings, rapid signal acquisition, and improved robustness against motion and lighting variability. CONCLUSION Emerging non-contact, AI-assisted HR monitoring technologies offer accurate, safe, and efficient alternatives for neonatal care, supporting faster clinical decisions and improved outcomes. Future multicenter studies are required to validate accuracy and confirm clinical utility before routine clinical implementation.
BACKGROUND Preterm birth remains the leading cause of neonatal morbidity and mortality worldwide. Data from tribal-district neonatal intensive care units (NICUs) in India are scarce, despite these populations bearing a disproportionate burden of adverse perinatal outcomes. AIM To evaluate morbidity patterns and identify predictors of mortality among preterm neonates in a tribal-district NICU. METHODS The present retrospective cohort study included total 1438 preterm neonates admitted between January 2022 and December 2024 to the tribal-district NICU. Clinical data were extracted from medical records. Mortality was analyzed by gestational age. Multivariable logistic regression, with multiple imputation for missing data, was used to identify independent predictors of in-hospital mortality. RESULTS Mortality demonstrated a steep inverse gradient with gestational age, decreasing from 49% among extremely preterm neonates to 4.6% among late preterm infants. The most common morbidities were respiratory distress syndrome (42%-55%) and neonatal sepsis (32%-45%). Early continuous positive airway pressure (CPAP) initiation (< 1 hour) was associated with reduced need for mechanical ventilation (P < 0.001). In multivariable analysis, increasing gestational age [adjusted odd ratios (AOR): 0.82 per week; 95%CI: 0.75-0.89], higher birth weight (AOR: 0.93 per 100 g; 95%CI: 0.89-0.97), culture-positive sepsis (AOR: 3.41; 95%CI: 1.98-5.89), delayed CPAP initiation (AOR: 1.94; 95%CI: 1.15-3.28), and outborn status (AOR: 1.67; 95%CI: 1.01-2.74) were independently associated with mortality. Discharge against medical advice rates remained high (9%-11%). CONCLUSION Lower gestational age, lower birth weight, infection, and delayed respiratory stabilization are associated with mortality. Strengthening early neonatal care may improve survival in tribal settings.
BACKGROUND This case report expands the limited literature on phosphoglucomutase-1 deficiency (GSD XIV), a rare disorder that combines features of glycogen storage disease and congenital disorders of glycosylation. Given its wide clinical spectrum and often subtle early signs, under-recognition remains common. We report this case to highlight its multisystem involvement, emphasize diagnostic challenges, and reinforce the need for early consideration of GSD XIV in patients with unexplained hepatic, metabolic, and neuromuscular abnormalities. CASE SUMMARY We describe a case of a three-year-old girl born to consanguineous parents who presented with a constellation of atypical features, including cleft palate with bifid uvula, transient ventricular septal defect, hepatomegaly, persistent transaminitis, recurrent ketotic hypoglycemia, coagulopathy, febrile seizures, and emerging proximal muscle weakness. Despite an extensive workup, including metabolic, infectious, and immunologic testing, no clear diagnosis was identified in early infancy. Whole-exome sequencing revealed a homozygous pathogenic variant in PGM1 (c.1294G>T), confirming the diagnosis of GSD XIV. CONCLUSION This case highlights that genetic analysis is highly useful for diagnosing and specifying the subtype of GSD in patients with suspected multiorgan involvement, particularly those presenting with persistent transaminitis and neurological abnormalities.
BACKGROUND The TNFRSF1A gene encodes TNFR1, which regulates inflammation and apoptosis. Variants in this gene present with an autoinflammatory phenotype and are linked to tumor necrosis factor receptor associated periodic syndrome (TRAPS), an orphan monogenic autoinflammatory disease (AID) that can mimic systemic juvenile idiopathic arthritis (sJIA) and other rheumatic diseases. Despite known mechanisms and classification criteria, diagnosing and choosing therapy for patients with TNFRSF1A variants remains challenging. Assessing phenotypic characteristics and considering alternative therapies for these patients is important. AIM To evaluate the clinical and laboratory features of sJIA associated with the TNFRSF1A gene and treatment outcomes. METHODS A single-center, retrospective, cross-sectional cohort study with longitudinal follow-up was performed. A total of 66 patients with fever and a referral diagnosis of sJIA were included: 33 (50%) had TNFRSF1A gene variants identified by molecular genetic testing, and 33 (50%) had no TNFRSF1A or other autoinflammatory gene variants. Demographic, clinical, laboratory, and treatment data were collected before and after verification of AID, and again at 3, 6, and 12 months. RESULTS Molecular genetic testing identified several TNFRSF1A variants. Of 33 patients, 4 (12%) had likely pathogenic variants, 1 (3%) had a pathogenic variant, and 3 (9.1%) had variants of uncertain significance; all were heterozygous. The most common, identified in 27 (82%), was a variant of uncertain significance (c.362G>A, p.Arg121Gln) with incomplete penetrance. These patients had paroxysmal (48.5%) or continuous fever (48.5%), rash (66.7%), joint syndrome (78.8%), abdominal pain (33.3%), gastrointestinal symptoms (27.2%), eye involvement (24.2%), chest pain (12.1%), hearing loss (9.1%), periorbital edema (9.1%), arrested development (6.1%), aseptic meningitis (3%), hydrocephalus (3%), and amyloidosis (3%). Endoscopic signs of intestinal damage were found in 20 patients (60.6%): 11 showed upper gastrointestinal tract issues; 9 had intestinal pathology. All patients with TNFRSF1A variants received antirheumatic therapy before genetic testing. Treatments included intravenous glucocorticoids (GC) (45.5%), oral GC (45.5%), intravenous immunoglobulin (18.1%), methotrexate (48.5%), cyclosporine (18.1%), azathioprine (3%), mesalazine (3%), sulfasalazine (3%), and biological (b) disease-modifying antirheumatic drugs (bDMARDs) (72.7%). Of those on bDMARDs, 39.4% received tocilizumab, 9.1% abatacept, 6.1% canakinumab, 6.1% infliximab, 3% rituximab, 3% etanercept, 3% adalimumab, and 3% certolizumab pegol. Among 24 patients with three prior bDMARD switches before genetic diagnosis, 17 (70.8%) achieved remission: 7 on tocilizumab, 6 on canakinumab, 2 on adalimumab, 1 on infliximab, and 1 on rituximab. After confirming AID, all patients received biological therapy: 9 previously untreated patients started canakinumab (3), tocilizumab (3), or etanercept (3); 7 switched drugs after ineffective prior therapy. After all therapy adjustments, all patients achieved remission: 13 on tocilizumab, 11 on canakinumab, 3 on adalimumab, 2 on etanercept, 1 on golimumab, 1 on rituximab, and 1 with GC and colchicine followed by withdrawal. Patients started on bDMARDs after genetic testing required fewer drug switches than those treated empirically before diagnosis (0.23 ± 0.42 vs 0.9 ± 0.6, P = 0.001). CONCLUSION Variants in the TNFRSF1A gene may cause a wide range of clinical symptoms, including eye and intestinal lesions that are not typical of sJIA. All patients with fever and unusual sJIA symptoms should have molecular genetic testing for TNFRSF1A variants to confirm or exclude AID early. Early diagnosis enables timely therapy and prevents complications. Tocilizumab (39.3%), canakinumab (33.3%), and TNF inhibitors (21.2%) achieved remission in children with TNFRSF1A variants. Some patients required multiple bDMARD switches to achieve remission, highlighting the complexity of treatment decisions in this group.
In infants who are born with a gestational age of 32 weeks or less, bronchopulmonary dysplasia (BPD) is persistently a significant cause of morbidity. Early gestational age, low birth weight, prolonged mechanical ventilation, prolonged oxygen exposure, and neonatal sepsis were found to be important predictors of BPD in Palestinian private hospitals by Algharabeh et al in a retrospective cohort study published in World Journal of Clinical Pediatrics . These results underline the ongoing significance of modifiable postnatal exposures and support the complex character of BPD. The study additionally shows several significant maternal-newborn relationships, including preeclampsia and patent ductus arteriosus, eclampsia and neonatal sepsis, preterm rupture of membranes and retinopathy of prematurity (ROP), and multiple gestations with late-onset sepsis and ROP. Impaired alveolarization and aberrant pulmonary vascular development due to oxidative stress, inflammation, and ventilator-associated lung injury are the main features of BPD. These findings necessitates the need for lung-protective ventilation strategies, judicious use of oxygen, infection prevention and control, and improvement in maternal health. The study by Algharabeh et al has limitations like a retrospective design and a single-center setting. But still, it provides useful insights and highlights the need for further prospective research design to refine prevention strategies and improve adverse respiratory outcomes.
Phenomenology offers a powerful methodological lens through which pediatric nursing researchers can explore the emotional, cultural, and relational dimensions of caring for children with chronic illnesses. Drawing on a series of qualitative studies conducted with Jordanian mothers of children living with conditions such as type 1 diabetes mellitus, cerebral palsy, autism spectrum disorder, end-stage renal failure, and glycogen storage disease, this article reflects on the practical and philosophical applications of phenomenological inquiry in pediatric contexts. The insights presented highlight how lived experiences reveal layers of meaning often overlooked within biomedical models of care, including spiritual interpretation, cultural expectations, stigma, maternal resilience, and the evolving identity of caregiving mothers. Ultimately, the article illustrates how phenomenological principles, particularly bracketing, reflexivity, and sustained engagement during interviews, support the development of nuanced, context-sensitive understandings that can inform pediatric nursing practice. By integrating lessons across multiple studies, this Field of Vision article demonstrates how phenomenology enriches pediatric nursing research and contributes to more holistic, empathetic, and culturally grounded approaches to clinical care.
BACKGROUND Acute respiratory tract infections (ARTIs) are a major cause of pediatric morbidity. Daycare centers (DCCs) are high-risk environments where close interpersonal contact facilitates rapid viral transmission. Effective and practical preventive strategies are therefore essential to reduce infection-related burden in these settings. AIM To determine the incidence of ARTIs in DCCs following implementation of a structured protocol designed to mitigate respiratory virus transmission. METHODS A cluster study was conducted in which two centers were centers to either intervention or control groups via lottery. Although allocation was randomized, the study was not designed as a randomized controlled trial; therefore, potential bias and confounding were considered. Participants were followed for 25 weeks. The primary outcome was physician-diagnosed ARTIs per 100 child-weeks. Incidence rate ratios (IRRs) with 95%CIs were estimated using Poisson regression with a log link and person-time offset, adjusting for covariates under the intention-to-treat principle. Results cautious interpretation Due to limited clusters, results require cautious interpretation. Statistical significance was defined as P < 0.05. RESULTS A total of 223 children (149 intervention, 74 control) across 2 clusters were enrolled. By week 25, the cumulative proportion of ARTIs was 18.1% in the intervention group compared with 60.8% in the control group. The incidence rate of ARTIs was lower in the intervention group, with adjusted rates of 1.09 per 100 child-weeks vs 13.00 per 100 child-weeks. The adjusted IRR was 0.14 (95%CI: 0.09-0.22; P < 0.001), suggesting an observed difference in incidence between groups under the study conditions. CONCLUSION Protocol implementation was associated with a lower observed incidence of ARTIs under the study conditions. However, interpretation is constrained by the study design, the small number of clusters, and potential sources of bias. Larger, well-designed randomized studies are required to further evaluate this association in daycare settings.
BACKGROUND Intercellular adhesion molecule-1 (ICAM-1) plays a key role in mediating leukocyte adhesion and endothelial injury. Elevated circulating levels of soluble ICAM-1 (sICAM-1) in patients undergoing hemodialysis (HD) have been linked to a higher incidence of cardiovascular complications. AIM To evaluate the impact of dialysis modality and membrane performance on post-dialysis sICAM-1 levels in children undergoing maintenance HD. METHODS This study included 26 children on low-flux HD for at least 3 months and 26 sex-matched and age-matched healthy controls. Patients were shifted to high-flux HD for 3 months, then subsequently to post-dilutional online hemodiafiltration (OL-HDF) for additional 3 months. At the end of each study phase, blood samples were obtained before and after a mid-week HD session for sICAM-1 measurement. To account for hemoconcentration, post-session ICAM-1 were hematocrit-adjusted using van Beaumont’s formula yielding corrected ICAM-1 (cICAM-1). RESULTS Circulating post-dialysis cICAM-1 levels increased significantly after low-flux HD compared with the corresponding pre-dialysis levels (P = 0.002), and were also significantly higher than those of the control group (P < 0.001). Following conversion to high-flux HD, post-dialysis cICAM-1 concentrations decreased significantly compared to pre-dialysis values (P < 0.001), although they remained elevated compared to controls (P = 0.026). In contrast, OL-HDF was associated with a substantial decline in post-session cICAM-1 levels (P < 0.001), yielding values comparable to those observed in the control group (P = 0.898). CONCLUSION Children on maintenance HD exhibit elevated sICAM-1 levels. Our findings suggest that higher-efficiency dialysis modalities, such as OL-HDF, may attenuate dialysis-related inflammation and endothelial activation in these patients.
