Background Pneumonia is the foremost cause of child death worldwide. M‐ficolin is encoded by the FCN1 gene and represents a novel link between innate and adaptive immunity. Objectives To investigate the FCN1 −144 C/A (rs10117466) polymorphism as a potential marker for pneumonia severity and adverse outcome namely complications or mortality in the under‐five Egyptian children. Methods This was a prospective multicenter study that included 620 children hospitalized with World Health Organization‐defined severe pneumonia and 620 matched healthy control children. Polymorphism rs10117466 of the FCN1 gene promoter was analyzed by PCR‐SSP, while serum M‐ficolin levels were assessed by ELISA. Results The FCN1 A/A genotype and A allele at the −144 position were more frequently observed in patients compared to the control children (43.4% vs 27.6%; odds ratio [OR]: 1.62; [95% confidence interval {CI}: 1.18‐2.2]; for the A/A genotype) and (60.8% vs 52.5%; OR: 1.4; [95% CI: 1.19‐1.65]; for the A allele); P < .01. The FCN1 −144 A/A homozygous patients had significantly higher serum M‐ficolin concentrations (mean: 1844 ± 396 ng/mL) compared with those carrying the C/C or C/A genotype (mean: 857 ± 278 and 1073 ± 323 ng/mL, respectively; P = .002). FCN1 −144 A/A genotype was an independent risk factor for adverse outcomes in children with severe pneumonia (adjusted OR = 4.85, [95% CI: 2.96‐10.25]; P = .01). Conclusion The FCN1 A/A genotype at the −144 position was associated with high M‐ficolin serum levels and possibly contributes to enhanced inflammatory response resulting in the adverse outcome of pneumonia in the under‐five Egyptian children.

Data on mitral valve replacement (MVR) in young children is still limited. Our objective was to evaluate MVR in children below 5 years and identify factors affecting the outcomes. This retrospective study included 29 patients who had MVR from 2002 to 2020. We grouped the patients into two groups according to their age: age ≤ 24 months (n = 18) and > 24 months (n = 11). Primary cardiac diagnoses were Shone complex (n = 7; 24%), isolated congenital mitral valve abnormality (n = 11; 38%), and complete atrioventricular septal defect (n = 3; 10%). The median age was 19 month (25th–75th percentile: 11–32) and 59% were females (n = 17). The hemodynamic lesions were mitral regurgitation in 66%, mitral stenosis in 10%, and combined mitral stenosis and regurgitation in 24% of the patients. St. Jude mitral valve was the most common valve implanted (n = 19, 66%), followed by CarboMedics in 21% of the patients (n = 6). The mitral valve was implanted in the supra-annular position in 6 cases (21%). Preoperative and operative data were comparable between both groups. There was no association between valve size and position with postoperative heart block (P > 0.99, for both). The median follow-up duration was 19.4 months (8.6–102.5). Nine patients had mitral valve reoperation, six had MVR, and three had clot removal from the mitral valve. There was no effect for age group on reoperation (SHR 0.89 (95% CI 0.27–2.87), P = 0.84). Valve size significantly affected reoperation (SHR 0.39 (95% CI 0.18–0.87), P = 0.02). The supra-annular position was associated with an increased risk of reoperation (SHR 3.1 (95% CI 1.003–9.4), P = 0.049). There was no difference in survival according to the age (Log-rank P = 0.57) or valve size (Log-rank P = 0.66). Mitral valve replacement in children is associated with low morbidity and mortality. The risk of reoperation could be affected by the valve size and position rather than the age.

Background Reinterventions after tetralogy of Fallot repair (TOF) remains a common clinical problem. The objective of this study was to evaluate types of reintervention after TOF repair and identify the risk factors for reinterventions. Methods This retrospective study was conducted from 2010 to 2022 and included 171 patients with complete TOF repair. Patients were grouped according to the occurrence of reintervention into two groups: patients who did not have reintervention (n = 138) and those who required reintervention (n = 33). Results Median follow-up was 36 (13–67) months. The first reintervention was required in 33 patients. Freedom from the first reintervention at 1, 3, 5, and 7 years was 91%, 85%, 81%, and 76%, respectively. Surgical reintervention was required in 12 patients and transcatheter intervention in 21 patients. Second reinterventions were required in 11 patients; 4 had surgery, and 7 had a transcatheter intervention. Third reinterventions were performed on two patients; one had surgery, and one had a transcatheter intervention. The most common interventions were performed at the level of pulmonary arteries (n = 17), followed by the pulmonary valve and the right ventricular outflow tract (n = 15). The risk of reintervention was associated with the low weight (HR: 0.65 (95% CI: 0.48–0.88); P = 0.005) and small LPA diameter (HR: 0.36 (95% CI: 0.21–0.60); P < 0.001) at the time of the primary intervention and the nonuse of the transannular patch (HR: 0.27 (95% CI: 0.08–0.85); P = 0.026). Conclusions The risk of reintervention is high after tetralogy of Fallot repair. In our experience, the smaller the left pulmonary artery and weight at the repair time increased the risk of reintervention. Using a transannular patch in our series was associated with a lower risk of reintervention.

Background Pediatric-onset SLE (pSLE) is a multisystem autoimmune disease. Recently, the ficolin-2 (FCN2) gene has emerged as a potential candidate gene for susceptibility to SLE. Objectives The objective of this study was to evaluate the association of the FCN2 gene polymorphisms at positions −986 (G/A), −602 (G/A), −4 (A/G) and SNP C/T (rs3124954) located in intron 1, with susceptibility to pSLE in Egyptian children and adolescents. Methods This was a multicenter study of 280 patients diagnosed with pSLE, and 280 well-matched healthy controls. The FCN2 promoter polymorphisms at –986 G/A (rs3124952), −602 G/A (rs3124953), −4 A/G (rs17514136) and SNP C/T (rs3124954) located in intron 1 were genotyped by polymerase chain reaction, while serum ficolin-2 levels were assessed using enzyme-linked immunosorbent assay. Results The frequencies of the FCN2 GG genotype and G allele at −986 and −602 positions were significantly more represented in patients with pSLE than in controls ( p < 0.001). Conversely, the FCN2 AA genotype and A allele at position −4 were more common in patients than in controls ( p < 0.001). Moreover, patients carrying the FCN2 GG genotype in −986 position were more likely to develop lupus nephritis (odds ratio: 2.6 (95% confidence interval: 1.4–4.78); p = 0.006). The FCN2 AA genotype at position −4 was also identified as a possible risk factor for lupus nephritis (odds ratio: 3.12 (95% confidence interval: 1.25–7.84); p = 0.024). Conclusion The FCN2 promoter polymorphisms may contribute to susceptibility to pSLE in Egyptian children and adolescents. Moreover, the FCN2 GG genotype at position −986 and AA genotype at position −4 were associated with low serum ficolin-2 levels and may constitute risk factors for lupus nephritis in pSLE.