Background/Objectives: We aimed to evaluate the etiologic distribution of markedly elevated IgE (≥2000 IU/mL) and the association of parasitic infections with longitudinal IgE dynamics and National Institutes of Health Hyper-IgE Syndrome (NIH-HIES) score trajectories in pediatric patients. Methods: We retrospectively enrolled 127 pediatric patients with IgE ≥2000 IU/mL and ≥1 year of longitudinal follow-up at a tertiary allergy clinic (2019–2024). The primary outcome was the IgE reduction percentage difference between parasitic and non-parasitic groups. Results: Atopic sensitization was identified in 81.0% of tested patients; genetic evaluation was performed in 40 patients (31.5%), with confirmed IEI in one patient (0.8% of the cohort; 2.5% of those evaluated). Parasitic infections were present in 24.4% of patients (n = 31; intestinal parasites 15.7%, scabies 8.7%, hydatid cyst 1.6%; two patients had concurrent intestinal parasitosis and scabies). Median IgE reduction was 63.8% vs. 27.0% in parasitic versus non-parasitic groups (p < 0.001), persisting after multivariable adjustment (p < 0.001). Parasitic infection independently predicted IgE normalization below 2000 IU/mL (OR = 8.26; 95% CI: 2.76–24.68; p < 0.001). All three NIH-HIES inflammatory components (IgE, eosinophilia, eczema) regressed more often in the parasitic group (all p ≤ 0.01); no patient reached the ≥40-point HIES threshold. Conclusions: Parasitic infections produce a clinical phenotype overlapping with hyper-IgE syndrome, constituting a reversible phenocopy of primary immune dysregulation. In populations with substantial parasitic prevalence, parasitological evaluation may be a useful consideration in children with markedly elevated IgE and indeterminate clinical scores; however, this approach should complement rather than replace comprehensive clinical assessment.

Objective: Conventional markers such as serum creatinine and eGFR may lack sensitivity for detecting early graft dysfunction. Since pancreatic enzymes are primarily eliminated via the kidneys, this study aimed to evaluate serum amylase and lipase levels in pediatric kidney transplant recipients and investigate their relationship with graft function.Materials and Methods: This retrospective, dual-center study included 52 pediatric kidney transplant recipients (2011–2021) and 50 age- and sex-matched healthy controls. eGFR was calculated using the modified Schwartz formula. The correlation between pancreatic enzymes and clinical/laboratory variables was statistically analyzed.Results: Serum amylase and lipase levels were significantly higher in the transplant group compared to the control group (p < 0.05). A significant negative correlation was found between eGFR and both amylase (r = −0.689, p < 0.01) and lipase (r = −0.443, p < 0.01). After multivariable adjustment, eGFR was the only independent correlate of serum amylase (β = −1.16, p < 0.001), whereas body mass index was the only independent correlate of lipase (β = 1.56, p = 0.006). On ROC analysis, amylase discriminated transplant recipients from controls with an area under the curve of 0.90. Obesity, hypertension, and dyslipidemia were more prevalent among recipients but showed no independent association with enzyme levels. No significant correlation was observed between immunosuppressive therapy and enzyme levels.Conclusions: Elevated amylase primarily reflected reduced eGFR and thus graft function, whereas lipase reflected adiposity. Whether these enzymes add clinical value beyond conventional graft function markers remains to be determined in prospective longitudinal studies.