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Admission inflammatory biomarker phenotypes and risk of severe community-acquired pneumonia and PARDS in young children

In brief

Hyper-inflammatory biomarker profile raises PARDS risk twelvefold in kids with pneumonia

In a cohort of 129 children under five hospitalized for community-acquired pneumonia, three inflammatory phenotypes were defined using routine labs; the hyper-inflammatory group had about a twelve-times higher odds of developing pediatric ARDS and nearly five-times higher odds of severe pneumonia at admission. Adding the phenotype improved prediction modestly, but neutrophil-to-lymphocyte ratio alone performed similarly, so external validation is needed.

Journal
European journal of pediatrics (Q1)
Published
8 August 2026
Study design
Prospective / inception cohort
Evidence level
Level 2, Moderate (CEBM 2b)
Authors
Duong T K Loan, Ngo C Quang, Ta V Tram, Tran D Hung, Nguyen T T Nhan
PMID
42570118
DOI
10.1007/s00431-026-07317-3

Why clinicians should know about it

  • Picked for Pediatrics and Child Health (paper of the day, 11 August 2026): Inflammatory biomarker phenotypes predict severe CAP and PARDS

Abstract

UNLABELLED: Advanced cytokine-based frameworks for pediatric acute respiratory distress syndrome (PARDS) are not readily applicable in routine practice. We investigated whether routinely available admission biomarkers could define inflammatory phenotypes in young children hospitalized with community-acquired pneumonia (CAP) and provide prognostic information for severe CAP and in-hospital PARDS, with potential relevance for resource-constrained settings. In this prospective cohort of children aged < 5 years hospitalized with CAP, seven admission biomarkers (neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, lymphocyte-to-monocyte ratio, systemic immune-inflammation index, systemic inflammation response index, C-reactive protein, and procalcitonin) were log1p-transformed, standardized, and analyzed using K-means clustering. Associations with severe CAP at admission and definite in-hospital PARDS were examined using age- and sex-adjusted logistic regression. Incremental prognostic performance was evaluated using nested models, receiver operating characteristic analysis, calibration, and decision curve analysis. Among 129 children, three biomarker phenotypes were identified: low-inflammatory (n = 40), intermediate-inflammatory (n = 60), and hyper-inflammatory (n = 29). Compared with the low-inflammatory phenotype, adjusted odds of PARDS were higher in the intermediate-inflammatory (OR 4.00, 95% CI 1.17-18.6; p = 0.043) and hyper-inflammatory phenotypes (OR 11.6, 95% CI 2.90-60.9; p = 0.001). Only the hyper-inflammatory phenotype was independently associated with severe CAP at admission (OR 4.79, 95% CI 1.54-16.2; p = 0.009). Adding biomarker phenotype to age and sex improved PARDS discrimination (AUC 0.571 to 0.716), but discrimination was similar to NLR alone (AUC 0.711), and gain beyond severe CAP was modest. CONCLUSIONS: Routine admission biomarkers identified inflammatory phenotypes associated with severe CAP and PARDS. This low-cost may be relevant in resource-constrained settings but requires external validation. WHAT IS KNOWN: • Hyperinflammatory biology is associated with worse outcomes in pediatric CAP and PARDS, but most biomarker frameworks rely on research-oriented cytokine panels. • Routine admission biomarkers such as CRP, PCT, and CBC-derived indices are widely available, but their value for inflammatory phenotyping remains unclear. WHAT IS NEW: • Routine admission biomarkers identified three clinically interpretable inflammatory phenotypes in young children hospitalized with CAP. • The hyper-inflammatory phenotype was associated with severe CAP and PARDS; this pragmatic approach may be relevant in resource-constrained settings, although discrimination was similar to NLR alone.

Abstract as published, via PubMed.

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For healthcare professionals. The summary is generated by AI from the published abstract, and the evidence level is assigned automatically from the study design on the Oxford CEBM hierarchy. Neither is medical advice. Read the full paper before changing practice.