ArticleTranslational pediatrics2025
IgG4 elevation dilemma at the crossroads of helminth infection and IgG4-related disease: insights from a case report of pediatric paragonimiasis with persistent pericardial effusion.
Article in Translational pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Quantitative total serum IgG4 reporting in human paragonimiasis: a scoping review.Tropical medicine and health · 2026Review
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4 authors.
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Abstract
Background: Immunoglobulin G4 (IgG4)-related disease (IgG4-RD) is a systemic fibroinflammatory disorder defined by elevated serum IgG4, tissue IgG4+ plasma cell infiltration, and multi-organ involvement. Paradoxically, helminth infections may also trigger IgG4 elevation through Th2-polarized immune responses, creating diagnostic ambiguity when overlapping features occur. Critically, no studies have addressed whether IgG4-RD with helminthiasis can coexist in children or how to differentiate them when histopathology is unavailable. Case Description: A 10-year-old boy with confirmed pulmonary paragonimiasis developed refractory pericardial effusion and markedly elevated IgG4 [11 g/L, 8.1× upper limit of normal (ULN)]. Despite five courses of praziquantel (75 mg/kg/day), effusions persisted for 8 weeks. Subsequent glucocorticoids (methylprednisolone 2 mg/kg/day) achieved rapid clinical resolution, though lacked histopathology IgG4-RD hallmarks. Longitudinal monitoring revealed a dynamic IgG4 decline (from 11 to 5.25 g/L) post-methylprednisolone therapy. However, residual IgG4 elevation (5.25 g/L, >3× ULN) and absent histopathological features of IgG4-RD left the diagnosis unresolved. Therapeutic monitoring revealed normalized eosinophils and imaging improvement, yet persistent IgG4 suggested potential immune dysregulation beyond parasitic clearance. Conclusions: This case highlights a critical diagnostic dilemma: IgG4 elevation in parasitic infections may mimic or coexist with IgG4-RD. The rapid glucocorticoid response argues against simple parasitic infections, yet incomplete IgG4 normalization post-treatment leaves coexistence unresolved. Clinicians must weigh these possibilities when anti-helminthic therapy fails, particularly when histopathology is absent. Prospective studies should define pediatric-specific IgG4 thresholds to disentangle infection from autoimmunity.
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