Autoinflammatory & rare systemic diseases
Clinical characteristics, inflammatory biomarkers and genetic background of patients with non-hereditary periodic fever syndromes
Authors' conclusion
Analysis of routine and experimental biomarkers revealed heterogeneous immune dysregulation. Elevation of several inflammatory mediators in afebrile sample of patients with periodic fever indicates subclinical inflammation with granulocyte colony-stimulating factor and interleukin-18 notably higher in SURF than in PFAPA. Our data provide new insights into the immune mechanisms of non-hereditary periodic fever syndromes and support further biomarker-driven research.
Study context
- Population
- Patients with non-hereditary periodic fever syndromes (syndrome of undifferentiated recurrent fever (SURF) and PFAPA), febrile controls and healthy controls94 patients and 35 controls · patients 94 · controls 35
- Exposure
- SURF vs PFAPA, and patients with periodic fever vs febrile and healthy controls, during febrile and afebrile conditions
- Outcome
- Rash, diarrhoea, arthralgia, myalgia and abdominalgia, and fever duration
Main finding
As reported in the abstract
- More frequent, with longer fever duration, in SURF than in PFAPA
Observational data: associations, not effects.
Further findings
| Outcome | P value |
|---|---|
| Response to episodic prednisonePFAPA vs SURF · significantly better response with PFAPA | P < 0.001 |
| Mediators in afebrile samples, SURF vs PFAPANine mediators higher and one lower in SURF | P < 0.05 |
Inflammatory parameters and cytokines in febrile samples
- Did not differ between groups apart from C-reactive protein (CRP) being higher in periodic fever than controls
Proinflammatory cytokines in afebrile samples, periodic fever vs healthy controls
- Proinflammatory cytokines significantly higher than in healthy controls
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Original publication
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