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Evaluation of subclinical inflammation in familial Mediterranean fever patients: relations with mutation types and
Fatih Mehmet Kelesoglu1, Erhan Aygun2, Nazli Kubra Okumus2
1Department of Pediatric Rheumatology, Istanbul Medical School, Istanbul University, Millet Caddesi, Fatih, Istanbul, 34093, Turkey. fatihmk@istanbul.edu.tr.
Abstract:
Familial Mediterranean fever (FMF) is an autosomal recessive autoinflammatory disease of childhood and adulthood. Development of systemic amyloidosis and frequent attack influence quality of life and survival. There is sporadic evidence indicating subclinical inflammation in patients with FMF. We aimed to assess subclinical inflammation using neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), and C-reactive protein (CRP) in pediatric patients with FMF in the attack-free period. In this retrospective study, we reviewed the files of all FMF patients in our pediatric rheumatology outpatient clinic in a tertiary center and enrolled those with sufficient clinical and laboratory data. We also enrolled 73 controls. We grouped the patients according to being in attack period or attack-free period. We compared CRP, NLR, PLR, and WBC (white blood cell) levels between different mutations and polymorphisms. We also compared patients in the attack period with those in attack-free period. We enrolled 61 patients in attack period, 509 patients in attack-free period, and 73 controls. There was no difference between patients with different mutations with respect to NLR or PLR levels in the attack-free period. However, CRP levels were higher in patients with homozygous exon 10 mutations, especially those with homozygous M694V mutations compared with other mutations. However, CRP levels were mostly normal in these patients. Our data are against the reported fact that patients with FMF have higher NLR or PLR levels in attack-free periods. However, CRP levels were higher in the presence of homozygous exon 10 mutations (in particular homozygous M694V mutations).
Insights
Subclinical inflammation in Familial Mediterranean Fever (FMF) was assessed using neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and C-reactive protein (CRP). CRP levels were elevated in patients with specific FMF mutations, even during attack-free periods.
Area of Science:
- Pediatric Rheumatology
- Autoinflammatory Diseases
- Clinical Immunology
Background:
- Familial Mediterranean Fever (FMF) is an autoinflammatory disorder impacting quality of life and survival due to systemic amyloidosis and frequent attacks.
- Subclinical inflammation in FMF patients, particularly during attack-free periods, requires further investigation.
- Biomarkers like neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and C-reactive protein (CRP) may indicate subclinical inflammation.
Purpose of the Study:
- To evaluate subclinical inflammation in pediatric FMF patients during attack-free periods.
- To assess the utility of NLR, PLR, and CRP as inflammatory markers in FMF.
- To compare inflammatory markers across different FMF mutations and between attack and attack-free periods.
Main Methods:
- Retrospective analysis of clinical and laboratory data from pediatric FMF patients and controls.
- Comparison of NLR, PLR, and CRP levels in FMF patients during attack and attack-free periods.
- Analysis of inflammatory markers based on FMF genotype, including homozygous exon 10 and M694V mutations.
Main Results:
- No significant difference in NLR or PLR was observed between FMF patients with different mutations in the attack-free period.
- C-reactive protein (CRP) levels were higher in patients with homozygous exon 10 mutations, particularly homozygous M694V, compared to other mutations.
- CRP levels were generally within normal limits, even in patients with elevated levels associated with specific mutations.
Conclusions:
- The study findings challenge the notion of elevated NLR or PLR in attack-free FMF periods.
- Elevated CRP levels may be associated with specific FMF genotypes, such as homozygous exon 10 mutations.
- Further research is needed to elucidate the role of these markers in FMF pathogenesis and management.
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