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Increased serum concentrations of neutrophil-derived protein S100A12 in heterozygous carriers of MEFV mutations
M. Lieber1, T. Kallinich2, P. Lohse3, J. Klotsche4, D. Holzinger5, D. Foell6, H. Wittkowski7
- Department of Paediatric Pneumology and Immunology, Charité University Hospital Berlin, Germany.
- Department of Paediatric Pneumology and Immunology, Charité University Hospital Berlin, Germany. tilmann.kallinich@charite.de
- Department of Clinical Chemistry, Großhadern, University of Munich, Munich, Germany.
- German Rheumatism Research Centre Berlin, a Leibniz Institute, Berlin; and Institute for Social Medicine, Epidemiology and Health Economics, Charité Universitaetsmedizin, Berlin, Germany.
- Department of Paediatric Rheumatology and Immunology, University Children’s Hospital Münster, Germany.
- Department of Paediatric Rheumatology and Immunology, University Children’s Hospital Münster, Germany.
- Department of Paediatric Rheumatology and Immunology, University Children’s Hospital Münster, Germany.
CER8488
2015 Vol.33, N°6 ,Suppl.94
PI 0113, PF 0116
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PMID: 26486615 [PubMed]
Received: 27/03/2015
Accepted : 30/06/2015
In Press: 19/10/2015
Published: 04/11/2015
Abstract
OBJECTIVES:
To assess subclinical inflammation in heterozygous carriers of Mediterranean fever (MEFV) gene mutations, analysis of classical inflammation markers and S100A12 was performed.
METHODS:
Exons 2, 3, and 10 of the MEFV gene, C-reactive protein (CRP), serum amyloid A protein (SAA), procalcitonin (PCT), and S100A12 concentrations, erythrocyte sedimentation rate (ESR), and differential blood count were analysed in apparently healthy parents (n=26) of homozygous children with familial Mediterranean fever (FMF). Their general health condition was assessed by a standardised questionnaire. In order to collect data on the disease course, subjects were reevaluated after 5 years by means of telephone interview and/or questionnaire.
RESULTS:
Twenty-two individuals with one typical mutation in the MEFV gene were included. Mean values (mean±SEM) of classical inflammation markers were within the normal range (ESR of 11.7±1.9 mm/h, SAA 4.7±0.4 mg/l, CRP 0.26±0.04 mg/dl), while PCT was non-detectable in all cases (<0.1 μg/l). Eleven subjects showed elevated S100A12 levels [>140 ng/ml] with a mean concentration of 205±43 ng/ml. Thus, the mean value of S100A12 was 1.5-fold higher than the regular cut-off.
CONCLUSIONS:
50% of the heterozygous MEFV mutation carriers exhibited elevated S100A12 levels, supporting previous observations that S100 molecules are very sensitive biomarkers of subclinical inflammation. Possibly, S100A12 could be a prognostic biomarker to detect individuals at risk of FMF manifestation who might benefit from colchicine therapy.
