Serum calprotectin may reflect inflammatory activity in patients with active rheumatoid arthritis despite normal to low C-reactive protein
Jazyk angličtina Země Německo Médium print-electronic
Typ dokumentu časopisecké články
Grantová podpora
023728
Project of the Ministry of Health of the Czech Republic for conceptual research development by organization
260373
Specific Academy Research Projects (SVV)
PubMed
29656372
DOI
10.1007/s10067-018-4091-5
PII: 10.1007/s10067-018-4091-5
Knihovny.cz E-zdroje
- Klíčová slova
- C-reactive protein, Calprotectin, Inflammation, Rheumatoid arthritis,
- MeSH
- biologické markery krev MeSH
- C-reaktivní protein analýza MeSH
- krevní sedimentace MeSH
- leukocytární L1-antigenní komplex krev MeSH
- lidé středního věku MeSH
- lidé MeSH
- referenční hodnoty MeSH
- revmatoidní artritida krev MeSH
- stupeň závažnosti nemoci MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Finsko MeSH
- Názvy látek
- biologické markery MeSH
- C-reaktivní protein MeSH
- leukocytární L1-antigenní komplex MeSH
Approximately half of patients with rheumatoid arthritis (RA) have normal C-reactive protein (CRP) levels. Calprotectin is a promising and likely more specific biomarker of disease activity than conventionally used acute phase reactants. We aimed to analyse the levels of serum calprotectin in RA patients with clinically active disease and with normal/low CRP. A total of 160 RA patients underwent clinical examination (DAS28-ESR and CDAI). The levels of calprotectin were analysed in patients with moderate to high disease activity with normal/low CRP levels and in 32 healthy subjects. The discriminatory capacity of calprotectin to identify clinically active patients in spite of normal/low CRP was assessed using ROC curves. Out of all RA patients, 74/160 (46.3%) were in remission or had low disease activity according to DAS28 and had normal/low CRP levels. However, 51/160 (32%) had normal/low CRP levels despite having moderate to high disease activity. In these patients, calprotectin levels were significantly higher than those in patients who had normal/low CRP and were in remission or showed low disease activity (2.7 ± 1.5 vs. 2.1 ± 1.2 μg/mL, p = 0.043), which differed from those in healthy subjects (2.7 ± 1.5 vs. 1.9 ± 1.2 μg/mL, p = 0.011). The discriminatory capacity for calprotectin to distinguish clinically active vs. inactive disease despite normal/low CRP using AUC of the DAS28 was 0.607 (95% CI 0.503 to 0.711, p = 0.043). The present study demonstrates that calprotectin may reflect inflammatory activity in RA patients where CRP fails to do so.
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