Complement lectin pathway protein levels reflect disease activity in juvenile idiopathic arthritis : a longitudinal study of the Nordic JIA cohort
BACKGROUND: To determine the serum levels of the lectin pathway proteins early in the disease course and 17 years after disease onset and to correlate the protein levels to markers of disease activity in participants from a population-based Nordic juvenile idiopathic arthritis (JIA) cohort. Additionally, to assess the predictive value of lectin pathway proteins with respect to remission status.
METHODS: A population-based cohort study of consecutive cases of JIA with a disease onset from 1997 to 2000 from defined geographical areas of Finland, Sweden, Norway and Denmark with 17 years of follow-up was performed. Clinical characteristics were registered and H-ficolin, M-ficolin, MASP-1, MASP-3, MBL and CL-K1 levels in serum were analyzed.
RESULTS: In total, 293 patients with JIA were included (mean age 23.7 ± 4.4 years; mean follow-up 17.2 ± 1.7 years). Concentrations of the lectin protein levels in serum were higher at baseline compared to the levels 17 years after disease onset (p ≤ 0.006, n = 164). At baseline, the highest level of M-ficolin was observed in systemic JIA. Further, high M-ficolin levels at baseline and at 17-year follow-up were correlated to high levels of ESR. In contrast, high MASP-1 and MASP-3 tended to correlate to low ESR. CL-K1 showed a negative correlation to JADAS71 at baseline. None of the protein levels had prognostic abilities for remission status 17 years after disease onset.
CONCLUSION: We hypothesize that increased serum M-ficolin levels are associated with higher disease activity in JIA and further, the results indicate that MASP-1, MASP-3 and CL-K1 are markers of inflammation.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2019 |
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Erschienen: |
2019 |
Enthalten in: |
Zur Gesamtaufnahme - volume:17 |
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Enthalten in: |
Pediatric rheumatology online journal - 17(2019), 1 vom: 09. Sept., Seite 63 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Glerup, Mia [VerfasserIn] |
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Links: |
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Anmerkungen: |
Date Completed 08.04.2020 Date Revised 13.12.2023 published: Electronic Citation Status MEDLINE |
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doi: |
10.1186/s12969-019-0367-9 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM301094888 |
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245 | 1 | 0 | |a Complement lectin pathway protein levels reflect disease activity in juvenile idiopathic arthritis |b a longitudinal study of the Nordic JIA cohort |
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520 | |a BACKGROUND: To determine the serum levels of the lectin pathway proteins early in the disease course and 17 years after disease onset and to correlate the protein levels to markers of disease activity in participants from a population-based Nordic juvenile idiopathic arthritis (JIA) cohort. Additionally, to assess the predictive value of lectin pathway proteins with respect to remission status | ||
520 | |a METHODS: A population-based cohort study of consecutive cases of JIA with a disease onset from 1997 to 2000 from defined geographical areas of Finland, Sweden, Norway and Denmark with 17 years of follow-up was performed. Clinical characteristics were registered and H-ficolin, M-ficolin, MASP-1, MASP-3, MBL and CL-K1 levels in serum were analyzed | ||
520 | |a RESULTS: In total, 293 patients with JIA were included (mean age 23.7 ± 4.4 years; mean follow-up 17.2 ± 1.7 years). Concentrations of the lectin protein levels in serum were higher at baseline compared to the levels 17 years after disease onset (p ≤ 0.006, n = 164). At baseline, the highest level of M-ficolin was observed in systemic JIA. Further, high M-ficolin levels at baseline and at 17-year follow-up were correlated to high levels of ESR. In contrast, high MASP-1 and MASP-3 tended to correlate to low ESR. CL-K1 showed a negative correlation to JADAS71 at baseline. None of the protein levels had prognostic abilities for remission status 17 years after disease onset | ||
520 | |a CONCLUSION: We hypothesize that increased serum M-ficolin levels are associated with higher disease activity in JIA and further, the results indicate that MASP-1, MASP-3 and CL-K1 are markers of inflammation | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Multicenter Study | |
650 | 4 | |a Observational Study | |
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650 | 4 | |a JIA | |
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700 | 1 | |a Thiel, Steffen |e verfasserin |4 aut | |
700 | 1 | |a Rypdal, Veronika |e verfasserin |4 aut | |
700 | 1 | |a Arnstad, Ellen Dalen |e verfasserin |4 aut | |
700 | 1 | |a Ekelund, Maria |e verfasserin |4 aut | |
700 | 1 | |a Peltoniemi, Suvi |e verfasserin |4 aut | |
700 | 1 | |a Aalto, Kristiina |e verfasserin |4 aut | |
700 | 1 | |a Rygg, Marite |e verfasserin |4 aut | |
700 | 1 | |a Nielsen, Susan |e verfasserin |4 aut | |
700 | 1 | |a Fasth, Anders |e verfasserin |4 aut | |
700 | 1 | |a Berntson, Lillemor |e verfasserin |4 aut | |
700 | 1 | |a Nordal, Ellen |e verfasserin |4 aut | |
700 | 1 | |a Herlin, Troels |e verfasserin |4 aut | |
700 | 0 | |a Nordic Study Group of Pediatric Rheumatology (NoSPeR) |e verfasserin |4 aut | |
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