The relation between C-reactive protein and serum amyloid A in patients with autoinflammatory diseases
Autoinflammatory diseases are rare disorders of the innate immune system characterized by fever and other signs of inflammation. A feared complication of autoinflammatory diseases is the development of AA amyloidosis. AA amyloidosis is caused by extracellular deposition of soluble serum amyloid A (S...
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Published in: | Pediatric rheumatology online journal Vol. 20; no. 1; p. 106 |
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Abstract | Autoinflammatory diseases are rare disorders of the innate immune system characterized by fever and other signs of inflammation. A feared complication of autoinflammatory diseases is the development of AA amyloidosis. AA amyloidosis is caused by extracellular deposition of soluble serum amyloid A (SAA) proteins as insoluble amyloid fibrils leading to organ damage. Prolonged high levels of SAA are a prerequisite to develop AA amyloidosis. Since measurement of SAA is relatively expensive and sometimes unavailable, C-reactive protein (CRP) is often used as a surrogacy marker to test for inflammation.
The aim of this research is to evaluate the possible relation between CRP and SAA.
A retrospective cohort of patients with autoinflammatory diseases (n = 99) where SAA and CRP blood testing was performed in the period between 2015 and 2021 in the University Medical Centre in Groningen was used to investigate the correlation between CRP and SAA.
CRP and SAA have a high correlation (rho = 0.755, p < 0.001). A CRP value below 0.45 mg/L results in 100% sensitivity for SAA below 4 mg/L. CRP below 5 mg/L is a good predictor of SAA below 4 mg/L with 85.4% sensitivity and 83.6% specificity. Only prednisone and erythrocyte sedimentation rate (ESR) significantly influence the relation between CRP and log
SAA.
There was a significant correlation between CRP and SAA in our retrospective cohort. CRP levels below 5 mg/L proved to be highly predictive of SAA levels below 4 mg/L. This may not be true for patients on steroids. |
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AbstractList | Abstract Background Autoinflammatory diseases are rare disorders of the innate immune system characterized by fever and other signs of inflammation. A feared complication of autoinflammatory diseases is the development of AA amyloidosis. AA amyloidosis is caused by extracellular deposition of soluble serum amyloid A (SAA) proteins as insoluble amyloid fibrils leading to organ damage. Prolonged high levels of SAA are a prerequisite to develop AA amyloidosis. Since measurement of SAA is relatively expensive and sometimes unavailable, C-reactive protein (CRP) is often used as a surrogacy marker to test for inflammation. Objective The aim of this research is to evaluate the possible relation between CRP and SAA. Methods A retrospective cohort of patients with autoinflammatory diseases (n = 99) where SAA and CRP blood testing was performed in the period between 2015 and 2021 in the University Medical Centre in Groningen was used to investigate the correlation between CRP and SAA. Results CRP and SAA have a high correlation (rho = 0.755, p < 0.001). A CRP value below 0.45 mg/L results in 100% sensitivity for SAA below 4 mg/L. CRP below 5 mg/L is a good predictor of SAA below 4 mg/L with 85.4% sensitivity and 83.6% specificity. Only prednisone and erythrocyte sedimentation rate (ESR) significantly influence the relation between CRP and log10 SAA. Conclusion There was a significant correlation between CRP and SAA in our retrospective cohort. CRP levels below 5 mg/L proved to be highly predictive of SAA levels below 4 mg/L. This may not be true for patients on steroids. Background Autoinflammatory diseases are rare disorders of the innate immune system characterized by fever and other signs of inflammation. A feared complication of autoinflammatory diseases is the development of AA amyloidosis. AA amyloidosis is caused by extracellular deposition of soluble serum amyloid A (SAA) proteins as insoluble amyloid fibrils leading to organ damage. Prolonged high levels of SAA are a prerequisite to develop AA amyloidosis. Since measurement of SAA is relatively expensive and sometimes unavailable, C-reactive protein (CRP) is often used as a surrogacy marker to test for inflammation. Objective The aim of this research is to evaluate the possible relation between CRP and SAA. Methods A retrospective cohort of patients with autoinflammatory diseases (n = 99) where SAA and CRP blood testing was performed in the period between 2015 and 2021 in the University Medical Centre in Groningen was used to investigate the correlation between CRP and SAA. Results CRP and SAA have a high correlation (rho = 0.755, p < 0.001). A CRP value below 0.45 mg/L results in 100% sensitivity for SAA below 4 mg/L. CRP below 5 mg/L is a good predictor of SAA below 4 mg/L with 85.4% sensitivity and 83.6% specificity. Only prednisone and erythrocyte sedimentation rate (ESR) significantly influence the relation between CRP and log.sub.10SAA. Conclusion There was a significant correlation between CRP and SAA in our retrospective cohort. CRP levels below 5 mg/L proved to be highly predictive of SAA levels below 4 mg/L. This may not be true for patients on steroids. Keywords: Amyloidosis, Familial Mediterranean fever, Hereditary autoinflammatory diseases, Inflammation, Acute-phase proteins, C-reactive protein, Serum amyloid A protein BACKGROUNDAutoinflammatory diseases are rare disorders of the innate immune system characterized by fever and other signs of inflammation. A feared complication of autoinflammatory diseases is the development of AA amyloidosis. AA amyloidosis is caused by extracellular deposition of soluble serum amyloid A (SAA) proteins as insoluble amyloid fibrils leading to organ damage. Prolonged high levels of SAA are a prerequisite to develop AA amyloidosis. Since measurement of SAA is relatively expensive and sometimes unavailable, C-reactive protein (CRP) is often used as a surrogacy marker to test for inflammation. OBJECTIVEThe aim of this research is to evaluate the possible relation between CRP and SAA. METHODSA retrospective cohort of patients with autoinflammatory diseases (n = 99) where SAA and CRP blood testing was performed in the period between 2015 and 2021 in the University Medical Centre in Groningen was used to investigate the correlation between CRP and SAA. RESULTSCRP and SAA have a high correlation (rho = 0.755, p < 0.001). A CRP value below 0.45 mg/L results in 100% sensitivity for SAA below 4 mg/L. CRP below 5 mg/L is a good predictor of SAA below 4 mg/L with 85.4% sensitivity and 83.6% specificity. Only prednisone and erythrocyte sedimentation rate (ESR) significantly influence the relation between CRP and log10SAA. CONCLUSIONThere was a significant correlation between CRP and SAA in our retrospective cohort. CRP levels below 5 mg/L proved to be highly predictive of SAA levels below 4 mg/L. This may not be true for patients on steroids. Autoinflammatory diseases are rare disorders of the innate immune system characterized by fever and other signs of inflammation. A feared complication of autoinflammatory diseases is the development of AA amyloidosis. AA amyloidosis is caused by extracellular deposition of soluble serum amyloid A (SAA) proteins as insoluble amyloid fibrils leading to organ damage. Prolonged high levels of SAA are a prerequisite to develop AA amyloidosis. Since measurement of SAA is relatively expensive and sometimes unavailable, C-reactive protein (CRP) is often used as a surrogacy marker to test for inflammation. The aim of this research is to evaluate the possible relation between CRP and SAA. A retrospective cohort of patients with autoinflammatory diseases (n = 99) where SAA and CRP blood testing was performed in the period between 2015 and 2021 in the University Medical Centre in Groningen was used to investigate the correlation between CRP and SAA. CRP and SAA have a high correlation (rho = 0.755, p < 0.001). A CRP value below 0.45 mg/L results in 100% sensitivity for SAA below 4 mg/L. CRP below 5 mg/L is a good predictor of SAA below 4 mg/L with 85.4% sensitivity and 83.6% specificity. Only prednisone and erythrocyte sedimentation rate (ESR) significantly influence the relation between CRP and log.sub.10SAA. There was a significant correlation between CRP and SAA in our retrospective cohort. CRP levels below 5 mg/L proved to be highly predictive of SAA levels below 4 mg/L. This may not be true for patients on steroids. Autoinflammatory diseases are rare disorders of the innate immune system characterized by fever and other signs of inflammation. A feared complication of autoinflammatory diseases is the development of AA amyloidosis. AA amyloidosis is caused by extracellular deposition of soluble serum amyloid A (SAA) proteins as insoluble amyloid fibrils leading to organ damage. Prolonged high levels of SAA are a prerequisite to develop AA amyloidosis. Since measurement of SAA is relatively expensive and sometimes unavailable, C-reactive protein (CRP) is often used as a surrogacy marker to test for inflammation. The aim of this research is to evaluate the possible relation between CRP and SAA. A retrospective cohort of patients with autoinflammatory diseases (n = 99) where SAA and CRP blood testing was performed in the period between 2015 and 2021 in the University Medical Centre in Groningen was used to investigate the correlation between CRP and SAA. CRP and SAA have a high correlation (rho = 0.755, p < 0.001). A CRP value below 0.45 mg/L results in 100% sensitivity for SAA below 4 mg/L. CRP below 5 mg/L is a good predictor of SAA below 4 mg/L with 85.4% sensitivity and 83.6% specificity. Only prednisone and erythrocyte sedimentation rate (ESR) significantly influence the relation between CRP and log SAA. There was a significant correlation between CRP and SAA in our retrospective cohort. CRP levels below 5 mg/L proved to be highly predictive of SAA levels below 4 mg/L. This may not be true for patients on steroids. |
ArticleNumber | 106 |
Audience | Academic |
Author | Nienhuis, H L A Dermer, C W E Legger, G E van Daele, P L A Brunger, A F |
Author_xml | – sequence: 1 givenname: G E orcidid: 0000-0002-9576-0904 surname: Legger fullname: Legger, G E email: g.e.legger@umcg.nl organization: Department of Pediatric Rheumatology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. g.e.legger@umcg.nl – sequence: 2 givenname: C W E surname: Dermer fullname: Dermer, C W E organization: Department of Pediatric Rheumatology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands – sequence: 3 givenname: A F surname: Brunger fullname: Brunger, A F organization: Department of Rheumatology and Clinical Immunology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands – sequence: 4 givenname: P L A surname: van Daele fullname: van Daele, P L A organization: Department of Internal medicine, section allergy and clinical Immunology, Erasmus University, University Medical Center Rotterdam, Rotterdam, The Netherlands – sequence: 5 givenname: H L A surname: Nienhuis fullname: Nienhuis, H L A organization: Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands |
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Cites_doi | 10.1002/art.37827 10.1056/NEJMoa070265 10.1007/s00403-019-02014-8 10.1007/s00393-020-00778-3 10.1136/annrheumdis-2013-204991 10.1080/13506129.2018.1549825 10.1080/00365510310001636 10.1007/s00296-006-0265-6 10.1136/annrheumdis-2013-203666 10.1080/21551197.2018.1564200 10.3109/1354750X.2011.607189 10.3109/00365519709084584 10.1136/vr.154.26.814 10.1042/cs0680233 10.1182/blood-2009-07-230722 10.1186/s10020-018-0047-0 10.1007/s10067-020-05249-3 10.1093/rheumatology/kei279 10.1084/jem.140.4.1102 10.1016/j.clinbiochem.2016.11.008 10.1159/000497375 10.1016/j.semarthrit.2007.03.005 10.1002/14651858.CD010893.pub3 10.1038/nri.2017.1 10.1016/j.proghi.2012.03.001 10.1097/RHU.0000000000001134 10.1056/NEJM199902113400607 10.1080/13506129.2019.1693359 |
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Keywords | C-reactive protein Acute-phase proteins Hereditary autoinflammatory diseases Amyloidosis Familial Mediterranean fever Inflammation Serum amyloid A protein |
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References | C Gabay (757_CR1) 1999; 340 S Martínez-Subiela (757_CR30) 2004; 154 757_CR18 757_CR16 757_CR14 T Fülöp (757_CR26) 2019; 65 S Can Sandikci (757_CR24) 2021; 40 M Tunca (757_CR10) 2005; 84 HJ Lachmann (757_CR4) 2007; 356 S Hallan (757_CR19) 1997; 57 KN Porter Starr (757_CR27) 2019; 38 M Piram (757_CR23) 2014; 73 F Yalçânkaya (757_CR8) 2007; 27 AF Brunger (757_CR2) 2020; 27 F Yalçinkaya (757_CR17) 2007; 27 757_CR9 CPJ Maury (757_CR15) 1985; 68 R Levy (757_CR11) 2015; 74 M Çakan (757_CR6) 2021; 27 HJ Lachmann (757_CR5) 2006; 45 S Takata (757_CR31) 2011; 16 MD Benson (757_CR20) 2018; 25 T Lane (757_CR12) 2013; 65 RP Linke (757_CR22) 2012; 47 JA Vrana (757_CR21) 2009; 114 DW Cain (757_CR29) 2017; 17 KS Stojanovic (757_CR7) 2017; 50 Y Berkun (757_CR13) 2007; 37 GH Sack (757_CR3) 2018; 24 N Akdogan (757_CR25) 2019; 312 T Shirahama (757_CR28) 1974; 140 |
References_xml | – volume: 65 start-page: 1116 issue: 4 year: 2013 ident: 757_CR12 publication-title: Arthritis Rheum doi: 10.1002/art.37827 contributor: fullname: T Lane – volume: 356 start-page: 2361 issue: 23 year: 2007 ident: 757_CR4 publication-title: N Engl J Med doi: 10.1056/NEJMoa070265 contributor: fullname: HJ Lachmann – volume: 312 start-page: 255 issue: 4 year: 2019 ident: 757_CR25 publication-title: Arch DermatolRes doi: 10.1007/s00403-019-02014-8 contributor: fullname: N Akdogan – ident: 757_CR9 doi: 10.1007/s00393-020-00778-3 – volume: 74 start-page: 2043 issue: 11 year: 2015 ident: 757_CR11 publication-title: Ann Rheum Dis doi: 10.1136/annrheumdis-2013-204991 contributor: fullname: R Levy – volume: 25 start-page: 215 issue: 4 year: 2018 ident: 757_CR20 publication-title: Amyloid doi: 10.1080/13506129.2018.1549825 contributor: fullname: MD Benson – ident: 757_CR18 – ident: 757_CR14 doi: 10.1080/00365510310001636 – volume: 27 start-page: 517 issue: 6 year: 2007 ident: 757_CR17 publication-title: Rheumatol Int doi: 10.1007/s00296-006-0265-6 contributor: fullname: F Yalçinkaya – volume: 73 start-page: 2168 issue: 12 year: 2014 ident: 757_CR23 publication-title: Ann Rheum Dis doi: 10.1136/annrheumdis-2013-203666 contributor: fullname: M Piram – volume: 38 start-page: 33 issue: 1 year: 2019 ident: 757_CR27 publication-title: J Nutr Gerontol Geriatr doi: 10.1080/21551197.2018.1564200 contributor: fullname: KN Porter Starr – volume: 16 start-page: 530 issue: 6 year: 2011 ident: 757_CR31 publication-title: Biomarkers doi: 10.3109/1354750X.2011.607189 contributor: fullname: S Takata – volume: 27 start-page: 517 year: 2007 ident: 757_CR8 publication-title: Rheumatol Int doi: 10.1007/s00296-006-0265-6 contributor: fullname: F Yalçânkaya – volume: 57 start-page: 373 issue: 5 year: 1997 ident: 757_CR19 publication-title: Scand J Clin Lab Invest doi: 10.3109/00365519709084584 contributor: fullname: S Hallan – volume: 154 start-page: 814 issue: 26 year: 2004 ident: 757_CR30 publication-title: Vet Record doi: 10.1136/vr.154.26.814 contributor: fullname: S Martínez-Subiela – volume: 68 start-page: 233 issue: 2 year: 1985 ident: 757_CR15 publication-title: Clin Sci doi: 10.1042/cs0680233 contributor: fullname: CPJ Maury – volume: 114 start-page: 4957 issue: 24 year: 2009 ident: 757_CR21 publication-title: Blood doi: 10.1182/blood-2009-07-230722 contributor: fullname: JA Vrana – volume: 24 start-page: 1 issue: 1 year: 2018 ident: 757_CR3 publication-title: Mol Med doi: 10.1186/s10020-018-0047-0 contributor: fullname: GH Sack – volume: 40 start-page: 669 issue: 2 year: 2021 ident: 757_CR24 publication-title: Clin Rheumatol doi: 10.1007/s10067-020-05249-3 contributor: fullname: S Can Sandikci – volume: 45 start-page: 746 issue: 6 year: 2006 ident: 757_CR5 publication-title: Rheumatology (Oxford) doi: 10.1093/rheumatology/kei279 contributor: fullname: HJ Lachmann – volume: 140 start-page: 1102 issue: 4 year: 1974 ident: 757_CR28 publication-title: J Exp Med doi: 10.1084/jem.140.4.1102 contributor: fullname: T Shirahama – volume: 50 start-page: 206 issue: 4–5 year: 2017 ident: 757_CR7 publication-title: Clin Biochem doi: 10.1016/j.clinbiochem.2016.11.008 contributor: fullname: KS Stojanovic – volume: 65 start-page: 495 issue: 5 year: 2019 ident: 757_CR26 publication-title: Gerontology doi: 10.1159/000497375 contributor: fullname: T Fülöp – volume: 37 start-page: 182 issue: 3 year: 2007 ident: 757_CR13 publication-title: Semin Arthritis Rheum doi: 10.1016/j.semarthrit.2007.03.005 contributor: fullname: Y Berkun – ident: 757_CR16 doi: 10.1002/14651858.CD010893.pub3 – volume: 17 start-page: 233 issue: 4 year: 2017 ident: 757_CR29 publication-title: Nat Rev Immunol doi: 10.1038/nri.2017.1 contributor: fullname: DW Cain – volume: 47 start-page: 61 issue: 2 year: 2012 ident: 757_CR22 publication-title: Prog Histochem Cytochem doi: 10.1016/j.proghi.2012.03.001 contributor: fullname: RP Linke – volume: 27 start-page: 1 issue: 1 year: 2021 ident: 757_CR6 publication-title: J Clin Rheumatol doi: 10.1097/RHU.0000000000001134 contributor: fullname: M Çakan – volume: 340 start-page: 448 issue: 6 year: 1999 ident: 757_CR1 publication-title: N Engl J Med doi: 10.1056/NEJM199902113400607 contributor: fullname: C Gabay – volume: 27 start-page: 1 issue: 1 year: 2020 ident: 757_CR2 publication-title: Amyloid doi: 10.1080/13506129.2019.1693359 contributor: fullname: AF Brunger – volume: 84 start-page: 1 issue: 1 year: 2005 ident: 757_CR10 publication-title: Med Int contributor: fullname: M Tunca |
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Snippet | Autoinflammatory diseases are rare disorders of the innate immune system characterized by fever and other signs of inflammation. A feared complication of... Background Autoinflammatory diseases are rare disorders of the innate immune system characterized by fever and other signs of inflammation. A feared... BACKGROUNDAutoinflammatory diseases are rare disorders of the innate immune system characterized by fever and other signs of inflammation. A feared... Abstract Background Autoinflammatory diseases are rare disorders of the innate immune system characterized by fever and other signs of inflammation. A feared... |
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SubjectTerms | Acute-phase proteins Amyloidosis Blood C-reactive protein C-Reactive Protein - metabolism Care and treatment Familial Mediterranean fever Hereditary autoinflammatory diseases Hereditary Autoinflammatory Diseases - diagnosis Humans Inflammation Medical examination Proteins Retrospective Studies Serum Amyloid A Protein - analysis Serum Amyloid A Protein - metabolism |
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Title | The relation between C-reactive protein and serum amyloid A in patients with autoinflammatory diseases |
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