Potential clinical applications of c‐reactive protein

Okamura, Jonathan; Miyagi, Junko; Terada, Keith Y.; Hokama, Y.

doi:10.1002/jcla.1860040316

Cited by 72 publications

(40 citation statements)

References 57 publications

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“…According to the present findings, IL-6 concentration was increased in TPE and PPE, but these findings were nonsignificant after fitting the logit model. CRP is an acute-phase protein widely used as a marker of inflammation and tissue injury [19]. CRP concentration level has been studied in pleural fluid and been found to be higher in benign than in malignant exudates [20].…”

Section: Biological Markers In Pleural Effusion Zd Daniil Et Almentioning

confidence: 99%

Discrimination of exudative pleural effusions based on multiple biological parameters

Daniil

Ζιντζαράς²,

Kiropoulos³

et al. 2007

Eur Respir J

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Pleural effusion is a common complication of various diseases. Conventional methods are not always capable of establishing the cause of pleural effusion, so alternative tests are needed. The aim of this study was to explore means of discriminating between different pleural effusion groups, malignant, parapneumonic and tuberculous, based on the combined function of seven biological markers.Adenosine deaminase (ADA), interferon-c, C-reactive protein (CRP), carcinoembryonic antigen, interleukin-6, tumour necrosis factor-a and vascular endothelial growth factor concentration levels were measured in pleural fluid from 45 patients with malignant, 15 with parapneumonic and 12 with tuberculous pleural effusion. Receiver operating characteristic curve analysis, multinomial logit modelling and canonical variate analysis were applied to discriminate the pleural effusion groups.The three groups could be discriminated successfully using the measured markers. The most important parameters for discrimination were ADA and CRP concentration levels. An individual with an ADA concentration level of .45 U?L -1 and a CRP concentration of ,4 mg?dL -1 was more likely to belong to the tuberculous pleural effusion group, whereas one with an ADA concentration level of ,40 U?L -1 and a CRP concentration of .6 mg?dL -1 was more likely to belong to the parapneumonic pleural effusion group, and one with a CRP concentration of ,4 mg?dL -1 to the malignant pleural effusion group. The combination of adenosine deaminase and C-reactive protein levels might be sufficient for discriminating between the three different groups of exudative pleural effusion: malignant, tuberculous and parapneumonic.

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Section: Biological Markers In Pleural Effusion Zd Daniil Et Almentioning

confidence: 99%

Discrimination of exudative pleural effusions based on multiple biological parameters

Daniil

Ζιντζαράς²,

Kiropoulos³

et al. 2007

Eur Respir J

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“…13,14 In fact, tear samples from glaucoma patients have been shown to have greater amounts of infl ammatory cytokines compared to their normal counterparts. 49 Although fi brinogen is suspected as being upregulated indirectly (secondary to the infl ammatory cytokines), 50 it (ie, fi brinogen), 12 CRP, 11 and multiple cytokines, 13,14 specifi cally IL-1α and β, IL-2, IL-4, IL-6, IL-10, IL-12, IL-23, and TNFα, have long been described as conventional markers of infl ammation. used in concentrations varying from 0.015% to 0.05%, 4 although the American College of Toxicology has concluded that BAK can be safely used as an antimicrobial agent at concentrations up to 0.1%.…”

Section: 3mentioning

confidence: 99%

“…8 BAK, is known to be degraded into hydrogen peroxide (H 2 O 2 ), 8 which, in even small amounts as low as 30 parts per million (0.003%), is known to be an ophthalmic irritant. 9,10 C-reactive protein (CRP), 11 fi brinogen, 12 and multiple cytokines, 13,14 specifi cally interleukin (IL-)1α and β, IL-2, IL-4, IL-6, IL-10, IL-12, IL-23, and tumor necrosis factor (TNF-)α, have long been described as conventional biomarkers of infl ammation. Increased toxicity should cause a localized infl ammatory response with concomitant increased elaboration of these infl ammatory biomarkers.…”

Section: Epstein Chen and Asbell 416mentioning

confidence: 99%

Evaluation of Biomarkers of Inflammation in Response to Benzalkonium Chloride on Corneal and Conjunctival Epithelial Cells

Epstein

Chen

Asbell

2009

Journal of Ocular Pharmacology and Therapeutics

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Purpose: Most eye drops contain preservatives; benzalkonium chloride (BAK) is most common. Recent data demonstrated BAK adding to toxicity. BAK is degraded into hydrogen peroxide (H 2 O 2 ), which in even small amounts is known to be an irritant. Increased toxicity should cause localized infl ammation with increased elaboration of infl ammatory biomarkers. To evaluate the infl ammation BAK causes to the ocular surface, enzyme linked immunosorbant assays (ELISAs) were utilized to quantify the levels of infl ammatory biomarkers in response to BAK and/or H 2 O 2 . Methods: Immortalized human conjunctival and corneal epithelial cells were exposed to: BAK (0.001%-0.1%), hydrogen peroxide (H 2 O 2 ) (0.01%-0.1%), and cell media for 1 h. Cytokine quantifi cation was performed via enzyme-linked immunosorbent assays [ELISAs]). Additional experimentation was performed in which testing solutions were replaced with media after 1 h and the resulting supernatants quantifi ed after 24 h. Results: BAK induced signifi cant amounts of interleukin (IL-) 1 and tumor necrosis factor (TNF), but only moderate amounts of C-reactive protein (CRP), IL-10 and 12, and H 2 O 2 . Lower concentrations of BAK induced proportionally less elaboration. Replacing the test solutions with media and providing 23 h for cytokine elaboration signifi cantly increased TNF, but not IL-1. Lipopolysaccharide (LPS) positive controls induced substantial elaboration/release of both IL-1 and TNF as did in increasing the exposure to the full 24 h. Conclusions: After 1 h of exposure, BAK increased quantities of all biomarkers. The biomarkers in decreasing order of induction/upregulation were: TNF ≥ IL-1 ≥ IL-12 ≥ IL-10 ≥ CRP. Even low concentrations caused some degree of infl ammation. Replacing the testing solution with media and providing 23 h for cytokine elaboration, signifi cantly increased the elaboration/release of TNF, but not IL-1, as compared to the 1-h BAK exposure. Whereas increasing the exposure to the full 24 h by not removing the testing solution at the 1-h time point signifi cantly increased the elaboration/release of both IL-1 and TNF.

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“…8 C-reactive protein (CRP) is secreted by the liver, and plasma CRP rapidly rises in response to inflammation, so it is an important biomarker of systemic inflammation. 9 CRP correlates with long-term mortality and morbidity in patients with COPD, rheumatoid disease, coronary artery disease, and chronic inflammation. 10,11 Response to antiinflammatory treatment can be monitored with CRP.…”

Section: Introductionmentioning

confidence: 99%

C-Reactive Protein Alone or Combined With Cardiac Troponin T for Risk Stratification of Respiratory Intensive Care Unit Patients

Özsu¹,

Yılmaz

Yılmaz³

et al. 2011

Respir Care

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BACKGROUND: Mortality is high among patients admitted to intensive care units (ICUs). Several prognostic markers have been described in such patients, but the literature contains no data comparing C-reactive protein (CRP) and cardiac troponin T (cTn-T), nor of a combination of CRP and cTn-T in the same patient group in the ICU. METHODS: This was a retrospective electronic data review of patients who presented to the emergency department for respiratory reasons between December 2007 and December 2009 and in whom CRP and cTn-T levels were measured. Patients with a diagnosis of pulmonary embolism and acute coronary syndrome were excluded. We recorded demographics, chronic diseases, admission diagnosis, Simplified Acute Physiology Score II (SAPS II), ICU stay, and CRP and cTn-T concentrations. RESULTS: We included the records of 158 patients. Mean ICU stay was 9.9 days (range 1-65 d), and mean hospital stay was 14.1 days (range 1-72 d). For predicting mortality, receiver operating characteristic analysis gave a CRP cutoff value of > 10 mg/dL, and a CTn-T cutoff value of > 0.01 ng/mL. For CRP the mortality area under the curve was 0.691 (95% CI 0.608 -0.775), the sensitivity was 65%, and the specificity was 70%. For cTn-T the mortality area under the curve was 0.733 (95% CI 0.655-0.812), the sensitivity was 78%, and the specificity was 56%. Of the patients who died, 65% had CRP > 10 mg/dL and 78% had cTn-T > 0.01 ng/mL. On multivariable regression analysis, CRP > 10 mg/dL was associated with 6.6-fold higher (95% CI 1.7-21.3) ICU mortality. There was no advantage for models that combined CRP and cTn-T. CRP alone was more valuable in predicting ICU mortality than in combination with troponin or SAPS II. CONCLUSIONS: Elevated CRP is an independent early prognostic marker of mortality risk in ICU patients. We suspect that a CRP-based prognosis strategy may be useful.

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Potential clinical applications of c‐reactive protein

Cited by 72 publications

References 57 publications

Discrimination of exudative pleural effusions based on multiple biological parameters

Discrimination of exudative pleural effusions based on multiple biological parameters

Evaluation of Biomarkers of Inflammation in Response to Benzalkonium Chloride on Corneal and Conjunctival Epithelial Cells

C-Reactive Protein Alone or Combined With Cardiac Troponin T for Risk Stratification of Respiratory Intensive Care Unit Patients

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