Dose-response association between C-reactive protein and risk of all-cause and cause-specific mortality: a systematic review and meta-analysis of cohort studies

Ni, Peng; Yu, Ming‐Whei; Zhang, Rongguang; Cheng, Cheng; He, Mengya; Wang, Haiyan; Chen, Shuaiyin

doi:10.1016/j.annepidem.2020.07.005

Cited by 33 publications

(31 citation statements)

References 56 publications

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“…CRP concentration may increase by 500-fold following an acute-phase stimulus due to enhanced hepatic transcription, primarily in response to the proinflammatory cytokine interleukin 6 (Pepys, 2003;Hage & Szalai, 2007). Clinically, CRP concentrations are used for the diagnosis and monitoring of inflammatory processes (Pepys, 2003) in rheumatologic disease (Rhodes et al, 2010;Ammitzbøll et al, 2014;Wieli nska et al, 2020), ankylosing spondylitis (Xu, Jiang & Zhang, 2020), inflammatory bowel disease (Vatay et al, 2003), pancreatitis (Windgassen et al, 2011), cardiovascular disease (Hage & Szalai, 2007;Ni et al, 2020), cancer (Windgassen et al, 2011), and infections (Pepys, 2003).…”

Section: Introductionmentioning

confidence: 99%

Quantile-dependent expressivity of serum C-reactive protein concentrations in family sets

Williams¹

2021

PeerJ

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Background “Quantile-dependent expressivity” occurs when the effect size of a genetic variant depends upon whether the phenotype (e.g., C-reactive protein, CRP) is high or low relative to its distribution. We have previously shown that the heritabilities (h2) of coffee and alcohol consumption, postprandial lipemia, lipoproteins, leptin, adiponectin, adiposity, and pulmonary function are quantile-specific. Whether CRP heritability is quantile-specific is currently unknown. Methods Serum CRP concentrations from 2,036 sibships and 6,144 offspring-parent pairs were analyzed from the Framingham Heart Study. Quantile-specific heritability from full-sib (βFS, h2 ={(1 + 8rspouseβFS)0.5 − 1}/(2rspouse)) and offspring-parent regression slopes (βOP, h2 = 2βOP/(1 + rspouse)) were estimated robustly by quantile regression with nonparametric significance determined from 1,000 bootstrap samples. Results Quantile-specific h2 (±SE) increased with increasing percentiles of the offspring’s age- and sex-adjusted CRP distribution when estimated from βOP (Ptrend = 0.0004): 0.02 ± 0.01 at the 10th, 0.04 ± 0.01 at the 25th, 0.10 ± 0.02 at the 50th, 0.20 ± 0.05 at the 75th, and 0.33 ± 0.10 at the 90th percentile, and when estimated from βFS (Ptrend = 0.0008): 0.03±0.01 at the 10th, 0.06 ± 0.02 at the 25th, 0.14 ± 0.03 at the 50th, 0.24 ± 0.05 at the 75th, and 0.53 ± 0.21 at the 90th percentile. Conclusion Heritability of serum CRP concentration is quantile-specific, which may explain or contribute to the inflated CRP differences between CRP (rs1130864, rs1205, rs1800947, rs2794521, rs3091244), FGB (rs1800787), IL-6 (rs1800795, rs1800796), IL6R (rs8192284), TNF-α (rs1800629) and APOE genotypes following CABG surgery, stroke, TIA, curative esophagectomy, intensive periodontal therapy, or acute exercise; during acute coronary syndrome or Staphylococcus aureus bacteremia; or in patients with chronic rheumatoid arthritis, diabetes, peripheral arterial disease, ankylosing spondylitis, obesity or inflammatory bowel disease or who smoke.

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Section: Introductionmentioning

confidence: 99%

Quantile-dependent expressivity of serum C-reactive protein concentrations in family sets

Williams¹

2021

PeerJ

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“…There is strong evidence that individuals with periodontitis have elevated CRP compared with controls (Paraskevas et al, 2008). Elevated levels of systemic inflammation, measured by CRP, have been independently associated with all‐cause mortality in numerous studies (Li et al, 2017; Ni et al, 2020). CRP in this specific context, thus, represents a potential mediator between periodontitis and all‐cause mortality.…”

Section: Discussionmentioning

confidence: 99%

Systemic inflammation and the relationship between periodontitis, edentulism, and all‐cause mortality: A 17‐year prospective cohort study

Winning

Patterson

Linden

et al. 2021

J Clinic Periodontology

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Aim The aim was to investigate the role of systemic inflammation in the relationship between periodontitis, edentulism, and all‐cause mortality in a group of men in Northern Ireland aged 58–72 years. Materials and methods A representative sample of 1558 men had a detailed dental examination between 2001 and 2003. The primary end point was death from any cause. Cox's proportional hazards model was used to assess the longitudinal relationship between periodontitis, edentulism, and all‐cause mortality. Accelerated failure time modelling was performed to investigate the mediating role of systemic inflammation. Results Mean age of the men at baseline was 64.3 (standard deviation 2.9) years. During a median follow‐up of 17 years, 500 (32.1%) men died. After adjustment for confounding variables, compared to men with no/mild periodontitis, edentulous men had a hazard ratio for all‐cause mortality of 1.52 (95% confidence interval [CI] 1.16–1.99) p < .01 and for those with severe periodontitis, it was 1.34 (95% CI 1.06–1.70) p = .01. Systemic inflammation accounted only for a minor mediating pathway effect of 10%. Conclusions There was evidence in this group of men that those who were edentulous or had severe periodontitis had a significantly increased risk of all‐cause mortality. Systemic inflammation was not a major explanatory mediator of this association.

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“…However, on multivariate analysis, both CRP and fibrinogen were not independent predictors for cancer mortality. A meta-analysis by Ni et al found a higher relative risk for cancer mortality among participants with high CRP levels; however, this study did not limit participants to solely women [ 34 ]. Similar to our findings, Wulaningsih et al was unable to demonstrate a significant association between CRP levels and cancer mortality in women using the NHANES III sample, but the authors did find this relationship in their male cohort [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Social isolation, inflammation, and cancer mortality from the National Health and Nutrition Examination Survey - a study of 3,360 women

et al. 2021

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Background This study evaluates the role of social isolation on inflammation and cancer mortality among women. Methods Data were abstracted from the U.S. National Health and Nutrition Examination Survey from 1988 to 1994. The Social Network Index was used to assess participants’ degree of social isolation. C-reactive protein and fibrinogen levels were included as markers of inflammation. We used the National Death Index to identify causes and dates of mortality. Chi-square and multivariable Cox regressions were employed for statistical analyses. Results Of 3360 women (median age: 54 years), the most isolated, very isolated, somewhat isolated, and not isolated comprised 14.5, 30.2, 37.1, and 18.2% of the sample, respectively. The most isolated participants were more likely to have low income (56.8% vs 12.2%, p < 0.001), have fewer years of education (40.8% vs 12.3%; p < 0.001), have low physical activity (27.3% vs 14.7%; p < 0.003), be obese (32.5% vs 24.4%; p = 0.02), and be current smokers (34.2% vs 10.3%; p < 0.001) compared to the not isolated ones. Mean fibrinogen levels increased with degree of social isolation (p = 0.003), but C-reactive protein showed no association (p = 0.52). Kaplan-Meier estimates indicated higher cancer mortality rates among participants with elevated fibrinogen levels, though not with statistical significance (p = 0.08). Furthermore, there was no association between social isolation and cancer mortality (p = 0.54). On multivariate analysis, obesity (HR = 1.56; 95% CI: 1.11–2.18), higher education (HR = 1.36; 95% CI: 1.01–1.83), and smoking (HR = 4.42, 95% CI: 2.84–6.88) were independent predictors for cancer mortality, while high physical activity predicted for lower mortality from cancer (HR = 0.67, 95% CI: 0.51–0.87). However, social isolation was not a predictor. Conclusion Social isolation among women was associated with an increased level of fibrinogen, but not associated with cancer mortality. The relationship between inflammation and cancer mortality warrants further investigation.

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Dose-response association between C-reactive protein and risk of all-cause and cause-specific mortality: a systematic review and meta-analysis of cohort studies

Cited by 33 publications

References 56 publications

Quantile-dependent expressivity of serum C-reactive protein concentrations in family sets

Quantile-dependent expressivity of serum C-reactive protein concentrations in family sets

Systemic inflammation and the relationship between periodontitis, edentulism, and all‐cause mortality: A 17‐year prospective cohort study

Social isolation, inflammation, and cancer mortality from the National Health and Nutrition Examination Survey - a study of 3,360 women

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