Quartile Of C-reactive Protein Research Articles

The admission level of CRP during cardiogenic shock is a strong independent risk marker of mortality

Inflammatory processes are involved not only in coronary artery disease but also in heart failure (HF). Cardiogenic shock (CS) and septic shock are classically distinct although intricate relationships are frequent in daily practice. The impact of admission inflammation in patients with CS is largely unknown. FRENSHOCK is a prospective registry including 772 CS patients from 49 centers. One-month and one-year mortalities were analyzed according to the level of C-reactive protein (CRP) at admission, adjusted on independent predictive factors. Within 406 patients included, 72.7% were male, and the mean age was 67.4 y ± 14.7. Four groups were defined, depending on the quartiles of CRP at admission. Q1 with a CRP < 8 mg/L, Q2: CRP was 8–28 mg/L, Q3: CRP was > 28–69 mg/L, and Q4: CRP was > 69 mg/L. The four groups did not differ regarding main baseline characteristics. However, group Q4 received more often antibiotics in 47.5%, norepinephrine in 66.3%, and needed more frequently respiratory support and renal replacement therapy. Whether at 1 month (Ptrend = 0.01) or 1 year (Ptrend < 0.01), a strong significant trend towards increased all-cause mortality was observed across CRP quartiles. Specifically, compared to the Q1 group, Q4 patients demonstrated a 2.2-fold higher mortality rate at 1-month (95% CI 1.23–3.97, p < 0.01), which persisted at 1-year, with a 2.14-fold increase in events (95% CI 1.43–3.22, p < 0.01). Admission CRP level is a strong independent predictor of mortality at 1 month and 1-year in CS. Specific approaches need to be developed to identify accurately patients in whom inflammatory processes are excessive and harmful, paving the way for innovative approaches in patients admitted for CS.NCT02703038.

C-reactive Protein and Risk of Right Ventricular Dysfunction and Mortality in Patients With Acute Symptomatic Pulmonary Embolism

BackgroundRight ventricle (RV) dysfunction increases the risk of death from pulmonary embolism (PE). C-reactive protein (CRP) might identify RV inflammation and dysfunction in patients with PE. MethodsThis cohort study enrolled consecutive stable patients with acute PE between 2017 and 2023. We stratified patients by quartiles of CRP. We evaluated the association between CRP quartiles and the presence of RV dysfunction, and used multivariable models to assess for an association between CRP and the outcomes of all-cause and PE-specific mortality during the 30 days of follow-up after PE diagnosis. ResultsThe study included 633 stable patients with PE. Patients without RV dysfunction had significantly lower median (IQR) CRP levels compared with patients with RV dysfunction (n=509, 31.7 [10.0–76.4]mg/L vs n=124, 45.4 [16.0–111.4]mg/L; P=0.018). CRP showed a statistically significant positive association with the presence of RV dysfunction (P<0.01). On multivariable analysis, CRP level was not significantly associated with 30-day all-cause mortality (adjusted odds ratio [OR] per mg/L increment, 1.00; 95% CI, 1.00–1.01; P=0.095), but higher CRP was associated with significantly higher PE-related mortality (adjusted OR, 1.01; 95% CI, 1.00–1.01; P=0.026). Compared with patients in CRP quartile 1, patients in quartiles 2, 3, and 4 had a stepwise increase in the adjusted odds of 30-day all-cause death of 2.41 (P=0.148), 3.04 (P=0.062), and 3.15 (P=0.052), respectively. ConclusionsAs an indicator of RV dysfunction, CRP may improve risk stratification algorithms for hemodynamically stable patients with acute symptomatic PE.

Relationship of Soluble Lectin-Like Low-Density Lipoprotein Receptor-1 (sLOX-1) With Inflammation and Coronary Plaque Progression in Psoriasis.

Psoriasis is a chronic inflammatory condition associated with coronary artery disease risk. Uptake of oxidized low-density lipoprotein by the lectin-like low-density lipoprotein receptor-1 triggers release of the soluble extracellular domain of the receptor (sLOX-1). We sought to characterize the relationship between sLOX-1, inflammation, and coronary plaque progression in psoriasis. A total of 327 patients with psoriasis had serum sLOX-1 levels measured at baseline by an ELISA-based assay. Stratification by high-sensitivity C-reactive protein ≥4.0 mg/L (quartile 4), identified 81 participants who had coronary plaque phenotyping at baseline and were followed longitudinally by coronary computed tomography angiography. Subjects within high-sensitivity C-reactive protein quartile 4 were middle-aged (51.47±12.62 years), predominantly men (54.3%) with moderate psoriasis disease severity (6.60 [interquartile range, 3.30-13.40]). In the study cohort, participants with sLOX-1 above the median displayed increased vulnerable coronary plaque features. At baseline, sLOX-1 was associated with total burden (rho=0.296; P=0.01), noncalcified burden (rho=0.286; P=0.02), fibro-fatty burden (rho=0.346; P=0.004), and necrotic burden (rho=0.394; P=0.002). A strong relationship between sLOX-1, noncalcified burden (β=0.19; P=0.03), and fibro-fatty burden (β=0.29; P=0.003) was found in fully adjusted models at baseline and 1- and 4-year follow-up. Finally, coronary plaque features progressed over 1 year regardless of biologic or systemic treatment in subjects with high sLOX-1. Patients with psoriasis with both high sLOX-1 and high-sensitivity C-reactive protein levels have increased coronary plaque burden associated with atherosclerotic plaque progression independent of biologic and systemic treatment. Thus, sLOX-1 might be considered as a promising marker in coronary artery disease risk estimation beyond traditional risk factors. URL: https://www.clinicaltrials.gov; Unique identifier: NCT01778569.

Coronary artery calcification score and 19 biomarkers on cardiovascular events; a 10-year follow-up DanRisk substudy

Abstract Background SCORE2 is recommended for the estimation of the 10-year risk of cardiovascular disease (CVD), and guideance of medical therapy. However, the prediction is deficient. Coronary artery calcification (CAC) score has been proven to improve the risk assessment in primary prevention of CVD, however, it is also resource-intensive. Biomarkers may be an advantageous alternative. Purpose This study aims to determine and compare the additive value of CAC-score and 19 biomarkers in risk prediction. Methods Classic cardiovascular (CV) risk factors, CAC-score, and a wide range of blood samples (including lipids, calcium-phosphate metabolism, troponin, inflammation, and kidney function), were collected from 1,211 randomly selected middle-aged men and women in this multicentre prospective cohort in 2009-2010. 10-year follow-up data on CV-events (death from CVD, stroke, myocardial infarction, heart failure or coronary artery revascularization) were obtained from the Danish Health Registries. The association between SCORE2, CAC-score, biomarkers, and CV-events was displayed in Kaplan Meier diagrams, assessed using cox proportional hazard rates (HR) and compared using area under the curve (AUC) calculation of receiver operating characteristic (ROC) curves. The net reclassification improvement (NRI) for CAC-score compared to SCORE2 was also calculated. Results 92 participants had CV-events. Events were seen in 29.3% of 41 participants with a very high risk (SCORE2 ≥10%) and 24.2% of 66 participants with CAC-score ≥400. Adjusted for risk factors, CAC-score was significantly associated with events adjusted HR 1.91 (95%CI: 1.10;3.31), 3.61 (95%CI: 1.93;6.76), and 5.2 (95%CI: 2.63;10.29) for CAC-score 1-99, CAC-score 100-399 and CAC-score ≥400, respectively. HR for the highest quartile of C-reactive protein (CRP) was 2.34 (95%CI: 1.15;4.47), while none of the remaining biomarkers improved HR. CAC-score improved AUC of the SCORE2 model (AUC_CAC+SCORE2: 0.72, AUC_SCORE2: 0.67, p&amp;lt;0.01) as seen in Figure 1. A combination of selected biomarkers (total cholesterol, low-density lipoprotein, phosphate, troponin I, CRP, and creatinine) borderline improved AUC (AUC_Biomarkers+SCORE2: 0.71, AUC_SCORE2: 0.67, p=0.06). Inclusion of CAC-score in the SCORE2 model improved the risk prediction. For participants with a CV-event, 73.9% had increased probabilities and 26.1% had decreased probabilities, compared to 42.4% increased and 57.6% decreased probabilities for participants without an event. NRI was 63% (p&amp;lt;0.0001) Conclusion CAC-score remained to improve the prediction of CV-events, while the selected biomarkers did not.ROC of SCORE2 versus CAC-score+SCORE2

C-Reactive Protein and Risk of Incident Heart Failure in Patients With Cardiovascular Disease

BackgroundPatients with established cardiovascular disease (CVD) are at high risk of incident heart failure (HF), which may in part reflect the impact of systemic inflammation. ObjectivesThe goal of this study was to determine the association between C-reactive protein (CRP) and incident HF in patients with established CVD. MethodsPatients from the prospective UCC-SMART (Utrecht Cardiovascular Cohort-Second Manifestations of ARTerial disease) cohort with established CVD, but without prevalent HF were included (n = 8,089). Incident HF was defined as a first hospitalization for HF. The association between baseline CRP and incident HF was assessed using Cox proportional hazards models adjusted for established risk factors (ie, age, sex, myocardial infarction, smoking, diabetes mellitus, body mass index, blood pressure, cholesterol, and kidney function). ResultsDuring a median follow-up of 9.7 years (IQR 5.4-14.1 years), 810 incident HF cases were observed (incidence rate 1.01/100 person-years). Higher CRP was independently associated with an increased risk of incident HF: HR per 1 mg/L: 1.10 (95% CI: 1.07-1.13), and for last vs first CRP quartile: 2.22 (95% CI: 1.76-2.79). The association was significant for both HF with reduced (HR: 1.09; 95% CI: 1.04-1.14) and preserved ejection fraction (HR: 1.12; 95% CI: 1.07-1.18) (P for difference = 0.137). Additional adjustment for medication use and interim myocardial infarction did not attenuate the association, and the association remained consistent beyond 15 years after the CRP measurement. ConclusionsIn patients with established CVD, CRP is an independent risk marker of incident HF. These data support ongoing trial efforts to assess whether anti-inflammatory agents can reduce the burden of HF.

Medium term moderate to low-level air pollution exposure is associated with higher C-reactive protein among healthy Danish blood donors

Air pollution is a significant contributor to the global burden of disease with a plethora of associated health effects such as pulmonary and systemic inflammation. C-reactive protein (CRP) is associated with a wide range of diseases and is associated with several exposures. Studies on the effect of air pollution exposure on CRP levels in low to moderate pollution settings have shown inconsistent results.In this cross-sectional study high sensitivity CRP measurements on 18,463 Danish blood donors were linked to modelled air pollution data for NOx, NO2, O3, CO, SO2, NH3, mineral dust, black carbon, organic carbon, sea salt, secondary inorganic aerosols and its components, primary PM2.5, secondary organic aerosols, total PM2.5, and total PM10 at their residential address over the previous month. Associations were analysed using ordered logistic regression with CRP quartile as individuals outcome and air pollution exposure as scaled deciles. Analyses were adjusted for health related and socioeconomic covariates using health questionnaires and Danish register data.Exposure to different air pollution components was generally associated with higher CRP (odds ratio estimates ranging from 1.11 to 1.67), while exposure to a few air pollution components was associated with lower CRP. For example, exposure to NO2 increased the odds of high CRP 1.32-fold (95%CI 1.16–1.49), while exposure to NH3 decreased the odds of high CRP 0.81-fold (95%CI 0.73–0.89).This large study among healthy individuals found air pollution exposure to be associated with increased levels of CRP even in a setting with low to moderate air pollution levels.

Inflammation and cholesterol as predictors of cardiovascular events among patients receiving statin therapy: a collaborative analysis of three randomised trials

Inflammation and hyperlipidaemia jointly contribute to atherothrombotic disease. However, when people are treated with intensive statin therapy, the relative contributions of inflammation and hyperlipidaemia to the risk of future cardiovascular events might change, which has implications for the choice of adjunctive cardiovascular therapeutics. We aimed to evaluate the relative importance of high-sensitivity C-reactive protein (CRP) and low-density lipoprotein cholesterol (LDLC) as determinants of risk for major adverse cardiovascular events, cardiovascular death, and all-cause-death among patients receiving statins. We did a collaborative analysis of patients with-or at high risk of-atherosclerotic disease, who were receiving contemporary statins and were participants in the multinational PROMINENT (NCT03071692), REDUCE-IT (NCT01492361), or STRENGTH (NCT02104817) trials. Quartiles of increasing baseline high-sensitivity CRP (a biomarker of residual inflammatory risk) and of increasing baseline LDLC (a biomarker of residual cholesterol risk) were assessed as predictors of future major adverse cardiovascular events, cardiovascular death, and all-cause death. Hazard ratios (HRs) for cardiovascular events and deaths were calculated across quartiles of high-sensitivity CRP and LDLC in analyses adjusted for age, gender, BMI, smoking status, blood pressure, previous history of cardiovascular disease, and randomised treatment group assignment. 31 245 patients were included in the analysis from the PROMINENT (n=9988), REDUCE-IT (n=8179), and STRENGTH (n=13 078) trials. The observed ranges for baseline high-sensitivity CRP and LDLC, and the relationships of each biomarker to subsequent cardiovascular event rates, were almost identical in the three trials. Residual inflammatory risk was significantly associated with incident major adverse cardiovascular events (highest high-sensitivity CRP quartile vs lowest high-sensitivity CRP quartile, adjusted HR 1·31, 95% CI 1·20-1·43; p<0·0001), cardiovascular mortality (2·68, 2·22-3·23; p<0·0001), and all-cause mortality (2·42, 2·12-2·77; p<0·0001). By contrast, the relationship of residual cholesterol risk was neutral for major adverse cardiovascular events (highest LDLC quartile vs lowest LDLC quartile, adjusted HR 1·07, 95% CI 0·98-1·17; p=0·11), and of low magnitude for cardiovascular death (1·27, 1·07-1·50; p=0·0086) and all-cause death (1·16, 1·03-1·32; p=0·025). Among patients receiving contemporary statins, inflammation assessed by high-sensitivity CRP was a stronger predictor for risk of future cardiovascular events and death than cholesterol assessed by LDLC. These data have implications for the selection of adjunctive treatments beyond statin therapy and suggest that combined use of aggressive lipid-lowering and inflammation-inhibiting therapies might be needed to further reduce atherosclerotic risk. Kowa Research Institute, Amarin, AstraZeneca.

Association between C-reactive protein and all-cause mortality among critically ill patients with acute kidney injury.

To explore the relationship between C-reactive protein (CRP) and mortality in critically ill patients with acute kidney injury (AKI). A total of 580 patients diagnosed with AKI within 48 hours of ICU admission between September 2017 and August 2019 were enrolled. Patients were followed for all-cause mortality in-hospital and then up to 2 years after discharge. We performed two multivariate regression analysis to assess the association between CRP and mortality, and conducted stratified analysis to assess whether the effect of the CRP differed across subgroups. According to initial CRP quartiles, patients were divided into 4 groups (quartile 1, CRP ≤2.87mg/L; quartile 2, CRP: 2.87-25.95mg/L; quartile 3, CRP: 25.95-111.51mg/L; quartile 4, CRP > 111.51 mg/L). Patients with high CRP levels have higher APACHE-II score, longer length of stay in the ICU, and higher mortality. In multivariate regression analysis, high CRP was associated with the increased risk of in-hospital mortality after adjusting for age, gender, surgical grade, heart rate, serum potassium, serum chloride, coronary heart disease, and atherosclerotic cerebral infarction (quartile 4 vs. quartile 1, OR: 3.810, 95%CI: 2.081-6.973). For 2-year mortality, the increased trend was still significant with the OR (95% CI) of the quartile 4 group of 5.117 (2.678-9.780) after adjusting for confounders. Subgroup analyses detected in each group showed that the in-hospital and 2-year risk of mortality increased with higher CRP levels. Higher CRP level was associated with the increased risk of mortality in critically ill patients with AKI.

Sepsis Related Mortality Associated with an Inflammatory Burst in Patients Admitting to the Department of Internal Medicine with Apparently Normal C-Reactive Protein Concentration.

Background: Patients who are admitted to the Department of Internal Medicine with apparently normal C-reactive protein (CRP) concentration impose a special challenge due the assumption that they might not harbor a severe and potentially lethal medical condition. Methods: A retrospective cohort of all patients who were admitted to the Department of Internal Medicine with a CRP concentration of ≤31.9 mg/L and had a second CRP test obtained within the next 24 h. Seven day mortality data were analyzed. Results: Overall, 3504 patients were analyzed with a mean first and second CRP of 8.8 (8.5) and 14.6 (21.6) mg/L, respectively. The seven day mortality increased from 1.8% in the first quartile of the first CRP to 7.5% in the fourth quartile of the first CRP (p < 0.0001) and from 0.6% in the first quartile of the second CRP to 9.5% in the fourth quartile of the second CRP test (p < 0.0001), suggesting a clear relation between the admission CRP and in hospital seven day mortality. Conclusions: An association exists between the quartiles of CRP and 7-day mortality as well as sepsis related cause of death. Furthermore, the CRP values 24 h after hospital admission improved the discrimination.

Association between C-reactive protein and risk of overall and 18 site-specific cancers in a Japanese case-cohort.

Evidence of the association between chronic low-grade inflammation, as reflected by C-reactive protein (CRP) measurements, and cancer risk is equivocal. Specifically, few studies have examined this in uncommon cancers and Asian populations. We utilised a case-cohort design consisting of multi-types of cancer (N = 3608), and a random subcohort (N = 4432) in a Japanese large population-based study, with a median follow-up time of 15.6 years, and measured baseline plasma CRP using high sensitivity assay. The hazard ratios (HRs) were estimated using weighted Cox proportional hazards methods. The multivariable-adjusted HR (95% confidence interval) for the top quartile of CRP was 1.28 (1.11‒1.48) (Ptrend < 0.001) for overall cancer compared to the bottom quartile of CRP. Among site-specific cancers, higher CRP levels were associated with an increased risk of colorectal, lung, breast, biliary tract, and kidney cancer, and leukaemia. These positive associations remained among participants after >3 years' follow-up. Furthermore, subgroup analyses for overall cancer robustly showed a positive association with CRP levels, regardless of sex and obesity. Our consistent findings suggested that chronic low-grade inflammation measured by CRP is associated with the risk of cancer.

The association between serum high-sensitivity cardiac troponin T and acute myocardial infarction in patients with suspected chronic coronary syndrome is modified by body mass index

BackgroundHigher systemic concentrations of cardiac troponins and biomarkers of inflammation and endothelial dysfunction as well as obesity are associated with increased risk of cardiovascular disease (CVD) and may share pathophysiological pathways. We sought to explore the association between serum high sensitive cardiac troponin T (hs-cTnT) and future acute myocardial infarction (AMI) according to body mass index (BMI) among patients with suspected chronic coronary syndrome (CCS), as well as interactions with C-reactive protein (CRP) and asymmetric dimethylarginine (ADMA). MethodsA total of 3879 patients with baseline hs-cTnT ≤ 30 ng/L who underwent elective coronary angiography due to chronic coronary syndrome (CCS) were followed to subsequent AMI or end of 2009. Risk associations between hs-cTnT and incident AMI were explored with Cox regression according to BMI categories <25 kg/m 2, 25–30kg/m2 and >30kg/m2 and quartiles of serum CRP and plasma ADMA. ResultsMedian (25 th −75 th percentile) age was 62 (54–69) years and 2773 (77.5%) were men. During median 7.5 (25 th −75 th percentile) (6.9–9.2) years of follow-up, 460 (11.9%) patients experienced an AMI. The risk relationship between hs-cTnT and incident AMI was stronger among patients in the higher vs lower BMI categories, HR 1.087 (1.055–1.119), P for interaction 0.043. A similar interaction was not found in categories of CRP or ADMA. ConclusionThe risk relationship of hs-cTnT with incident AMI was stronger in patients with higher BMI. Our results motivate further studies into potential pathophysiological mechanisms connecting hs-cTnT with increased cardiovascular risk.

Association of C-Reactive Protein and Motoric Cognitive Risk Syndrome in Community-Dwelling Older Adults: The China Health and Retirement Longitudinal Study.

Motoric cognitive risk syndrome (MCR) is a newly described pre-dementia syndrome characterized by cognitive complaints and slow gait and is associated with numerous adverse outcomes. Previous studies have indicated an association between C-reactive protein (CRP) and cognitive decline, but no clear relationship between CRP and MCR has been reported. The purpose of the study is to examine the associations between CRP with MCR and MCR subtypes. Participants were 5,642 adults aged ≥60 years from the China Health and Retirement Longitudinal Study (CHARLS). MCR was defined as cognitive complaints and slow gait speed without dementia or impaired mobility. Two subtypes of MCR were defined by whether memory impairment (MI) was also present, such as MCR-MI and MCR-non-MI. MI was evaluated through the immediate recall and delayed recall in a word recall test during the CHARLS and was defined as 1.0 standard deviation or more below the mean values of the test scores in this cohort. Of the participants, 421 (7.46%) met the criteria for MCR. After multivariate adjustment, participants with higher CRP levels had an increased likelihood of MCR (fourth quartile: adjusted odds ratio [OR]=1.44; 95% confidence interval [CI]: 1.06-1.95) compared with those in the first quartile group. The OR for MCR-MI was 2.04 (95% CI: 1.35-3.09) for the highest quartile of CRP compared to the lowest quartile. No significant associations between CRP levels and odds of MCR-non-MI were observed. Higher CRP levels were associated with increased odds of prevalent MCR-MI but not MCR-non-MI among community-dwelling older adults.

Systemic Inflammation in the First 2 Weeks after Birth as a Determinant of Physical Growth Outcomes in Hospitalized Infants with Extremely Low Gestational Age

To examine associations of systemic inflammation with growth outcomes at neonatal intensive care unit discharge or transfer among infants with extremely low gestational ages. We studied 850 infants at born at 23-27weeks of gestation. We defined inflammatory protein elevation as the highest quartile of C-reactive protein (CRP), Interleukin (IL)-6, tumor necrosis factor-∝, or IL-8 on postnatal days 1, 7, and 14. We compared z-scores of weight, length, and head circumference at neonatal intensive care unit discharge or transfer between infants with vs without inflammatory protein elevation, adjusting in linear regression for birth size z-score, sex, gestational age, diet, comorbidities, medications, and length of hospitalization. The mean gestational age was 25weeks (range, 23-27weeks) and birth weight z-score 0.14 (range, -2.73 to 3.28). Infants with a high CRP on day 7 had lower weights at discharge or transfer (-0.17 z-score; 95% CI, -0.27 to -0.06) than infants without CRP elevation, with similar results on day 14. Infants with CRP elevation on day 14 were also shorter (-0.21 length z-scores; 95% CI, -0.38 to -0.04), and had smaller head circumferences (-0.18 z-scores; 95% CI, -0.33 to -0.04) at discharge or transfer. IL-6 elevation on day 14 was associated with lower weight (-0.12; 95% CI, -0.22 to -0.02); IL-6 elevation on day 7 was associated with shorter length (-0.27; 95% CI, -0.43 to -0.12). Tumor necrosis factor-∝ and IL-8 elevation on day 14 were associated with a lower weight at discharge or transfer. Postnatal systemic inflammation may contribute to impaired nutrient accretion during a critical period in development in infants with extremely low gestational ages.

Psychosocial stressors at work and inflammatory biomarkers: PROspective Quebec Study on Work and Health

BackgroundChronic low-grade inflammation has been associated with high risk of several chronic diseases such as cardiovascular diseases, diabetes, depression, and dementia. As low-grade inflammation could be present long before the apparition of the disease, identifying modifiable risk factors could allow to act upstream. Psychosocial stressors at work have been suggested as modifiable risk factors of low-grade inflammation, but few longitudinal studies have evaluated the association between these stressors and inflammatory biomarkers, such as C-reactive protein (CRP) and interleukin-6 (IL-6). ObjectiveThis longitudinal study evaluate the associations between exposure to psychosocial stressors at work and CRP and IL-6, separately and combined into an inflammatory index. MethodsData came from a cohort of 9188 white-collar workers recruited in 1991–1993 (T1) and followed-up after 8 (T2, 1999–2000) and 24 (T3, 2015–2018) years. Participants included in this study were randomly selected at T3 for serum biomarkers studies (n = 2557). CRP and IL-6 were measured using standardized protocols. Psychosocial stressors at work were assessed at T2 according to recognized models: Karasek’s Demand-Control-Support model and Siegrist’s Effort-Reward Imbalance (ERI) model, using validated questionnaires. High job strain was defined by an exposure to high psychological demand combined with low job control, and iso-strain was defined by an exposure to high job strain combined with low social support at work. ERI was defined by an imbalance between psychological demand and social, economic, and organizational reward. Several covariates were considered including sociodemographic, anthropometric, and lifestyle characteristics, and comorbidities. Prevalence ratios (PRs) and 95% confidence interval (CI) for the highest quartile of CRP, IL-6 and inflammatory index at T3 according to psychosocial stressors at work measured at T2 were calculated using generalized estimating equations. Multiple imputation and inverse probability of censoring weighting were done. ResultsIn men, an association was observed between exposure to iso-strain and the inflammatory index (PR of 1.42 (95% CI: 1.06;1.90)), mainly among men aged less than 65 years (PR of 2.00 (95% CI: 1.37;2.92)). In this same age group, associations with inflammatory biomarkers were also observed among men with exposure to ERI, and among women with exposure to low reward at work or moderate social support at work. ConclusionThese results suggest that psychosocial stressors at work may increase low-grade inflammation. However, further studies are needed to corroborate these results and to clarify the potential differences between men and women. As these stressors are frequent and modifiable, their reduction is important for public health and could play a role in the primary prevention of chronic diseases.

C-reactive protein in adult Samoans: Population variation and physiological correlates.

C-reactive protein (CRP) has been associated with adiposity and cardiometabolic disease risk in many populations but remains remarkably understudied in Pacific Islander populations. Here, we provide the first examination of correlates of CRP in adult Samoans (n=108, ages 35-55 years) to test the hypotheses that CRP exhibits sex-dependent associations with measures of BMI, adiposity, and cardiometabolic disease risks. We analyzed associations between measures of adiposity (total fat mass, visceral fat mass, percent total body fat), body mass index (BMI), cardiometabolic risks, behaviors, demographics, and CRP. Unadjusted analyses of CRP were undertaken using Pearson's pairwise, and Spearman's rank correlations; one-way analysis of variance and Kruskal-Wallis tests assessed variables by CRP quartiles. Adjusted analyses of CRP correlates were examined using generalized linear regression. Serum CRP ranged from 0.08 to 13.3mg/L (median 1.4mg/L) and varied significantly by sex t (108)=-2.47, p=.015. CRP was weakly to moderately associated with measures of adiposity and BMI (r and ρ ranged between 0.25 and 0.50, p < .05) and some cardiometabolic markers (including HbA1c, fasting insulin, and insulin resistance). CRP was significantly associated with percent body fat in women and men, adjusting for other variables. These data are among the first to demonstrate CRP correlates in a sample of adult Samoans. CRP differed by sex and was associated with BMI, adiposity, and some cardiometabolic risk markers. These data align with findings in other populations.

Mental health symptoms and inflammatory markers among HIV infected patients in Tanzania

BackgroundHIV and mental disorders are predicted to be the leading causes of illness worldwide by the year 2030. HIV-infected patients are at increased risk of developing mental disorders which are significantly associated with negative clinical outcomes and propagation of new HIV infections. There is little evidence that links inflammation to development of mental disorders among HIV patients. Therefore, the main objective of this study was to evaluate if mental health symptoms were associated with biomarkers of inflammation in HIV infected subjects.MethodsA cross-sectional study was conducted in Dar es Salam, Tanzania from March to May 2018. Standardized tools were used to collect data based on the World Health Organisation's (WHO) stepwise approach for non-communicable diseases (NCD) surveillance. A total of 407 HIV+ patients on antiretroviral therapy were recruited. The WHO stepwise approach for NCD surveillance was used to collect data together with anthropometric measurements. Mental health symptoms were determined based on self-reported thoughts of helplessness, suicide ideation, depression, despair, discouragement, and feelings of isolation. Enzyme-linked immunosorbent assay was used to test for inflammatory markers:- C-reactive protein (CRP), Iinterleukin-6 (IL-6), interleukin-18 (IL-18), soluble tumour necrosis factor receptor-I (sTNFR-I), and soluble tumour necrosis factor receptor-II (sTNFR-II). Bivariate and multi-variate analysis was conducted to examine the association between biomarkers and mental health symptoms.ResultsThe prevalence of self-reported mental health symptoms was 42% (n = 169). Participants with self-reported symptoms of mental health had elevated CRP, were less likely to walk or use a bicycle for at least 10 minutes, were less likely to participate in moderate-intensity sports or fitness activities, and had poor adherence to HIV treatment (p < 0.005). CRP remained significant in the sex adjusted, age-sex adjusted, and age-sex-moderate exercise adjusted models. In the fully adjusted logistic regression model, self-reported mental health symptoms were significantly associated with a higher quartile of elevated CRP (OR 4.4; 95% CI 1.3–5.9) and sTNFR-II (OR 2.6; 95% CI 1.4–6.6) and the third quartile of IL-18 (OR 5.1;95% CI 1.5–17.5) as compared with those reporting no mental health symptoms. The significance of sTNFR-II and IL-18 in the fully adjusted model is confounded by viral load suppression rates at the sixth month.ConclusionHigh CRP and sTNFR II were important contributors to the prevalence of mental health symptoms. This study is among the minimal studies that have examined mental health issues in HIV, and therefore, the findings may offer significant knowledge despite the potential reverse causality. Regardless of the nature of these associations, efforts should be directed toward screening, referral, and follow-up of HIV patients who are at-risk for mental health disorders.

Leukocyte count, C-reactive protein level and incidence risk of type 2 diabetes among non-smoking adults: A longitudinal finding over 12 years from the Korean Genome and Epidemiology Study

AimsChronic low-grade inflammation is closely linked to the development and progression of type 2 diabetes mellitus (T2DM). Since inflammatory markers tend to be chronically elevated in current smokers, we examined the association of inflammatory markers, including leukocyte counts and C-reactive protein (CRP) levels, with incidence risk of T2DM in non-smoking adults. Methods5568 non-smoking participants aged 40–69 years without diabetes at baseline were selected from the Korean Genome and Epidemiology Study (KoGES), a large prospective cohort study. The hazard ratios (HRs) with 95% confidence intervals (CIs) for incident T2DM according to leukocyte and CRP quartiles, respectively, were calculated using multivariate Cox proportional hazards regression models. ResultsDuring the 12-year follow-up period, T2DM developed in 1030 subjects (18.5%, 1030/5568), with an incidence rate of 3.1–4.9 per 2 years. The cumulative incidence of T2DM increased proportionally with increasing leukocyte and CRP quartiles. Compared with the reference first quartile, the HRs of incident T2DM in the second, third, and fourth quartiles of leukocyte counts and third and fourth quartiles of CRP levels increased in a dose-dependent manner after adjusting for potentially confounding variables. ConclusionsLeukocyte counts and CRP levels are predictors of incident T2DM independent of tobacco smoking.

Abstract 13104: The Concomitant Inflammation Affect the Ratio of N-terminal Pro B-type Natriuretic Peptide to B-type Natriuretic Peptide in Patients With Heart Failure and Preserved Ejection Fraction

Backgrounds: Although B-type natriuretic peptide (BNP) and N-terminal pro B-type natriuretic peptide (NT-proBNP ) are interrelated parameters in assessment heart failure severity and prognosis, the ratio of NT-proBNP to BNP (NT-proBNP/BNP) are affected by various clinical factors, such as renal function. However, little is known about the influence of inflammation on NT-proBNP/BNP in patients with heart failure and preserved ejection fraction (HFpEF). Methods and Results: Patients data were extracted from PURSUIT-HFpEF registry, which is a multicenter prospective observational study including patients hospitalized for acute heart failure with left ventricular ejection fraction of &gt;50%. Of 871 patients, data of BNP and NT-proBNP was available in 654 patients. The median baseline concentration of BNP was 474 pg/ml (299-720), NT-proBNP was 3310 pg/ml (1740-6840), and NT-proBNP/BNP was 7.6 (5.0-11.8). In multivariable linear regression analyses, older age [odds ratio (OR); 1.05, 95% confidence interval (CI); 1.02-1.09, p=0.001], higher creatinine [OR; 2.63, 95% CI; 1.66-4.16, p&lt;0.001], and higher C-reactive protein (CRP) [OR; 1.17, 95% CI; 1.06-1.28, p&lt;0.001] were significantly associated with a higher NT-proBNP/BNP (&gt;median value of 7.6). However, other factors expected to affect NT-proBNP/BNP, such as atrial fibrillation and body mass index, were not associated with a higher NT-proBNP/BNP in this study. Patients in the highest CRP quartile had significantly higher NT-proBNP/BNP than those with other quartiles. Conclusion: In HFpEF patients, concomitant inflammation was associated with high NT-proBNP/BNP, which indicated that we need a careful interpretation on these two natriuretic peptides of patients with HFpEF and inflammatory status, such as infection.

Association between indicators of systemic inflammation biomarkers during puberty with breast density and onset of menarche

BackgroundSystemic inflammation may play a role in shaping breast composition, one of the strongest risk factors for breast cancer. Pubertal development presents a critical window of breast tissue susceptibility to exogenous and endogenous factors, including pro-inflammatory markers. However, little is known about the role of systemic inflammation on adolescent breast composition and pubertal development among girls.MethodsWe investigated associations between circulating levels of inflammatory markers (e.g., interleukin-6 (IL-6), tumor necrosis factor receptor 2 (TNFR2), and C-reactive protein (CRP)) at Tanner stages 2 and 4 and breast composition at Tanner stage 4 in a cohort of 397 adolescent girls in Santiago, Chile (Growth and Obesity Cohort Study, 2006–2018). Multivariable linear models were used to examine the association between breast composition and each inflammatory marker, stratifying by Tanner stage at inflammatory marker measurement. Accelerated failure time models were used to evaluate the association between inflammatory markers concentrations at each Tanner stage and time to menarche.ResultsIn age-adjusted linear regression models, a doubling of TNFR2 at Tanner 2 was associated with a 26% (95% CI 7–48%) increase in total breast volume at Tanner 4 and a 22% (95% CI 10–32%) decrease of fibroglandular volume at Tanner 4. In multivariable models further adjusted for body fatness and other covariates, these associations were attenuated to the null. The time to menarche was 3% (95% CI 1–5%) shorter among those in the highest quartile of IL-6 at Tanner 2 relative to those in the lowest quartile in fully adjusted models. Compared to those in the lowest quartile of CRP at Tanner 4, those in the highest quartile experienced 2% (95% CI 0–3%) longer time to menarche in multivariable models.ConclusionsSystemic inflammation during puberty was not associated with breast volume or breast density at the conclusion of breast development among pubertal girls after adjusting for body fatness; however, these circulating inflammation biomarkers, specifically CRP and IL-6, may affect the timing of menarche onset.

C-reactive protein for prediction of atrial fibrillation recurrence after catheter ablation

BackgroundInflammation plays an important role in the initiation and progression of atrial fibrillation (AF), but data about the relationship between subclinical inflammation and recurrence of AF after catheter ablation remains poorly studied. We aimed to assess whether plasma levels of C-reactive protein (CRP) are associated with long-term AF recurrence following catheter ablation.MethodsPrior to the intervention, plasma CRP concentrations were measured in patients who underwent first catheter ablation for AF. AF recurrence was evaluated after 12 months and defined as any AF episode longer than 30 s recorded on either 12-lead electrocardiogram, 24-h Holter or 7-day Holter monitoring. Multivariable adjusted Cox models were constructed to examine the association of CRP levels and AF recurrence.ResultsOf the 711 patients (mean age: 61 years, 25% women) included in this study, 247 patients (35%) experienced AF recurrence after ablation. Patients who were in the highest CRP quartile had a higher rate of recurrent AF compared to those who were in the lowest quartile (53.4 vs. 33.1% at 1 year of follow-up; P = 0.004). The adjusted hazard ratios (aHR) of recurrent AF across increasing quartiles of CRP were 1.0 (reference), 1.26 (95% confidence interval [CI], 0.86–1.84), 1.15 (95% CI, 0.78–1.70) and 1.60 (95% CI, 1.10–2.34) (P trend = 0.015). A similar effect was observed when CRP was analyzed as continuous variable (aHR per unit increase, 1.21; 95% CI, 1.05–1.39; P = 0.009). When a predefined CRP cut-off of 3 mg/l was applied, patients with CRP levels of 3 mg/l or above had a higher risk of AF recurrence than those with levels below (aHR, 1.44; 95% CI, 1.06–1.95; P = 0.019).ConclusionsIncreasing pre-interventional CRP levels are associated with a higher risk of AF recurrence in patients undergoing catheter ablation for AF.Trail registrationClinicalTrials.gov identifier, NCT03718364.