Elevated hs-CRP Research Articles

Physical exercise, systemic inflammation and adult-onset asthma: a 12-year follow-up study

Physical exercise in treatment of asthma is scarcely studied with no clear exercise guidelines for asthmatics. We aimed to investigate the associations between physical exercise frequency, systemic inflammation and asthma control. This has not been previously studied in adult-onset asthma. This study is part of Seinäjoki Adult Asthma Study (SAAS), where 203 patients with adult-onset asthma were evaluated in 2012-2013. Exercise frequency was recorded with a structured lifestyle questionnaire. Study population was divided into two categories by exercise frequency: Low frequency group exercised ≤2 times/week and high frequency group >2 times/week. Blood inflammatory markers were measured and IL-6 > 1.55 pg/ml and hs-CRP > 4.12 mg/l indicated systemic inflammation. High exercise frequency group had lower levels of hs-CRP (p = 0.007), IL-6 (p = 0.015), suPAR (p = 0.008) and adipsin (p = 0.031) and higher levels of adiponectin (p = 0.010) than low exercise frequency group. In logistic multivariate regression models higher exercise frequency lowered odds for elevated hs-CRP (OR = 0.37, 95% CI 0.15-0.94) and IL-6 levels (OR = 0.43, 95% CI 0.20-0.91), after adjusting for possible confounding factors. There was no difference in lung function tests, asthma control test or airways questionnaire 20 scores between the exercise frequency groups. However, differences were found in single symptom questions; high exercise frequency group had less symptoms during light housework and laughing but experienced more limitation of activity in self-reports. Higher exercise frequency is associated with lower level of systemic inflammation in patients with adult-onset asthma but no clear association was found to asthma outcomes. Exercise frequency may be associated with lesser amount of some individual asthma symptoms.

Can high-sensitivity C reactive protein (hsCRP) be used as a prognostic marker of functional disability after acute ischaemic stroke? A cross-sectional study at a tertiary care centre in Eastern India

ObjectivesThis study was conducted with the aim of assessing the correlation between highly sensitive C reactive protein (hsCRP) levels and indicators of disability and functional impairment in individuals presenting with...

Efficacy of dual antiplatelet therapy after ischemic stroke according to hsCRP levels and CYP2C19 genotype

Both high-sensitive C-reactive protein (hsCRP) and CYP2C19 genotypes are independent predictors of clinical outcomes after ischemic stroke. We aim to evaluate the association of CYP2C19 loss-of-function alleles (LoFA) carrying status with the effects of dual/single antiplatelet therapy at different hsCRP levels using the CHANCE trial. Subjects with both of CYP2C19 major alleles information (*2, *3, and *17) and hsCRP measurements were enrolled from the prespecified subgroup. CYP2C19 LoFA carriers were defined as patients with either*2 or *3 allele. Cox proportional hazards models were used to assess the interaction of CYP2C19 LoFA carrying status with the effects of dual/single antiplatelet therapy at different hsCRP levels. The primary outcome was recurrent stroke within 90 days. Among 2,801 patients, 1,646 (58.8%) were LoFA carriers, and 922 (32.9%) had elevated hsCRP. In patients with nonelevated hsCRP, there was a significant interaction effect between CYP2C19 LoFA carrying status and dual/single antiplatelet regimens for prevention of recurrent stroke and combined vascular events (P = .048, .048, respectively), but, not in patients with elevated hsCRP (P = .502, .472, respectively). Only among patients with nonelevated hsCRP and noncarrier of CYP2C19 LoFA, dual antiplatelets significantly reduced the risk of recurrent stroke compared with aspirin alone (hazard ratio = 0.44 [0.26-0.74], P = .003). No significant differences in bleeding were found. Nonelevated hsCRP and noncarrier of CYP2C19 LoFA may predict a better response to dual antiplatelet therapy in reducing stroke recurrence and composite vascular events for patients with minor stroke and high-risk TIA. clinicaltrials.gov Identifier: NCT00979589.

Risankizumab Is Associated With Normalization of Biomarkers in Patients With Crohn's Disease: Results From the Phase 3 ADVANCE, MOTIVATE, and FORTIFY Studies.

Normalization of high-sensitivity C-reactive protein [hs-CRP] and fecal calprotectin [FCP] are suggested Crohn's disease [CD] intermediate treatment targets. This analysis evaluates achievement of biomarker normalization and the relationship between improvements in biomarker concentrations and clinical and endoscopic outcomes among patients treated with risankizumab. This post hoc analysis included patients with moderately to severely active CD and elevated baseline hs-CRP [> 5mg/L] or FCP [> 250 µg/g] concentrations from the 12-week ADVANCE and MOTIVATE induction studies, and the 52-week FORTIFY maintenance study. We assessed the proportion of patients achieving biomarker normalization, defined as hs-CRP ≤ 5mg/L and FCP ≤ 250 µg/g, and the association between achieving biomarker normalization and improved clinical and endoscopic outcomes. Among 748 patients with elevated baseline hs-CRP or FCP concentrations, higher proportions of patients treated with risankizumab vs placebo achieved normalization of hs-CRP [week 12: placebo, 17.5%; risankizumab 600mg, 48.5%; week 52: placebo, 29.5%; risankizumab 180mg, 45.2%; risankizumab 360mg, 40.8%] and FCP [week 12: placebo, 9.1%; risankizumab 600mg, 26.0%; week 52: placebo, 28.0%; risankizumab 180mg, 43.0%; risankizumab 360mg, 44.0%; nominal p < 0.05 vs placebo for all comparisons]. Achievement of both clinical or endoscopic outcomes and improvement of biomarker concentrations occurred at higher rates among patients treated with risankizumab vs placebo, regardless of prior exposure to biologic therapies. Risankizumab treatment led to sustained normalization of inflammatory biomarkers with improved clinical and endoscopic results.

Association of Uric Acid, High-Sensitivity C-Reactive Protein, and 90-Day Risk of Poor Function Outcome in Patients with Ischemic Stroke or Transient Ischemic Attacks.

The interaction between inflammatory biomarkers (high-sensitivity C-reactive protein, hsCRP) and antioxidants (uric acid, UA) regarding prognosis after ischemic stroke or transient ischemic attack (TIA) remains inadequately explored. This study aimed to assess (1) the individual and joint effects of hsCRP and UA, and (2) the neuroprotective role of UA in patients with elevated hsCRP levels concerning poor functional outcomes at 90 days. A prospective cohort study was conducted involving 2140 consecutive ischemic stroke or TIA patients with hsCRP and UA levels. The primary outcome was defined as a poor functional outcome, indicated by a modified Rankin Scale (mRS) score of 3-6 at 90 days, with a shift in the mRS score as a secondary outcome. Logistic regression and propensity score (PS) analyses were employed to ensure robustness. Poor functional outcome occurred in 345 (16.1%) patients. Individual effects found that the highest quartiles of hsCRP (adjusted OR = 3.090; 95% CI 2.150-4.442) and UA (adjusted OR = 0.671; 95% CI 0.551-0.883) were associated with increased or decreased risk of poor functional outcome, respectively. Joint effects (adjusted OR = 3.994; 95% CI 2.758-5.640) between hsCRP and UA on the primary outcome were more apparent in patients with high hsCRP levels (hsCRP > 1.60 mg/L) and low UA levels (UA ≤ 291.85 µmol/L). For the patients with high hsCRP levels, patients with low UA levels had a higher risk of primary and secondary outcomes, compared with those with high UA levels, after unadjusted or adjusted for hsCRP. Similar and reliable results were observed in PS-based models. In patients with ischemic stroke or TIA, joint high levels of hsCRP and low UA levels significantly correlate with increased risk of poor functional outcome at 90 days. In addition, high UA levels could reduce the risk of poor functional outcome for patients with high hsCRP levels.

Effect of interleukin 1b inhibition with canakinumab on inflammation and viral persistence in people with human immunodeficiency virus

Abstract Introduction Effectively treated people with HIV (PWH) have elevated risk of cardiovascular disease (CVD). Inflammatory markers are predictive of CVD and mortality among PWH. The role of the myeloid system in driving inflammation and atherosclerosis has been recently recognized. Canakinumab (a monoclonal antibody to IL-1β) reduces inflammation and CVD events among people with elevated hsCRP after myocardial infarction without HIV. We evaluated the impact of IL-1β inhibition using canakinumab on HIV parameters, inflammation, HIV persistence markers, arterial inflammation, and hematopoietic activity in PWH. Methods PWH on effective ART who had CVD or were at risk for CVD were randomized 2:1 to receive 150 mg of canakinumab subcutaneously or matched placebo at weeks 0 and 12. Arterial inflammation and bone marrow metabolic activity were assessed using F18 FDG PET/CT at baseline and week 18. T cell and monocyte activation were evaluated using multiparameter spectral cytometry. The viral reservoir was quantified using Tat/rev Induced Limiting Dilution Assay (TILDA), HIV DNA and cell-associated RNA. The primary endpoints were change in CD4 and CD8 count. We assessed group effects over time using linear mixed effects models. Results 33 individuals were randomized (median age of 60 years old (IQR 57.5, 64.5) and 94% male); 25 received canakinumab and 8 received placebo. There were no significant differences at baseline. As expected, IL-1β increased among those treated with canakinumab at weeks 4- 24 (p&amp;lt;0.01 for each) and returned to baseline at week 36. There was one death from sepsis in an individual aged 84 with CVD and poorly controlled diabetes who received canakinumab. There were no significant changes in CD4 count, CD8 count, platelet count, creatinine, AST, or ALT by group. Treatment was not associated with a greater reduction in arterial inflammation in the most diseased segment compared to placebo (-6.9%; 95% CI -30.4 to 24.5%; p=0.62). However, bone marrow metabolic activity decreased in the canakinumab group versus placebo (-14.4%, 95% CI -26.5% to -0.2%; p=0.047). Treatment was associated with increased CD163 expression on monocytes at weeks 24 (p=0.03) and 36 (p&amp;lt;0.001), and lower caspase activity at week 36 (p=0.02). There was expansion of anti-inflammatory CD16+ patrolling monocytes that co-express CD163+CX3CR1+ and a decrease in pro-inflammatory CD16+ patrolling monocytes that are Caspase1+CCR2+. Treatment was not associated with differences in hsCRP, IL-6, IL-16, IL-18, MCP-1, sCD14, sCD163, T cell subsets, NK cell subsets, or viral persistence markers. Conclusion Among treated PWH, targeted inhibition of IL-1β using canakinumab results in decreased bone marrow metabolic activity and a shift toward anti-inflammatory monocyte populations. These findings shed light on mechanisms underlying how targeted IL-1β inhibition using canakinumab prevents CVD events by altering monocyte populations and reducing systemic inflammation.

Inflammation and cholesterol associated residual cardiovascular risk and its dependence on chronic kidney disease in statin treated patients with coronary artery disease

Abstract Background/Aim In statin-treated patients with chronic coronary syndrome (CCS) there is uncertainty about the relative contribution of inflammation and dyslipidaemia to residual cardiovascular risk, particularly in the presence of chronic kidney disease. We thus aimed to evaluate high sensitive C-reactive protein (hsCRP) and low density lipoprotein-cholesterol (LDL-C) as predictors of future events in these patients, stratified by estimated glomerular filtration rate (eGFR). Methods We identified patients with CCS on stable statin treatment from a contemporary all-comers cohort recruited at a large tertiary care center in Germany. We excluded patients with active malignancy, infectious disease or in a post-operative state. Cox regression for major adverse cardiovascular events (MACE, composite of cardiovascular death, myocardial infarction, stroke) and all-cause death was performed adjusting for age, sex, arterial hypertension, diabetes mellitus, active smoking, body mass index and change in the intensity of statin therapy at discharge, with log(hsCRP) or LDL-C as the exposure variables. Interaction with eGFR (&amp;lt; vs. ≥ 60 ml/min/1.73m²) was investigated. Results 937 patients with CCS (mean age 71.1 years, 78.7% male, median hsCRP 2.0 mg/L, median LDL-C 73.0 mg/dl, median eGFR 71.3 ml/min/1.73m²) were followed-up over 4 years, with 101 cases of MACE and 171 cases of all-cause death recorded. The hazard ratios (HR) for MACE per standard deviation (SD) increase were as follows: log(hsCRP) 1.08 (95% confidence interval (CI) 0.87, 1.34; p = 0.48), LDL-C 1.10 (95% CI 0.89, 1.35; p = 0.37). For all-cause death the HRs for log(hsCRP) and LDL-C were 1.60 (95% CI 1.36, 1.88; p &amp;lt;0.001) and 0.88 (95% CI 0.74, 1.04; p = 0.14), respectively. Kaplan-Meier curves stratifying the cohort by median values of LDL-C and hsCRP consistently demonstrated a significantly higher risk of death in the subgroups with elevated hsCRP (Figure 1). Contrastingly for LDL-C, levels below (vs. above) the median were associated with a higher mortality rate. This is in part a reflection of a higher prevalence of high-intensity statin therapy in this subgroup (21.0 vs. 14.2%, p = 0.0081), in turn a reflection of greater severity of coronary artery disease (history of myocardial infarction 43.9 vs. 31.9%, p &amp;lt;0.001). Further confounding by unadjusted for diseases with a catabolic metabolism is possible. Interaction analysis with eGFR revealed that log(hsCRP) was predictive of all-cause mortality both in the presence and absence of chronic kidney disease, whilst lower LDL-C values were found to be predictive only at eGFR &amp;lt;60 ml/min/1.73m² (Table 1). Conclusion Residual inflammation as measured by hsCRP predicts all-cause mortality in statin-treated patients with CCS in this contemporary all-comers cohort, both in the presence and absence of chronic kidney disease. The predictive utility of LDL-C is limited, likely due to confounding e.g. by the intensity of lipid lowering medication.Kaplan-Meier curves (all-cause death)Interaction analysis with eGFR

Clinical impact of systemic inflammation across the spectrum of different high-sensitivity CRP values in patients undergoing percutaneous coronary intervention

Abstract Background Systemic inflammation enhances atherosclerosis progression and is a well-established determinant of cardiovascular risk. High-sensitivity C-reactive protein (hsCRP), the most widely available biomarker of inflammation, has indeed been associated with the occurrence of major adverse cardiovascular and cerebrovascular events (MACCE) in patients undergoing percutaneous coronary intervention (PCI). However, some heterogeneity exists in the threshold to define high hsCRP associated with increased cardiovascular risk, with the 2 and 3 mg/L cut-offs being used more commonly. Purpose We aimed to evaluate the clinical impact of systemic inflammation in patients undergoing PCI across the spectrum of baseline hsCRP values. Methods We retrospectively evaluated consecutive patients undergoing PCI with drug-eluting stent implantation from 2012 to 2022 at Mount Sinai Hospital (NY, USA). We excluded patients presenting with acute myocardial infarction or active cancer and those for whom baseline hsCRP was not available or was above 10 mg/L. Patients were stratified into three groups according to baseline hsCRP levels: &amp;lt;2.0, 2.0 to 3.0, and &amp;gt;3.0 mg/L. We estimated the risk of 12-month adverse events using the lowest hsCRP group (&amp;lt;2.0 mg/L) as reference. The primary endpoint was MACCE, defined as the composite of all-cause death, myocardial infarction (MI), or stroke. Secondary endpoints were MACCE individual components, target vessel revascularization (TVR), stent thrombosis and bleeding. Results A total of 10,811 patients were included in the analysis. Of these, 6,210 (57.4%) had hsCRP &amp;lt;2.0 mg/L, 1,624 (15.0%) between 2 and 3 mg/L and 2,977 (27.6%) &amp;gt;3.0 mg/L. Incidence of anemia, diabetes mellitus, peripheral and cerebrovascular artery disease, atrial fibrillation and chronic kidney disease increased stepwise across hsCRP groups. Moreover, patients with higher hsCRP tended to present more frequently with unstable angina and higher baseline LDL cholesterol levels. As regards procedural variables, coronary artery disease severity and PCI complexity did not differ significantly across groups. When compared with patients with hsCRP &amp;lt; 2, hsCRP &amp;gt; 3 mg/L was associated with a greater adjusted risk of MACCE (4.9% vs 2.4%; HR 1.75 % CI 1.35 - 2.28), all-cause death (2.5% vs 0.9%, HR 2.34, 95%CI 1.57-3.47) and MI (2.5% vs 1.3%; HR 1.58 95%CI 1.11-2.26) (Figure 1). Risks of stroke, TVR, stent thrombosis and bleeding did not significantly differ across hsCRP groups (Table 1) Conclusions In patients undergoing PCI, elevated hsCRP values exceeding 3 mg/L exhibit a more robust association with the risk of MACCE and all-cause mortality, as compared with both hsCRP &amp;lt; 2.0 and between 2.0 and 3.0 mg/L. In this context, the use of hsCRP might improve the stratification of patients associated with higher inflammatory burden.

Hs-CRP modifies the impact of stress hyperglycemia ratio on long-term outcomes in patients with acute coronary syndrome

Abstract Background In recent years, studies have demonstrated the promising predictive value of stress hyperglycemia ratio (SHR) for adverse outcomes in patients with acute coronary syndrome (ACS). Nevertheless, knowledge regarding the effects of inflammation on the risks associated with SHR remains limited. Considering the potential interplay, we hypothesize that the well-recognized biomarker reflecting residual inflammation, high-sensitivity C-reactive protein (hs-CRP), may exert an influence on SHR-related cardiovascular risks. Purpose The objective of this study was to investigate the association between hs-CRP level and SHR-related long-term adverse events in ACS patients. Methods Among 10,724 consecutive patients who underwent percutaneous intervention treatment throughout the year 2013, 6149 ACS patients were eventually enrolled. SHR was calculated employing the formula: SHR = admission blood glucose (ABG) / [1.59 x HbA1c (%) – 2.59]. Based on their levels of hs-CRP, patients were stratified into two groups, with the cut-off set at 2 mg/L. The primary endpoint was defined as all-cause mortality, and the secondary endpoint was the major adverse cardiac and cerebrovascular events (MACCE), consisting of all-cause death, non-fatal myocardial infarction, coronary revascularization, and ischemic stroke. Results 238 (3.7%) all-cause mortality and 1275 (20.0%) MACCE occurred during the 5-year follow-up. The average age of the overall cohort was 58.39 ± 10.38 years, and 4723 (76.8%) were male. After adjusting for the potential confounders, multivariable Cox regression revealed a significant correlation between hs-CRP level and SHR for all-cause mortality (P for interaction = 0.009), and there were diverse associations between SHR and long-term risks depending on the levels of hs-CRP: With hs-CRP &amp;lt; 2mg/L, there was no significant risk of all-cause mortality at any SHR quantiles, while the lowest SHR quantile showed a 1.321-fold increased risk of MACCE [Hazard Ratio (HR): 1.321, 95% confidence interval (CI) 1.034-1.688, P = 0.026]. Conversely, with hs-CRP ≥ 2mg/L, significant association was observed between SHR and all-cause mortality (all P &amp;lt; 0.05). Notably, the highest SHR quantile exhibited the greatest risk for both all-cause mortality (HR: 4.030, 95% CI 1.778-9.134, P &amp;lt; 0.001) and MACCE (HR: 1.299, 95% CI 1.010-1.672, P = 0.042). Conclusions This large-scale real-world study was the first to report that the pattern of SHR-associated long-term cardiovascular risks in ACS patients was modified by the levels of hs-CRP, suggesting a potential interaction between inflammation and stress hyperglycemia that contributes to poor prognosis. When applying risk stratification, both factors should be comprehensively considered, and patients exhibiting high SHR along with concomitantly elevated hs-CRP may merit more rigorous risk management.Figure 1.Multivariable COX regression

The combined effects of depression or anxiety with high-sensitivity C-reactive protein in predicting the prognosis of coronary heart disease patients

BackgroundDepression, anxiety and high-sensitivity C-reactive protein (hs-CRP) are individually associated with poor prognosis in patients with coronary heart disease (CHD). However, the combined effects of depression with inflammation or anxiety with inflammation on the prognosis have been rarely explored.MethodsThis prospective cohort study included 414 patients diagnosed with CHD. The Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder-7 (GAD-7) were used to assess depression and anxiety. A score ≥ 5 points was defined as elevated depression or anxiety. High hs-CRP was defined as ≥ 3 mg/L. Follow-up was performed 2 years after the patients were discharged. The clinical results included noncardiac readmission, cardiac readmission, major cardiovascular events (MACEs), and composite events. The composite events included noncardiac readmission and MACEs. The Cox proportional hazard regression model was used to analyze the prognostic risk.ResultsAfter full adjustment, patients with elevated depression and high hs-CRP had a higher risk in predicting noncardiac readmission (hazard ratio (HR) = 3.87, 95% confidence interval (CI) = 1.10–9.02, p = 0.002) and composite events (HR = 1.93, 95% CI = 1.13–3.30, p = 0.016) than those with high hs-CRP alone. For the anxiety and hs-CRP group, high hs-CRP alone predicted a higher risk of noncardiac readmission (HR = 3.32, 95% CI = 1.57–7.03, p = 0.002) and composite events (HR = 1.75, 95% CI = 1.12–2.76, p = 0.015) than references. Elevated anxiety had no significant effects on all the endpoints. Furthermore, we didn’t find interactions between depression and hs-CRP or anxiety and hs-CRP.ConclusionIn patients with CHD, elevated depression with high hs-CRP was found to be significant in predicting the risk of noncardiac readmission and composite events. Early diagnosis and treatment of depression with inflammation are necessary in CHD patients.

Altered anthropometrics and HA1c levels, but not dyslipidemia, are associated with elevated hs-CRP levels in middle-aged adults: A population-based analysis.

Population-based studies of cardiovascular disease markers, such as hs-CRP, are crucial. However, studies exploring the effect of metabolic indices on hs-CRP while controlling for confounding variables adequately in middle-aged adults are limited. Using Wave 5 data from the National Longitudinal Study of Adolescent Health (Add Health), we examined the impact of various metabolic indices on hs-CRP in adults aged 32-42, controlling for eight allergic and infectious factors that may elevate hs-CRP levels. We used multiple linear regression analysis to determine which factors predict hs-CRP levels after log transformation of the dependent variable. The total number of participants was N = 1839 (weighted N = 1390763), with a mean age of 38.1 (SD = 2.0) and 46.4% having obesity. Among the controlled variables, recent surgery was the only confounder to significantly predict increased hs-CRP levels (P = 0.029, exponentiated estimate (EE) = 1.61; 95% Cl: [1.31-1.91]). Notably, current smoking and altered LDL or TG levels did not show a significant association with hs-CRP levels (P > 0.05). However, a significant increase in hs-CRP levels was observed in females compared to males (P < 0.001, EE = 1.43; 95%Cl: [1.35-1.51]). Similar findings were noted for diabetic HbA1c levels (P = 0.001, EE = 1.6; 95%CL: [1.42-1.78]), high waist circumference (P = 0.015, EE = 1.25; 95%CL: [1.15-1.35]), and grade 3 obesity (P = 0.006, EE = 7.62; 95%CL: [2.86-12.38]). Although not statistically significant, hs-CRP levels exhibited a gradual increase with rising BMI after controlling for other variables. These findings will improve the clinical application of hs-CRP in predicting coronary artery disease, especially in younger adults.

Impact of high-sensitivity C-reactive protein on metabolic syndrome in an elderly population: Findings from a hospital-based cross-sectional study in J&amp;K, India

ABSTRACT Background: Due to affluent lifestyles, primary care physicians are concerned about metabolic syndrome (MetS). Inflammation and insulin resistance are caused by extra adipose tissue. Our study seeks to evaluate, taking into account numerous variables, the relationship between high-sensitivity C-reactive protein (hsCRP) levels and MetS in adults aged 50+ in Northern Kashmir, India. Materials and Methods: In Northern Kashmir, India, a hospital-based cross-sectional study looked into the relationship between hsCRP and MetS in people over 50. The recruitment process included people looking for basic healthcare services. Utilising modified NCEP-ATP III criteria, MetS was established. The association between MetS and hsCRP levels was evaluated statistically while taking into account various variables. Results: The waist circumference, body mass index, systolic and diastolic blood pressure, as well as the prevalence of hypertension, diabetes mellitus (DM), and dyslipidemia were all greater in those with MetS. While demonstrating decreased levels of high-density lipoprotein cholesterol (HDL-C), they also showed higher levels of high-sensitive C-reactive protein (hsCRP) and fasting plasma glucose. A study of correlations revealed a substantial inverse relationship between hsCRP and HDL-C. Elevated hsCRP levels were found to be substantially linked with MetS by the use of logistic regression, along with obesity, uric acid levels, hypertension, DM, and dyslipidemia. These results underline how crucial it is to keep an eye on these variables in order to recognize and treat MetS as soon as possible. Conclusion: Among this investigation, we found strong evidence that high- hsCRP, an independent risk factor for MetS, was present among middle-aged and elderly residents of the northern Kashmir region of India.

Impact of Fixed Orthodontic Appliances on Blood Count and High-Sensitivity C-Reactive Protein Levels

ABSTRACT Background: Fixed orthodontic appliances are widely used in dental practice to correct malocclusions and improving oral health. However, their impact on systemic inflammation and hematological parameters remains under-explored. Materials and Methods: A cohort of 60 patients, aged 12 –30 years, undergoing fixed orthodontic treatment, were enrolled in the study. Blood samples were collected at baseline, 1 month, and 6 months post-appliance placement. Hematological parameters, including white blood cell (WBC) count, red blood cell (RBC) count, hemoglobin levels, and hs-CRP levels, were measured using standard laboratory techniques. A statistical analysis was performed to determine significant changes over time. Results: At 1-month post-appliance placement, a significant increase in WBC count (mean increase of 12%) and hs-CRP levels (mean increase of 18%) was observed compared to baseline (P &lt; 0.05). RBC count and hemoglobin levels remained relatively unchanged. By 6 months, WBC count and hs-CRP levels showed a decreasing trend, approaching baseline values, though hs-CRP levels remained slightly elevated (mean increase of 5% from baseline, P &gt; 0.05). Conclusion: The use of fixed orthodontic appliances induces a transient inflammatory response, as evidenced by elevated WBC count and hs-CRP levels within the first month of treatment.

Efficacy and safety of tocilizumab in Chinese patients with systemic juvenile idiopathic arthritis: a multicentre phase IV trial

ObjectivesGiven the limited tocilizumab (TCZ) treatment data for systemic juvenile idiopathic arthritis (sJIA) in China, we evaluated the long-term efficacy and safety of TCZ in Chinese patients with sJIA.MethodIn this multicentre, interventional Phase IV study, patients with sJIA and inadequate clinical response to non-steroidal anti-inflammatory drugs/corticosteroids received TCZ infusions every 2 weeks based on body weight (< 30 kg, 12 mg/kg; ≥ 30 kg, 8 mg/kg), over a 52-week open-label period and an 8-week safety follow-up period. The primary endpoint was the proportion of patients with a JIA American College of Rheumatology (ACR) 30 response and absence of fever at Week 12.ResultsSixty-two patients were enrolled and treated (12-mg/kg group, 34; 8-mg/kg group, 28). At Week 12, 87.1% (95% confidence interval 78.8%–95.4%) of patients had JIA ACR 30 response and absence of fever; Week 52 results were similar. The proportion of JIA ACR 30/50/70/90 responders rapidly increased at Week 12, up to Week 52. High-sensitivity C-reactive protein (hsCRP) levels decreased within 4 weeks; 44/58 patients (75.9%) with elevated baseline hsCRP recovered at Week 52. Childhood Health Assessment Questionnaire pain scores, disability index scores, and mean corticosteroid dose decreased over time. Height standard deviation score changes at Week 52 indicated catch-up growth. Most adverse events (AEs) were mild (serious AE incidence, 17.7%). No deaths or macrophage activation syndrome occurred.ConclusionThis is the first multicentre trial to report the efficacy and safety of TCZ in Chinese patients with sJIA at 52 weeks. No new safety concerns were found.Key points• This is the first multicentre trial providing strong evidence for tocilizumab (TCZ) treatment for systemic juvenile idiopathic arthritis (sJIA) in China.• The study reported TCZ had good efficacy and favourable safety profiles in Chinese sJIA patients in the long term (52 weeks).• TCZ treatment showed rapid disease control, which was maintained over time, catch-up growth benefits in patients, tapering and discontinuation of corticosteroids, and improved quality of life.

Abstract P397: Effects of Dietary Sodium Reduction on Systemic Inflammation: Findings from DASH-Sodium Study

Background: High sodium intake is a significant risk factor for hypertension and cardiovascular disease. Animal studies have demonstrated that high salt diet promotes tissue inflammation and increases systemic inflammation, such that it is plausible that sodium induced inflammation might be another pathway to hypertension. However, whether the link between dietary sodium intake and systematic inflammation in humans remains unclear due to limited human studies, different designs and inconsistent findings. Therefore, we tested the hypothesis that dietary sodium reduction reduces systemic inflammation in humans by leveraging the randomized controlled trial design of the DASH-Sodium study. Methods: DASH-Sodium study was a multicenter, randomized trial comparing the effects on blood pressure (BP) of three levels of sodium intake (3450 mg/d, 2300mg/d, and 1150 mg/d) in two diets (DASH vs American) among US adults. Five systematic inflammatory markers including hs-CRP, IFN-γ, IL-6, IL-10, and TNF-α were measured at each study visit in stored plasma samples from 224 participants. Two-level mixed-effects linear regression models were used to assess the effect of sodium reduction on inflammatory markers with adjustment of covariates. Results: A total of 224 participants (aged 49.4±9.5 yrs, 61% female, 62% black, and 2% other races) from the DASH-Sodium study were included in the analyses. Overall, compared to high sodium group, low sodium group had slightly elevated hs-CRP ( p =0.013), and intermediate sodium group had decreased TNF-α ( p =0.011). Both significances, however, disappeared after adjusting for multiple testing ( p adjust &gt;0.01). Conclusion: Modest dietary sodium reduction as recommended did not induce significant changes in systematic inflammation in humans.

Investigating the impact of dietary guidelines transition on cardiometabolic risk profile: a forensic analysis using diet quality metrics

Evaluating dietary guidelines using diet quality (DQ) offers valuable insights into the healthfulness of a population’s diet. We conducted a forensic analysis using DQ metrics to compare the Malaysian Dietary Guidelines (MDG-2020) with its former version (MDG-2010) in relation to cardiometabolic risk (CMR) for an adult Malaysian population. A DQ analysis of cross-sectional data from the Malaysia Lipid Study (MLS) cohort (n = 577, age: 20-65yrs) was performed using the healthy eating index-2015 (HEI-2015) framework in conformation with MDG-2020 (MHEI2020) and MDG-2010 (MHEI2010). Of 13 dietary components, recommended servings for whole grain, refined grain, beans and legumes, total protein, and dairy differed between MDGs. DQ score associations with CMR, dietary patterns and sociodemographic factors were examined. Out of 100, total DQ scores of MLS participants were ‘poor’ for both MHEI2020 (37.1 ± 10.3) and MHEI2010 (39.1 ± 10.4), especially among young adults, males, Malays, and those frequently ‘eating out’ as well as those with greatest adherence to Sugar-Sweetened Beverages pattern and lowest adherence to Food Plant pattern. Both metrics shared similar correlations with CMR markers, with MHEI2020 exhibiting stronger correlations with WC, BF%, TG, insulin, HOMA2-IR, and smallLDL than MHEI2010, primarily attributed to reduced refined grain serving. Notably, participants with the highest adherence to MHEI2020 scores exhibited significantly reduced odds for elevated TG (AOR 0.44, 95% CI 0.21–0.93, p = 0.030), HOMA2-IR (AOR 0.44, 95% CI 0.21–0.88, p = 0.022), and hsCRP (AOR 0.54, 95% CI 0.31–0.96, p = 0.040, compared to those with the lowest adherence. Each 5-unit increase in MHEI2020 scores reduced odds for elevated BMI (− 14%), WC (− 9%), LDL-C (− 32%), TG (− 15%), HOMA2-IR (− 9%) and hsCRP (− 12%). While MHEI2020 scores demonstrated better calibration with CMR indicators, the overall sub-optimally ‘poor’ DQ scores of this population call for health promotion activities to target the public to achieve adequate intake of healthful fruits, non-starchy vegetables and whole grain, and moderate intake of refinedgrain, added sugar and saturated fat.

Vitamin D Insufficiency with Elevated ADMA and hs-CRP: A Single-center Study of Chronic Kidney Disease Patients Undergoing Hemodialysis

Background: Vitamin D deficiency is a common issue among patients with chronic kidney disease (CKD) due to its ability to convert vitamin D into the active form of calcitriol, which is crucial for controlling cell inflammation. Low vitamin D levels are associated with increased inflammation and higher levels of biomarkers such as c-reactive protein and asymmetric dimethylarginine as an endogenous inhibitor of nitric oxide synthase. Those two combined become a specific marker for cardiovascular diseases, which become one of the common causes of CKD mortality. Objective: This study examines the correlation between vitamin D insufficiency, elevated high-sensitivity c-reactive protein, and asymmetric dimethylarginine in CKD patients receiving hemodialysis. Methods: This study used a cross-sectional design of CKD patients receiving hemodialysis in Dr. Kariadi Central General Hospital, Semarang, Indonesia, in November 2021. Thirty-six patients were randomly enrolled after meeting inclusion and exclusion criteria. Primary outcomes of Vitamin D, hs-CRP, and ADMA were measured from patients’ blood after hemodialysis. A statistical analysis of Pearson's correlation was used for primary outcomes. Results: No significant difference was found in the patient's baseline characteristics. A significant correlation between vitamin D and ADMA has been found; however, no correlation between vitamin D and hs-CRP has been found Conclusion: Vitamin D deficiency is correlated with elevated ADMA, indicative of endothelial dysfunction.

Cardiovascular disease risk factors and their associations with inflammation among US adolescents: NHANES, 2015 to March 2020

IntroductionThe prevalence of obesity and glycemic dysfunction in adolescents has increased over the past several decades but less is known on how these conditions are associated with systemic inflammation in...

Correlation Between Hemoglobin A1c (HbA1c) and High-Sensitivity C-Reactive Protein (hs-CRP) in Myocardial Infarction Patients and Their Six-Month Mortality Follow-Up.

Background Acute coronary syndrome (ACS), encompassing unstable angina (UA), non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI), poses significant global health challenges because of its associated high mortality and morbidity rates. Vascular inflammation plays a crucial role in the pathogenesis of atherosclerosis, and it is often assessed using biomarkers such as high-sensitivity C-reactive protein (hs-CRP). Hyperglycemia, common in myocardial infarction patients, is linked to increased complications and mortality, with glycosylated hemoglobin A1c (HbA1c) serving as a key indicator of long-term glycemic control. Objective This study investigates the correlation between hs-CRP and HbA1c levels in patients with acute myocardial infarction (AMI) and type 2 diabetes mellitus (T2DM) and evaluates their impact on six-monthmortality outcomes. Methods A prospective observational study was conducted with 80 patients diagnosed with AMI. Data collection included demographic information, medical history, clinical assessments, laboratory investigations (including hs-CRP and HbA1c levels), and imaging studies. Patients received standard treatment and were followed up for six months. Statistical analyses were performed to examine the relationships between hs-CRP, HbA1c, and clinical outcomes. Results Higher HbA1c levels at admission were significantly correlated with elevated hs-CRP levels (p < 0.05). Both biomarkers showed a reduction at six months, correlating with improved glycemic control and reduced inflammation. Each unit increase in HbA1c was associated with a 21% increase in the hazard of mortality, and, similarly, each unit increase in hs-CRP was associated with a 17% increase in the hazard of mortality. The positive correlation between HbA1c and hs-CRP suggests that HbA1c can serve as an independent marker for predictingmortality in this patient population. Conclusion The study demonstrates a significant correlation between hs-CRP and HbA1c levels in patients with AMI and T2DM, with both biomarkers serving as strong predictors of six-monthmortality. HbA1c, because of its positive correlation with hs-CRP, could be used as an independent marker for assessing the risk of adverse outcomes in these patients. These findings highlight the importance of managing both glycemic control and inflammation in diabetic patients with ACSs.

Association between Breakfast Consumption Frequency and Chronic Inflammation in Korean Adult Males: Korea National Health and Nutrition Examination Survey 2016-2018.

Skipping breakfast is associated with an increased risk of chronic inflammatory diseases. This study aimed to examine the association between breakfast-eating habits and inflammation, using high-sensitivity C-reactive protein (hs-CRP) as a marker. A total of 4,000 Korean adult males with no history of myocardial infarction, angina, stroke, diabetes, rheumatoid arthritis, cancer, or current smoking were included. Data from the 2016-2018 Korea National Health and Nutrition Examination Survey were used for analysis. The frequency of breakfast consumption was assessed through a questionnaire item in the dietary survey section asking participants about their weekly breakfast consumption routines over the past year. Participants were categorized into two groups, namely "0-2 breakfasts per week" and "3-7 breakfasts per week"; hs-CRP concentrations were measured through blood tests. Comparing between the "infrequent breakfast consumption (0-2 breakfasts per week)" and "frequent breakfast consumption (3-7 breakfasts per week)" groups, the mean hs-CRP was found to be significantly higher in the "infrequent breakfast consumption" group, even after adjusting for age, body mass index, physical activity, alcohol consumption, systolic blood pressure, blood pressure medication, fasting blood glucose, and triglycerides (mean hs-CRP: frequent breakfast consumption, 1.36±0.09 mg/L; infrequent breakfast consumption, 1.17±0.05 mg/L; P-value=0.036). Less frequent breakfast consumption was associated with elevated hs-CRP levels. Further large-scale studies incorporating adjusted measures of daily eating patterns as well as food quality and quantity are required for a deeper understanding of the role of breakfast in the primary prevention of chronic inflammatory diseases.