hs-CRP Levels Research Articles

Effect of scaling on serum high-sensitivity C-reactive protein levels and periodontal parameters in systemically healthy women of reproductive age group with gingivitis.

Varying levels of sex hormones across the menstrual cycle in young systemically healthy females may alter tissue responses to plaque, resulting in increased gingival inflammation. Also, higher severity and prevalence of gingivitis has been demonstrated in adult women than men, attributed to hormonal changes. Further, it has been reported that gingivitis raises the levels of systemic inflammatory markers such as C-reactive protein. This interventional trial aimed to evaluate the effect of supragingival scaling on serum high-sensitivity C-reactive protein (hsCRP) levels along with periodontal parameters in systemically healthy women of reproductive age with natural gingivitis. In total, 57 women of reproductive age were enrolled into two groups. The test group (n = 30) comprised systemically healthy women with gingivitis who received supragingival scaling. The control group (n = 27) included systemically and periodontally healthy women. Periodontal parameters (Gingival Index, Plaque Index, pocket probing depth, bleeding on probing) and serum hsCRP levels were recorded at baseline for both the groups. Follow-up of test group participants was done at 3 and 6 months. Serum hsCRP and periodontal parameters were significantly higher in the test group than in the control group at baseline, and this decreased significantly after treatment in the test group at the 6-month follow-up (P ≤ .05). Gingival Index, bleeding on probing, and hsCRP in the test group at 6 months were reduced to the baseline levels of systemically and periodontally healthy women. Treatment of gingival inflammation can help in lowering the systemic and local inflammation to the levels of systemically and periodontally healthy women.

Burst steroid therapy for acute heart failure: The CORTAHF randomized, open-label, pilot trial.

Burst steroid therapy, effective in acute respiratory diseases, may benefit patients with acute heart failure (AHF) in whom inflammatory activation is associated with adverse outcomes. CORTAHF assessed whether burst steroid therapy reduces inflammation and results in better quality of life and clinical outcomes in AHF. Patients with AHF, N-terminal pro-B-type natriuretic peptide >1500 pg/ml, and high-sensitivity C-reactive protein (hsCRP) >20 mg/L were randomized 1:1 to oral, once daily 40 mg prednisone for 7 days or usual care, without blinding. Patients were followed for 90 days. A total of 101 patients were randomized. At day 7 the primary endpoint, hsCRP decreased in both arms-adjusted geometric mean ratios (GMRs) were 0.30 and 0.40 in the prednisone and usual care arms (ratio of GMRs 0.75, 95% confidence interval [CI] 0.56-1.00, p = 0.0498). The 90-day risk of worsening heart failure (HF), HF readmission or death as reported by the unblinded investigators was significantly lower in the prednisone group (10.4%) than in usual care (30.8%) (hazard ratio 0.31, 95% CI 0.11-0.86, p = 0.016). The EQ-5D visual analogue scale score as reported by the unblinded patients increased more in the prednisone group on day 7 (least squares mean difference 2.57, 95% CI 0.12-5.01 points, p = 0.040). All effects were statistically significant in the pre-specified subgroup with centrally-measured interleukin-6 >13 pg/ml. Adverse events, particularly hyperglycaemia, occurred more in the prednisone group with no difference in infection rate. In this small open-label study of patients with AHF, burst steroid therapy was associated with reduced inflammation as measured by hsCRP levels at day 7 (primary endpoint). Secondary endpoints showed improved quality of life at day 7 and reduced 90-day risk of death or worsening HF. Large prospective studies are needed to evaluate these findings.

Impaired left ventricular function in lean women with PCOS: Insights from speckle tracking echocardiography

Aims: We aimed to conduct a study examining left ventricular function (LVEF) in lean women PCOS patients with speckle tracking echocardiography. Methods: The study included 60 patients diagnosed with PCOS and 30 healthy controls matched for age and body mass index. Morning fasting blood samples were collected to measure levels of glucose, insulin, high-sensitivity C-reactive protein (hs-CRP), and lipids. Left ventricular function (LVF) was evaluated using two-dimensional speckle tracking echocardiography (2D-STE) and real-time three-dimensional echocardiography (3D-Echo). Global strain was assessed from three standard apical views using 2D-STE. Results: The hs-CRP levels in lean women with PCOS were significantly higher compared to the control group (2.34±1.07 vs. 1.13±0.54; p=0.01). The peak longitudinal strain values in the 2-chamber, 4-chamber, and long-axis views were lower in lean women with PCOS compared to the control group (15.9±1.2 vs. 19.4±1.2; p=0.01, 17.0±1.1 vs. 19.2±1.4; p=0.01, 16.3±1.3 vs. 19.2±1.5; respectively, p=0.01). According to the multiple regression model, global strain was independently associated with hs-CRP (β=0.31, p=0.04), the ratio of early diastolic mitral inflow velocity (E) to early diastolic annular velocity (E/E’ ratio) (β=0.33, p=0.01), and ejection fraction (EF) (β=0.35, p=0.01). Conclusion: Our findings reveal that lean women with PCOS exhibit significantly higher levels of high-sensitivity C-reactive protein (hs-CRP) compared to healthy controls. Furthermore, the peak longitudinal strain values across multiple cardiac views were notably lower in the PCOS group, suggesting impaired left ventricular function. These results highlight the importance of monitoring cardiovascular health in lean women with PCOS, as they are at an increased risk of developing left ventricular dysfunction despite their lean body mass index.

Posttraumatic stress disorder increases thrombosis risk: Evidence from a biobank data set.

Depression and anxiety are linked to deep venous thrombosis (DVT) and posttraumatic disorder (PTSD) increases risk of venous thromboembolism in women. However, the mechanisms underlying this relationship remain unknown. We hypothesized that PTSD would associate with increased DVT risk, that neuroimmune mechanisms would mediate the PTSD-DVT link, and that these associations would be stronger in women. This cohort study included N = 106 427 participants from a large biobank. PTSD and DVT were defined using ICD-10 codes. A subset (N = 1520) underwent imaging, from which we assessed stress-associated neural activity (SNA). High-sensitivity C-reactive protein (hs-CRP) levels and heart rate variability (HRV) were used as indicators of systemic inflammation and autonomic activity, respectively. Linear, logistic, and Cox regressions and mediation analyses were used to test our hypotheses. Of 106 427 participants, 4192 (3.9%) developed DVT. PTSD associated with increased DVT risk (HR [95% CI]: 1.66 [1.34, 2.07], p < .001), and this finding remained significant after adjustment for age, sex, and traditional DVT risk factors. When analyzed separately by sex, PTSD was significantly associated with DVT risk in women but not men. Further, heightened SNA and lower HRV mediated the effect of PTSD on DVT risk. Results suggest that individuals with PTSD are at increased risk for DVT, and that risk is higher in women. This relationship was partially driven by alterations in stress-associated neural activity and autonomic function, suggesting potential targets for preventive therapies. Future studies are needed to investigate whether intervening on PTSD-DVT mechanisms has downstream beneficial effects on DVT, especially among women.

The Efficacy and Safety of Probiotic Combinations Lobun Forte® Versus Renadyl® in Patients With Chronic Kidney Disease: A Comparative, Phase IV, Randomized, Open-Label, Active-Controlled, Parallel Study.

Chronic kidney disease (CKD) often leads to gut microbiota imbalance, accelerating disease progression and increasing uremic toxins and inflammation. We conducted a randomized clinical trial comparing outcomes between two multi-strain probiotic supplements Lobun Forte® (Sanzyme P Ltd, Hyderabad, India) containing Streptococcus thermophilus, Lactobacillus acidophilus, Bifidobacterium longum, and Bacillus coagulans and Renadyl® (Kibow Biotech, LLC., Pennsylvania, United States) containing S. thermophilus, L. acidophilus, and B. longum. Sixty patients with stage 3-4 CKD were randomized to receive either Lobun Forte (n=30) or Renadyl (n=30) for six months, with each supplement providing 45 billion CFU/capsule, twice daily. Primary outcomes included quality of life (QoL) (Short-Form 8 (SF-8) score), reductions in uremic toxins (p-cresyl sulfate (PCS), 3-indoxyl sulfate (IS), indole-3-acetic acid (IAA)), blood urea nitrogen (BUN), serum creatinine, and serum uric acid. Secondary outcomes assessed oxidative stress, inflammatory biomarkers, and estimated glomerular filtration rate (eGFR). Results: Both Lobun Forte and Renadyl groups showed significant improvements in QoL, with Lobun Forte achieving a 53.5% improvement (16.43 point increase) and Renadyl a 51.1% improvement (15.27 point increase) in SF-8 scores (p < 0.0001). Thelevels of IS decreased significantly in both groups (p < 0.0001), with Lobun Forte reducing IS by 29.72% and Renadyl by 24.20%. In terms of other uremic toxins, Lobun Forte showed non-significant (p > 0.05) reductions in mean PCS (7.63%) and IAA (15.57%), whereas Renadyl demonstrated a significant (p = 0.0314) decrease in PCS (20.75%) and a non-significant (p > 0.05) reduction in IAA (12.35%). Both groups showed significant (p < 0.0001) reductions in BUN and serum creatinine levels. Serum uric acid levels showed a significant (p = 0.0448) reduction with Lobun Forte while Renadyl exhibited a non-significant reduction (p = 0.1034). Lobun Forte significantly (p = 0.0359) reduced mean high-sensitivity C-reactive protein (hsCRP) levels, while Renadyl showed a non-significant reduction (p = 0.0876). Both groups had non-significant reductions in interleukin-6 and tumor necrosis factor-alpha levels (p > 0.05). Further, both groups experienced significant (p < 0.0001) increases in mean glutathione levels and nitric oxide levels. Additionally, Renadyl resulted in a significant reduction in mean malondialdehyde, whereas Lobun Forte showed a non-significant reduction. Both probiotics significantly (p < 0.0001) improved eGFR, with Lobun Forte increasing it by 40.4% and Renadyl by 36.9%. Both probiotics were well tolerated, with a favorable safety profile throughout the study. Conclusion: Both Lobun Forte and Renadyl effectively improve the quality of life in patients with stage 3-4 CKD by modulation of uremic toxins, renal parameters, inflammatory biomarkers, oxidative biomarkers, and eGFR. These findings suggest that both probiotics may help delay CKD progression by modulating the gut-kidney axis.

Maternal Soluble Programmed Death Ligand-1 (sPD-L1) and T-regulatory Cells (Tregs) Alteration in Preeclampsia: A Cross-Sectional Study From Eastern India.

Background Studies have shown that aberrant reactions of the immune system play an important role in the pathogenesis of preeclampsia. The immune checkpoint molecules programmed cell death protein 1/programmed death-ligand 1 (PD-1/PD-L1) system and the T-regulatory cells (Tregs) system are decisive in the regulation of immune responses and can be the target molecules in preeclampsia. In this study, an attempt has been made to evaluate the soluble PD-L1 (sPD-L1) in the serum of preeclampsia cases and correlate it with Tregs and inflammatory markers to have an insight into the link between these immunomodulatory molecules in the pathogenesis of preeclampsia. Materials and methods Ten normal fertile women, 20 trimester-matched normal pregnancy cases, and 20 preeclampsia cases were enrolled in the study. Serum sPD-L1, transforming growth factor beta 1 (TGF-β1), and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA). High-sensitive C-reactive protein (hsCRP) was estimated using a clinical biochemistry autoanalyzer. Tregs were evaluated using flow cytometry. Results and discussion The immune checkpoint molecule PD-L1 inversely correlated with Tregs in preeclampsia cases. Associated inflammation was seen by raised IL-6 and hsCRP. The breakdown of immunological tolerance is mainly caused by the dysregulating the Tregs/Th17 balance, which leads to conditions of autoimmunity and chronic inflammatory disorders. PD-L1 can be the link between this immunological misbalance. Conclusion Our study, showing an increase in sPD-L1 and TGF and a decrease in Tregs with an increase in inflammatory markers like IL-6 and hsCRP levels in preeclampsia, has potential implications for early diagnosis and management of the condition. PD-L1 and Tregs can be target molecules for early management of preeclampsia.

Prediction of in-hospital mortality in patients with myocardial infarction and type 2 diabetes: the role of cellular indices of systemic inflammation

Aim. To assess the value of cellular indices of systemic inflammation in the prognosis of in-hospital mortality in patients with ST-segment elevation myocardial infarction (MI) in combination with type 2 diabetes (T2D).Material and methods. The retrospective case-control study included 125 patients with myocardial infarction and T2D, 25 of whom died during the index hospitalization. The cellular composition of the blood and the level of high-sensitivity C-reactive protein (hsCRP) were determined on the first and third days of hospitalization. In the groups of deceased and surviving patients, cellular indices of systemic inflammation were calculated and compared (neutrophil-lymphocyte ratio (NLR), neutrophil-monocyte ratio (NMR), monocyte-lymphocyte ratio (MLR), platelet-lymphocyte ratio (PLR), systemic inflammation index (SII), systemic inflammation response index (SIRI)) and average hsCRP levels). The prognostic role of the studied parameters was assessed using univariate and multivariate logistic regression.Results. Deceased patients, compared with survived ones, had higher Killip class, body mass index, number of stents implanted, higher hsCRP levels, and lower left ventricular ejection fraction. Inhospital mortality was associated with hsCRP (odds ratio of 1,03 with 95% confidence interval of 1,003-1,05, p=0,029), NLR (2,56 [1,73-9,78], p&lt;0,001), NMR (1,16 [1,001-1,35], p=0,04), MLR (23,7 [3,1-182,6], p=0,002), SII (1,001 [1,0-1,001], p=0,028), SIRI (1,29 [1,09-1,52], p=0,003) 48 hours after admission, as well as with the degree of hsCRP change (1,03 [1,003-1,05], p=0,025), NLR (1,58 [1,21-2,06], p=0,001), SII (1,001 [1,0-1,001], p=0,028) during the first three days. Adjusted multivariate regression analysis identified a set of independent predictors with greatest accuracy in assessing the death probability: NLR, SII and SIRI 48 hours after admission, the degree of hsCRP change, body mass index and the num ber of implanted stents.Conclusion. The work demonstrated the significance of cellular indices of systemic inflammation (NLR, SII and SIRI) in assessing the prognosis of in-hospital mortality in patients with MI combined with T2D.

Elevated C-Reactive Protein in Older Men With Chronic Pain: Association With Plasma Amyloid Levels and Hippocampal Volume.

Chronic pain leads to tau accumulation and hippocampal atrophy, which may be moderated through inflammation. In older men, we examined associations of chronic pain with Alzheimer's disease (AD)-related plasma biomarkers and hippocampal volume as moderated by systemic inflammation. Participants were men without dementia. Chronic pain was defined as moderate-to-severe pain in 2+ study waves at average ages 56, 62, and 68. At age 68, we measured plasma amyloid-beta (Aβ42, n = 871), Aβ40 (n = 887), total tau (t-tau, n = 841), and neurofilament light chain (NfL, n = 915), and serum high-sensitivity C-reactive protein (hs-CRP, n = 968), a marker of systemic inflammation. A subgroup underwent structural MRI to measure hippocampal volume (n = 385). Analyses adjusted for medical morbidities, depressive symptoms, and opioid use. Chronic pain was related to higher Aβ40 (β = 0.25, p = .009), but hs-CRP was unrelated to AD-related biomarkers (ps > .05). There was a significant interaction such that older men with both chronic pain and higher levels of hs-CRP had higher levels of Aβ42 (β = 0.36, p = .001) and Aβ40 (β = 0.29, p = .003). Chronic pain and hs-CRP did not interact to predict levels of Aβ42/Aβ40, t-tau, or NfL. Furthermore, there were significant interactions such that Aβ42 and Aβ40 were associated with lower hippocampal volume, particularly when levels of hs-CRP were elevated (hs-CRP × Aβ42: β = -0.19, p = .002; hs-CRP × Aβ40: β = -0.21, p = .001), regardless of chronic pain status. Chronic pain was associated with higher plasma Aβ, especially when hs-CRP was also elevated. Higher hs-CRP and Aβ levels were both related to smaller hippocampal volumes. Chronic pain, when accompanied by systemic inflammation, may elevate the risk of neurodegeneration in AD-vulnerable regions.

The effects of inulin supplementation on clinical indices, oxidative stress and inflammatory biomarkers in women with migraine: A double-blind, placebo-controlled, randomized trial

The present study aimed to investigate the effects of 12 weeks inulin supplementation (10 g/d) on clinical indices and biomarkers of inflammation, gut permeability, and oxidative stress in eighty women with migraine. Before and after the trial, we assessed the migraine index (MI), migraine headache index score (MHIS), headache diary results (HDR), high-sensitivity C-reactive protein (hs-CRP), zonulin, nitric oxide (NO), and oxidative stress factors. Inulin supplementation improved total antioxidant capacity (284.07 vs. 26.92, P=0.046), and reduced hs-CRP (−0.69 vs. 0.14), NO (−5.65 vs. 2.57) and oxidative stress index levels (−0.21 vs. 0.05) compared to placebo. Moreover, inulin supplementation resulted in a significant decrease in the score of MHIS, MI, and HDR (all P-values < 0.05). However, no significant change was observed in total oxidative status, and zonulin levels. This study showed that inulin supplementation can favorably improve clinical symptoms, inflammatory and oxidative stress biomarkers in women with migraine.

Activation of NLRP3 inflammasome in patients with renal transplantation: relation to allograft dysfunction, inflammation, and renal fibrosis

ABSTRACT Background Chronic allograft dysfunction (CAD) represents a complex process of inflammatory response, fibrosis, and tissue restoration, mediated by a myriad of proinflammatory cytokines, enzymes, and growth factors. NOD-like receptor protein3 (NLRP3) inflammasome is one of the NLR protein families. It drives proteolysis of proinflammatory caspases which induces maturation of pro-interleukin (IL)-1β and pro-IL-18. The aim of this work is to study NLRP3 inflammasome activation in patients with renal transplantation in relation to allograft function, inflammation, and renal fibrosis. Methods Thirty renal transplant recipients (RTR): 15 patients with stable renal function (Group I), 15 patients with CAD (Group II), and 15 healthy subjects (Group III) were included. Serum and urinary NLRP3, caspase-1, and interleukin-1β were measured using an enzyme-linked immunosorbent assay (ELISA) kit. Serum high sensitivity C-reactive protein (hs-CRP) level was measured, and neutrophil-lymphocyte ratio (NLR) was calculated. Renal function was evaluated by serum creatinine (S.Cr) and estimated glomerular filtration rate (eGFR). Resistive index (RI) was calculated with Doppler ultrasonography. In patients with CAD, renal interstitial fibrosis (RIF) was graded in renal biopsies. Results Serum NLRP3, caspase-1, serum and urinary IL-1β, and hs-CRP showed a statistically significant increase in RTR, particularly in those with CAD compared to the controls with a positive correlation with each other, their urinary level, S. Cr, hs-CRP, NLR, RI, and RIF (p < 0.001). The receiver operating characteristic curve showed high diagnostic accuracy of serum NLRP3, caspase-1, and IL-1β in discriminating patients with CAD from patients with stable renal function. Conclusion The NLRP3-caspase1-IL-1β cascade is activated and upregulated in renal transplant recipients, particularly those with advanced renal impairment, and thus may play a role in developing CAD and renal fibrosis. They could be potential biomarkers for post-transplant outcome, follow-up, and early diagnosis. Moreover, their cascade could be a target for future anti-inflammatory therapeutic strategies for allograft dysfunction.

First time ACS in patients with on-target lipid levels: Inflammation at admission and re-event rate at follow-up.

Dyslipidaemia, inflammation and elevated Lp(a) levels are associated with the progression of atherosclerosis. This study investigates whether patients with a first-time presentation of chest pain and on-target LDL-C levels and intermediate FRS/ESC-Score risks, display a high inflammatory burden linked to myocardial injury and whether inflammation at admission affects the re-event rate up to 6 years follow-up. Blind assessments of novel inflammatory markers such as Glycoprotein A and B via nuclear magnetic resonance (NMR), cytokines, hsCRP, Neutrophil-to-Lymphocyte ratio (NLR) and Lipoprotein(a) levels were examined. Out of 198 chest pain patients screened, 97 met the inclusion criteria at admission. cTnI(+) patients (>61 ng/L) with elevated Lipoprotein(a), showed significantly increased levels of Glycoprotein A and B, hsCRP, IL-6, a high NLR and a reduced left ventricular ejection fraction (%) compared to cTnI(-) individuals. Those patients, with a higher inflammatory burden at hospital admission (hsCRP, IL-6, Glycoprotein A and B, and Lipoprotein(a)) had a higher re-event rate at follow-up. Inflammation and Lipoprotein(a) levels were particularly prominent in patients presenting with reduced left ventricular ejection fraction. Notably, Glycoproteins A/B emerge as novel markers of inflammation in these patients. Our study highlights the significantly higher impact of inflammatory burden in patients with chest pain and high level of myocardial damage than in those with lower myocardial affectation, even when they all had lipid levels well controlled. Inflammation at the time of admission influenced the re-event rate over a follow-up period of up to 6 years.

Efficacy and Safety of Bempedoic Acid in Lipid Disorder Therapy: A Review of Clinical Trials

LDL levels are a key risk factor for atherosclerotic cardiovascular disease. Bempediic acid is an innovative hypolipemic drug, particularly useful for patients intolerant of statins. The article focuses on analyzing the results of clinical trials on the mechanisms of action, efficacy and safety of bempediic acid used both as monotherapy and in combination with other hypolipemic drugs. Scientific evidence based on the CLEAR: Tranquility, Harmony, Serenity, Wisdom, Outcomes study, among others, is presented. Its significant effects on lowering LDL-C, non-HDL-C, and hsCRP levels are highlighted, with important implications for the prevention and treatment of cardiovascular disease. It also outlines how bempedic acid is included in current Polish guidelines for the treatment of lipid disorders. The paper also points to new areas of research, including potential applications of bempediic acid in specific patient groups, such as pregnant women. In addition, the article addresses issues related to the long-term use and safety of bempediic acid, particularly in the context of reducing cardiovascular risk and lowering blood lipid levels, which is crucial for patients with statin intolerance.

Socioeconomic adversity, maternal nutrition, and the prenatal programming of offspring cognition and language at two years of age through maternal inflammation

Increasing rates of child neurodevelopmental vulnerability are a significant public health challenge. The adverse effect of socioeconomic adversity on offspring cognition may be mediated through elevated prenatal maternal systemic inflammation, but the role of modifiable antecedents such as maternal nutrition has not yet been clarified. This study aimed to examine (1) whether prenatal factors, with an emphasis on maternal nutrition, were associated with prenatal maternal systemic inflammation at 28 weeks’ gestation, including the metabolomic marker glycoprotein acetyls (GlycA); (2) the extent to which the association between prenatal maternal nutrition and child cognition and language at age two years was mediated by elevated maternal inflammation in pregnancy; (3) the extent to which the associations between prenatal socioeconomic adversity and child neurodevelopment were mediated through prenatal maternal nutrition and GlycA levels. We used a prospective population-derived pre-birth longitudinal cohort study, the Barwon Infant Study (Barwon region of Victoria, Australia), where 1074 mother–child pairs were recruited by 28 weeks’ gestation using an unselected sampling frame. Exposures included prenatal factors such as maternal diet measured by a validated food frequency questionnaire at 28 weeks’ gestation and dietary patterns determined by principal component analysis. The main outcome measures were maternal inflammatory biomarkers (GlycA and hsCRP levels) at 28 weeks’ gestation, and offspring Bayley-III cognition and language scores at age two years. Results showed that the ‘modern wholefoods’ and ‘processed’ maternal dietary patterns were independently associated with reduced and elevated maternal inflammation respectively (GlycA or hsCRP p < 0.001), and also with higher and reduced offspring Bayley-III scores respectively (cognition p ≤ 0.004, language p ≤ 0.009). Associations between dietary patterns and offspring cognition and language were partially mediated by higher maternal GlycA (indirect effect: cognition p ≤ 0.036, language p ≤ 0.05), but were less evident for hsCRP. The maternal dietary patterns mediated 22 % of the association between socioeconomic adversity (lower maternal education and/or lower household income vs otherwise) and poorer offspring cognition (indirect effect p = 0.001). Variation in prenatal GlycA levels that were independent of these dietary measures appeared less important. In conclusion, modifiable prenatal maternal dietary patterns were associated with adverse child neurocognitive outcomes through their effect on maternal inflammation (GlycA). Maternal diet may partially explain the association between socioeconomic adversity and child neurocognitive vulnerability. Maternal diet-by-inflammation pathways are an attractive target for future intervention studies.

Assessment of ventilatory functions and associated inflammatory markers among workers in slaughterhouses

ObjectiveMeat processing is among the most extensive industries globally. However, data on the effects of occupational exposure on the pulmonary health of slaughterhouse workers is limited. Ascertaining the impact of the slaughterhouse atmosphere on the breathing habits of laborers exposed to it and the inflammatory markers associated with it was the aim of the current investigation.MethodsA cross-sectional study was performed on 82 non-smoker subjects of 41 male workers working in one of the major slaughterhouses in Cairo, Egypt, matched to 41 controls of administrative personnel. An elaborate questionnaire encompassing medical and occupational history was administered to each participant in the research. General and local systemic examinations and ventilatory function tests were carried out, and serum levels of interleukin 6 (IL-6) and high-sensitivity C-reactive protein (hsCRP) were measured.ResultsRespiratory symptoms were more prevalent with a statistically significant decline in ventilatory function parameters (FVC%, FEV1%, FEV1/FVC, FEF 25%, FEF 50%, FEF 75%, and PEF%) among the exposed group compared to those of control. In addition, there was a significantly higher serum level of inflammatory markers (IL-6 and hsCRP) among the exposed group compared to the control group, with a negative correlation with ventilatory functions. Moreover, there was a positive association between levels of serum IL-6 and hsCRP and the age and duration of employment of workers.ConclusionThere was a notable increase in the prevalence of respiratory disorders and inflammatory markers among slaughterhouse workers. Additionally, there was a substantial decrease in ventilatory function parameters, which could be attributed to the bioaerosols they encountered in the workplace.

Obesity is associated with higher levels of circulating cytokines involved in the development of cardiovascular disease in people living with HIV.

Obesity is increasingly described in people living with HIV (PLWH), but its impact on immune activation and inflammation in HIV is still poorly characterised. We aimed to analyse the difference in circulating cytokines involved in pathways associated with co-morbidities in PLWH according to the presence or absence of obesity. Age and sex matched PLWH with and without obesity (BMI ≥30 kg/m2) from a multicentre, prospective cohort were recruited with a 1:2 ratio. Twenty-three biomarkers covering pathways associated with systemic inflammation (hsCRP, IL-2, IL-6, TNFR1, TNFR2, TNF-α, IFN-γ, IL-18), coagulation (vWF, D-dimer, sCD40L), endothelial function (E-selectin, P-selectin, sICAM-1, sVCAM-1), atherosclerosis (MPO, Lp-PLA2), immune regulation (IL-1RA), innate immune activation (MIP-1, MCP-1, sCD163, sCD14) and microbial translocation (LBP) were measured in the two groups. Between-group difference in biomarkers were assessed using Mann-Whitney test. Associations between obesity and biomarkers were assessed using logistic regression adjusted for age, gender, ethnicity, smoking status, and antiretroviral therapy (ART). Ninety-nine ART-treated PLWH were included in the analysis (33 with obesity, 66 without obesity). PLWH with obesity had higher levels of hsCRP, IL-6, vWF, D-dimer, E-selectin, MPO, IL-1RA, and LBP. Six markers (hsCRP, IL-6, vWF, E-selectin, MPO, IL-1RA), reflecting systemic inflammation, coagulation and atherosclerosis pathways were associated with increased odds of obesity in the adjusted logistic regression model: hsCRP (aOR 2.7, 95% CI [1.7, 4.29]), IL-6 (3.77 [1.43, 9.93]), vWF (5.33 [1.51, 18.75]), E-selectin (6.28 [1.36, 29.04]), MPO (6.85 [1.87, 25.04]), IL-1RA (6.45 [2.28, 18.2]). No association was observed between obesity and markers of innate immune activation and gut microbial translocation. Obesity in PLWH was associated with activation of systemic inflammatory, endothelial, atherosclerosis and coagulation pathways, rather than those associated with innate immune activation and gut microbial translocation. These pathways point towards an unfavourable cardiovascular profile in PLWH with obesity, which will have to be further explored in future studies on long-term outcomes.

Elevated monomeric C-reactive protein levels are associated with premature coronary artery disease in patients with normal hsCRP levels

Elevated monomeric C-reactive protein levels are associated with premature coronary artery disease in patients with normal hsCRP levels

The Effect of Phototherapy on Systemic Inflammation Measured with Serum Vitamin D-Binding Protein and hsCRP in Patients with Inflammatory Skin Disease.

Vitamin D plays a role in inflammatory skin disease, but the exact mechanisms and the clinical significance remain unclear. According to the free hormone hypothesis, it is the free concentration of 25-hydroxy vitamin D (25(OH)D) that is biologically active. Vitamin D-binding protein (DBP) acts as the major transporter of vitamin D in the circulation, and DBP concentration defines the free 25(OH)D levels. DBP levels are elevated in various inflammatory conditions, including psoriasis. Narrowband-ultraviolet B (NB-UVB) is the most widely used phototherapy and is an established first-line treatment for psoriasis and atopic dermatitis (AD), often used before proceeding to systemic treatment. The aim of this study was to investigate the influence of NB-UVB phototherapy on DBP and high-sensitivity C-reactive protein (hsCRP) levels, as markers of systemic inflammation, in inflammatory skin disease. Thirty adults (psoriasis (n = 20) and AD (n = 10)) were treated with NB-UVB. Serum DBP, hsCRP, total and free 25(OH)D, and 1,25-dihydroxy vitamin D (1,25(OH)2D) were measured before and after NB-UVB. Disease severity was assessed with Psoriasis Area and Severity Index (PASI), SCORing Atopic Dermatitis (SCORAD), and Visual Analogue Scale (VAS). DBP decreased in psoriasis patients and varied with no clear trend in AD patients. HsCRP decreased in both groups, but this did not reach statistical significance. PASI, SCORAD, and VAS improved, and vitamin D levels increased after NB-UVB. Sub-analysis indicated a better response to NB-UVB for patients with vitamin D deficiency and insufficiency compared to vitamin D-sufficient patients. The decrease in DBP after NB-UVB in psoriasis patients suggests a potential systemic anti-inflammatory effect of phototherapy. Measurement of vitamin D levels may potentially serve as a tool to identify patients who would derive the greatest benefit from NB-UVB phototherapy.

Dapagliflozin and sacubitril on myocardial microperfusion in patients with post-acute myocardial infarction heart failure and type 2 diabetes.

Coronary heart disease and type 2 diabetes mellitus (T2DM) frequently coexist, creating a complex and challenging clinical scenario, particularly when complicated with acute myocardial infarction (AMI). To examine the effects of dapagliflozin combined with sakubactrovalsartan sodium tablets on myocardial microperfusion. In total, 98 patients were categorized into control (n = 47) and observation (n = 51) groups. The control group received noxital, while the observation group was treated with dapagliflozin combined with noxital for 6 months. Changes in myocardial microperfusion, blood glucose level, cardiac function, N-terminal prohormone of brain natriuretic peptide (NT-proBNP) level, growth differentiation factor-15 (GDF-15) level, and other related factors were compared between the two groups. Additionally, the incidence of major adverse cardiovascular events (MACE) and adverse reactions were calculated. After treatment, in the observation and control groups, the corrected thrombolysis in myocardial infarction frame counts were 37.12 ± 5.02 and 48.23 ± 4.66, respectively. The NT-proBNP levels were 1502.65 ± 255.87 and 2015.23 ± 286.31 pg/mL, the N-terminal pro-atrial natriuretic peptide (NT-proANP) levels were 1415.69 ± 213.05 and 1875.52 ± 241.02 ng/mL, the GDF-15 levels were 0.87 ± 0.43 and 1.21 ± 0.56 g/L, and the high-sensitivity C-reactive protein (hs-CRP) levels were 6.54 ± 1.56 and 8.77 ± 1.94 mg/L, respectively, with statistically significant differences (P < 0.05). The cumulative incidence of MACEs in the observation group was significantly lower than that in the control group (P < 0.05). The incidence of adverse reactions was 13.73% (7/51) in the observation group and 10.64% (5/47) in the control group, with no statistically significant difference (P > 0.05). Dapagliflozin combined with nocinto can improve myocardial microperfusion and left ventricular remodeling and reduce MACE incidence in patients with post-AMI heart failure and T2DM. The underlying mechanism may be related to the reduction in the expression levels of NT-proANP, GDF-15, and hs-CRP.

The effect of hsCRP on TyG index-associated cardiovascular risk in patients with acute coronary syndrome undergoing PCI

The effect of systemic inflammation, represented by high-sensitivity C-reactive protein (hsCRP), on triglyceride glucose (TyG) index-associated cardiovascular risk in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI) has not yet been determined. This study was a retrospective analysis of a single-center prospective registry and finally included 1701 patients (age, 60 ± 10 years; male, 76.7%). The primary endpoint was defined as major adverse cardiovascular events (MACE), including cardiovascular mortality, non-fatal stroke, and non-fatal myocardial infarction. In the multivariate COX regression model that included the GRACE risk score, higher TyG index was significantly associated with a greater incidence of MACE in patients with hsCRP levels less than 2 mg/L but not 2 mg/L or more (P for interaction = 0.039). Each unit increase in the TyG index was independently associated with a 52% increased risk of MACE only in patients with hsCRP levels less than 2 mg/L (P = 0.021). After adjustment for other confounding factors, including the GRACE risk score, compared with those in the group of TyG index < 8.62 and hsCRP < 2 mg/L, patients in the group of TyG index ≥ 8.62 and hsCRP ≥ 2 mg/L had a 3.9 times higher hazard ratio for developing MACE. The addition of both TyG index and hsCRP had an incremental effect on the predictive ability of the GRACE risk score-based prognostic model for MACE (C-statistic: increased from 0.631 to 0.661; cNRI: 0.146, P = 0.012; IDI: 0.009, P < 0.001). In conclusion, there was a significant interaction between the TyG index and hsCRP for the risk of MACE, and the TyG index was reliably and independently associated with MACE only when hsCRP levels were less than 2 mg/L. Furthermore, high TyG index and high hsCRP levels synergistically increased the risk of MACE, suggesting that the prognostic value of TyG index combined with hsCRP might be promising in patients with ACS undergoing PCI.

The Impact of Combined Application of Donepezil and Nimodipine on Patients with Comorbid Cerebral Small Vessel Disease and Cognitive Dysfunction: Efficacy and Influence on Nutritional Status.

Cerebral small vessel disease (CSVD) often coexists with cognitive dysfunction in patients, leading to significant challenges in treatment and management. This study aimed to examine the efficacy of combined application of donepezil and nimodipine on patients with comorbid CSVD and cognitive dysfunction and the effects on patients' albumin and prealbumin levels. The records of 112 patients with comorbid CSVD and cognitive dysfunction treated at the People's Hospital of Suzhou New District from January 2019 to December 2022 were analysed retrospectively. A total of 50 patients receiving donepezil were allocated to the control group, and 62 patients receiving both nimodipine and donepezil to the study group. Outcomes compared between the two groups included serum homocysteine (Hcy), high sensitivity C-reactive protein (hs-CRP), albumin, and prealbumin before and after therapy, efficacy, and adverse reactions. Additionally, logistic regression was performed to analyze the risk factors impacting patient prognosis. Prior to therapy, the two groups did not differ significantly in Hcy and hs-CRP levels (p > 0.05), whereas after therapy, the levels in both groups dropped significantly (p < 0.01), with more obvious lower levels in the study group (p < 0.05). After treatment, the study group presented significantly higher albumin and prealbumin levels than the control group (p < 0.001). An obvious higher overall response rate was observed in the study group compared to the control group (p = 0.012). No significant inter-group discrepancy was found regarding the total incidence of adverse reactions (p = 0.752). Univariate analysis identified age, course of disease, heart rate (HR), Montreal Cognitive Assessment (MoCA) score, diastolic blood pressure (DBP), systolic blood pressure (SBP), drinking history, as well as medication regimen as risk factors impacting patient prognosis. Multivariate logistic regression analysis identified SBP, DBP, and medication regimen as the independent risk factors. Combined application of donepezil and nimodipine can effectively treat patients with comorbid CSVD and cognitive dysfunction. It can significantly lower the Hcy and hs-CRP levels and improve the nutritional status without increasing the frequency of adverse reactions. In addition, for CSVD patients with cognitive dysfunction, age, course of disease, MoCA score, HR, SBP, DBP, drinking history, and medication regimen are risk factors impacting patient prognosis, while SBP, DBP, and medication regimen are independent risk factors.