Plasma Pentraxin 3 Concentrations Research Articles

Pentraxin 3 concentration is associated with poor outcomes in patients with coronary artery disease: a systematic review and dose–response meta-analysis

Background The amount of plasma pentraxin 3 (PTX3) is gradually being considered as a novel biomarker in forecasting poor clinical outcomes in patients with coronary artery disease (CAD). However, very little is known about the connection between PTX3 and CAD. This dose–response meta-analysis was carried out to quantify the relationship between circulating PTX3 concentration and CAD prognosis. Methods A systematic literature search was conducted using PubMed, EuropePMC, ProQuest, EBSCOhost, SCOPUS, Cochrane Library, and Google Scholar up until April 2021. The primary outcome of this study consisted of mortality and major adverse cardiovascular events (MACEs). Results The current meta-analysis comprised 15 studies with a total of 11.365 participants. High circulating PTX3 concentrations were associated with a higher risk of composite poor outcomes as compared to low circulating PTX3 concentrations (OR: 1.36 [1.18, 1.54], p < 0.001; I 2 = 86.69%, P heterogeneity<0.001), mortality (OR: 1.43 [1.15, 1.71], p < 0.001; I 2 = 87.58%, P heterogeneity<0.001), and MACEs (OR: 1.28 [1.08, 1.48], p < 0.001; I 2 = 35.86%, P heterogeneity = 0.08) in patients with CAD. Consistent results were obtained during meta-regression analyses and in all examined subgroups. The adjusted odds ratios (aORs) for composite poor outcomes increased by 32% per 1 ng/mL increment (OR: 1.32 [1.21, 1.43]) in line with the dose–response meta-analysis. Conclusion A significant positive dose-dependent association between circulating PTX3 concentration and the risk of poor outcomes in patients with CAD was found in this dose–response meta-analysis.

The Protective Role of the Long Pentraxin PTX3 in Spontaneously Hypertensive Rats with Heart Failure.

Pentraxin 3 (PTX3) is synthesized locally and released into the circulation, reflecting local inflammation in the cardiovascular system. Therefore, we conducted a study to explore the effect of PTX3 in spontaneously hypertensive heart failure (SHHF) rats. Sprague Dawley (SD) and SHHF rats were treated with recombinant PTX3 protein, and the blood pressure (BP) and echocardiographic parameters were collected. Radioimmunoassay, enzyme immunoassay and enzyme-linked immunosorbent assay (ELISA) were applied to detect plasma levels of atrial/B-type natriuretic peptide (ANP/BNP) and PTX3. The pathological changes in the myocardial tissues were observed by hematoxylin and eosin (HE) and Masson stainings. The mRNA and protein expressions were detected by quantitative real-time reverse-transcription polymerase chain reaction (qPCR) and western blotting. Cardiomyocyte apoptosis was evaluated by TUNEL staining and DNA fragmentation test. Increased plasma concentrations of PTX3 were found in SHHF rats compared with SD rats, which was further enhanced by recombinant PTX3 protein. After injection with recombinant PTX3 protein, the heart function was improved in SHHF rats with the decreased systolic and diastolic BP, and the reduced plasma levels of ANP and BNP. Moreover, PTX3 improved the myocardial damage and interstitial fibrosis in SHHF rats with reduced cardiomyocyte apoptosis and decreased mRNA expressions of pro-inflammatory factors in myocardial tissues. PTX3 could decrease the BP and plasma levels of ANP and BNP in SHHF rats, as well as improve the inflammation, cardiomyocyte apoptosis, and pathological changes of myocardial tissues, suggesting it may be a useful intervention in the treatment of SHHF.

Impact of acute high-intensity interval exercise on plasma pentraxin 3 and endothelial function in obese individuals-a pilot study.

Pentraxin 3 (PTX3) has been shown to be a predictor of endothelial dysfunction in patients with increased risk of cardiovascular disease (CVD) (e.g., obesity). Circulating PTX3 concentrations are dysregulated in obese individuals and are elevated following acute aerobic exercise. High-intensity interval exercise (HIIE) has been demonstrated to be as effective as continuous moderate-intensity exercise in improving endothelial function, as indicated by brachial artery flow-mediated dilation (BAFMD), in patients with CVD. Therefore, the purpose of this study was to examine the effect of acute HIIE on plasma PTX3 and BAFMD responses in obese individuals. Eight obese and six normal-weight young males participated in acute HIIE (4 intervals of 4min at 80-90% of VO2max; 3min of active recovery at 50-60% VO2max). Plasma PTX3 and BAFMD were measured prior to, immediately following exercise, and one and 2hours into recovery. Plasma PTX3 concentrations significantly increased following HIIE, yet the PTX3 response to HIIE was significantly blunted in obese compared to normal-weight participants. While the kinetic responses of BAFMD were also significantly different in obese compared to normal-weight participants, similar increases above the baseline were observed 2hours into recovery in both groups. Finally, plasma PTX3 concentrations were not associated with BAFMD at baseline or in response to HIIE. The utilization of HIIE may serve as a time-efficient exercise prescription strategy to transiently improve endothelial function, independent of elevated plasma PTX3 concentrations, in obese individuals.

PTX3 as a biomarker of lowered arterial stiffness due to weight loss in overweight and obese Japanese men

Background: Obesity, an independent cardiovascular disease risk factor, is the leading cause of death in the world. It has been previously shown that arterial stiffness,which is an index of cardiovascular disease, is significantly higher in Japanese overweight and obese men. Increased levels of pentraxin3 (PTX3), a novel anti-inflammatory substance mainly produced in the atherosclerotic region, due to weight reduction has been proposed to reflect an improvement in arterial stiffness. However, this has not been investigated. Methods: Here, we elucidate whether an individual who has significantly increased plasma PTX3 concentration result in a significantly decreased arterial stiffness compared to a smaller change in PTX3 level after a 12-week dietary modified weight reduction program in twenty overweight or obese Japanese men. A well-balanced dietary modification weight-loss program was implemented for overweight and obese men over a course of 12-week. Results: Prior to and after the program, we measured anthropometric variables, blood pressure, arterial stiffness, and circulating biochemistry, including plasma PTX3 concentrations. We then compared the differences in arterial stiffness between two groups, low or high ΔPTX3 groups, based on the median of delta of plasma PTX3 levels before and after weight reduction via modified diet habit in men with overweight and obesity. Carotid-femoral pulse wave velocity (PWV) as index of central arterial stiifness and brachial-ankle PWV as index of whole body arterial stiffness were significantly decreased in the high ΔPTX3 group after dietary modification. Conclusions: Our present results suggest that PTX3 could be a clinically useful biochemical index for monitoring appropriate arterial function maintenance in obese weight control.

Macrophage expression and prognostic significance of the long pentraxin PTX3 in COVID-19.

Long pentraxin 3 (PTX3) is an essential component of humoral innate immunity, involved in resistance to selected pathogens and in the regulation of inflammation1-3. The present study was designed to assess the presence and significance of PTX3 in Coronavirus Disease 2019 (COVID-19)4-7. RNA-sequencing analysis of peripheral blood mononuclear cells, single-cell bioinformatics analysis and immunohistochemistry of lung autopsy samples revealed that myelomonocytic cells and endothelial cells express high levels of PTX3 in patients with COVID-19. Increased plasma concentrations of PTX3 were detected in 96 patients with COVID-19. PTX3 emerged as a strong independent predictor of 28-d mortality in multivariable analysis, better than conventional markers of inflammation, in hospitalized patients with COVID-19. The prognostic significance of PTX3 abundance for mortality was confirmed in a second independent cohort (54 patients). Thus, circulating and lung myelomonocytic cells and endothelial cells are a major source of PTX3, and PTX3 plasma concentration can serve as an independent strong prognostic indicator of short-term mortality in COVID-19.

Association of microRNA-224 and microRNA-155 expressions with coronary microvascular obstruction following primary angioplasty for acute ST-segment elevation myocardial infarction

Abstract Background Proinflammatory stimuli induce a variety set of microRNAs (miRs) expressions in human mononuclear cells that regulate long pentraxin-3 (PTX3) gene, which associates with a procoagulant state in the endothelial cells. Purpose We evaluated, for the first time, the association of miR-224 and miR-155 expressions with coronary microvascular obstruction (MVO) and plasma PTX3 concentration in patients with acute ST-segment elevation myocardial infarction (STEMI) treated by primary angioplasty. Methods The expression levels of miR-224 and miR-155 on admission were evaluated in 217 consecutive patients with STEMI (symptom onset &amp;lt;12h) undergoing primary angioplasty between January 2018 and August 2018, and results were analyzed by the median values. The miRs expression and plasma PTX3 concentration were measured by TaqMan real-time PCR and human ELISA kit, respectively. The primary outcome of the study was the occurrence of angiographic MVO, defined as a post-primary angioplasty TIMI grade &amp;lt;3 flow or TIMI grade 3 flow with myocardial blush grade 0 or 1. Results After adjustment with sex, age and plasma PTX3 concentration, miR-244 ≥ median group was associated with angiographic MVO (odds ratio, 2.81; 95% confidence interval 1.34 to 5.92, p=0.006). Spearman analysis showed no correlations between miR-224 and miR-155 expressions with plasma PTX3 concentration. Conclusion This study suggests that miR-224 expression, (but not miR-155), associates with angiographic MVO following primary angioplasty for STEMI. However, miR-224 and miR-155 expressions did not correlate with plasma PTX3 concentration. Future studies are needed to find the molecular inflammatory pathway related with miR-224 expression in MVO. Funding Acknowledgement Type of funding source: None

Pentraxin-3 is a candidate biomarker on the spectrum of severity from pre-eclampsia to HELLP syndrome: GenPE study.

Pentraxin-3 has been reported as a promising biomarker of pre-eclampsia and its severity; however, available studies have small sample sizes, and analyses are not always adjusted for confounders. The aim of this study is to establish the strength of the association between maternal Pentraxin-3 level and pre-eclampsia or HELLP syndrome. It was a case-control study. Women with pre-eclampsia or HELLP syndrome were defined as cases, and women with healthy pregnancies at term (>37 weeks) were classified as controls. Plasma concentrations of Pentraxin-3 were determined at the time of delivery by quantitative enzyme immunoassay. Associations between Pentraxin-3 and pre-eclampsia and HELLP syndrome were assessed by multinomial logistic regression. Subsidiary analysis for the time of disease onset was also carried out. Odds ratios and 95% confidence intervals are reported. A total of 1024 pregnant women were included (461 controls, 368 pre-eclampsia, 195 HELLP). A positive log-linear relationship was found between the top pentraxin-3 quintile and HELLP syndrome. After adjustment for confounders (maternal age, ethnicity, socioeconomic position, date and place of recruitment, family history of pre-eclampsia, smoking, body mass index at beginning of pregnancy, gestational age and multiple pregnancy), the strength of the association was higher for HELLP syndrome [OR 1.13 (95% CI 1.08; 1.18)] than for pre-eclampsia [OR 1.03 (95% CI 1.03; 1.10)]. No difference according to time of onset or pentraxin-3 level was found. In summary, pentraxin-3 level was associated with pre-eclampsia, but it was more strongly associated with HELLP syndrome. Longitudinal studies with a lower probability of residual confounding are necessary to improve our knowledge about the role of pentraxin-3 in pre-eclampsia.

P16 Relationship of plasma long Pentraxin-3 concentration with clinical and angiographic outcomes of patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary

Abstract Background Inflammation has an important role for the progression of coronary plaque vulnerability to acute coronary thrombosis. Long pentraxin-3 (PTX3) is a sensitive marker of inflammation released upon exposure to primary inflammatory signals. Whether concentration of PTX3 affects coronary thrombus severity and impaired coronary flow in patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) is unknown. Purpose This study sought to evaluate the relationship of plasma PTX3 concentration with coronary thrombus severity and final TIMI flow after primary PCI in patients with acute STEMI. Methods We prospectively enrolled 335 consecutive patients with acute STEMI undergoing primary PCI between 1 January 2018 and 2 August 2018. Plasma PTX3 concentrations were measured at admission by ELISA method. Results Compared to low PTX3 group (&amp;lt;0.33 ng/mL; N = 223), patients in the high PTX3 group (≥ 0.33 ng/mL; N = 112) had higher proportion of thrombus grade 4 and 5 on initial coronary angiogram (83% vs. 72%, p= 0.03), final TIMI flow &amp;lt;3 (66% vs. 51%, p= 0.01), incomplete ST segment resolution after primary PCI (85% vs. 72%, p= 0.002) and Killip classification II-IV at entry (34.8% vs. 13%, adjusted odds ratio= 3.38, p&amp;lt; 0.001). High PTX3 concentration was associated with an increased risk of 30-day mortality (adjusted hazard ratio= 3.41, 95% confidence interval, 1.27 to 9.11, p= 0.01). Conclusion High plasma PTX3 concentration is associated with worse clinical and angiographic outcomes among patients undergoing primary PCI for STEMI. Further study is needed to eludicate whether PTX3 is a causal agent for adverse outcomes and whether therapies directed at reducing PTX3 levels are effective. Table 1. Variable Hazard ratio (95% confidence interval) P-value Long pentraxin-3 ≥0.33 ng/mL 3.41 (1.27 - 9.11) 0.01 Age &amp;gt;65 years 0.38 (0.11 - 1.41) 0.15 Male gender 0.43 (0.13 - 1.44) 0.16 Diabetes Mellitus 1.24 (0.44 - 3.52) 0.68 Hypertension 0.64 (0.23 - 1.80) 0.39 Baseline creatinine ≥1.3 mg/dL 4.06 (1.43 - 11.53) 0.009 TIMI risk score &amp;gt; 4 8.31 (2.69 - 25.59) &amp;lt; 0.001 Multivariable Cox regression analysis showing association between PTX3 concentration and selected confounding variables for all-cause death at 30 day.

Correlates of pentraxin 3 serum concentration in men and women with type 2 diabetes

Elevated levels of plasma pentraxin 3 (PTX3), a marker of inflammation, are associated with the risk of developing cardiovascular diseases in the general population, as well as in patients with type 2 diabetes (DM2). In this study, we aimed to determine factors associated with PTX3 serum concentrations in men and women with DM2. The study included 116 consecutive patients (67 men and 49 women) with DM2 from an outpatient diabetic clinic. Men were characterised by lower age and higher uric acid, creatinine and bilirubin concentrations and waist/hip ratio than women. In women, low-density lipoprotein cholesterol (LDL-C) levels were higher than in men. In men, median (interquartile range) values of PTX3 concentration were 4.02 (1.99), and in women they were 4.53 (3.31) ng/ml (NS). In men, PTX3 concentrations correlated with total cholesterol (TC), triglycerides, apolipoprotein (Apo) C3, Apo B48, Glc and creatinine levels. In women, PTX3 correlated significantly with TC and LDL-C and Apo B100. Partial regression analysis revealed that after adjusting for age, PTX3 concentrations in men were significantly associated with TC, LDL-C, triglycerides, creatinine, Apo C3 and Apo B48, while in women they were associated with TC, LDL-C and Apo B100. The results could be of importance in sex-specific prevention of vascular complications in DM2 patients.

Association of plasma pentraxin 3 concentration with angiographic and clinical outcomes in patients with acute ST-segment elevation myocardial infarction treated by primary angioplasty.

To evaluate the association of plasma long pentraxin 3 (PTX3) concentration with angiographic and clinical outcomes in patients with acute ST-segment elevation myocardial infarction (STEMI) treated by primary angioplasty. Whether concentration of PTX3, a sensitive marker of inflammation, associates with angiographic and clinical outcomes in STEMI patients treated by primary angioplasty is unknown. We prospectively enrolled 335 consecutive patients with acute STEMI undergoing primary angioplasty. Blood samples for plasma PTX3 measurement were drawn in all patients at the emergency department before primary angioplasty, and were measured by ELISA method. The median PTX3 concentrations were higher in patients with thrombus burden grade 4 and 5 versus grade <4 on initial coronary angiogram (0.29 ng/ml vs. 0.24 ng/ml, p = .02), thrombolysis in myocardial infarction (TIMI) grade <3 vs. TIMI grade-3 flow after primary angioplasty (0.31 ng/ml vs. 0.24 ng/ml, p < .001), incomplete versus complete ST-segment resolution within 12 hr after angioplasty (0.29 ng/ml vs. 0.22 ng/ml, p = .001) and in patients who did not survive versus those who survived at 30 days (0.44 ng/ml vs. 0.26 ng/ml, p = .001). A linear correlation was observed between PTX3 concentration and baseline leukocyte count (Spearman correlation = 0.21, p < .001). After adjustment for laboratory and selected clinical variables, patients in the highest quartile of PTX3 concentration (≥0.4 ng/ml) were associated with increased risk of 30-day mortality (hazard ratio = 11.83; 95% confidence interval = 1.52-92.27, p = .01). This study suggests that higher plasma PTX3 concentration associates with worse angiographic and clinical outcomes in STEMI patients treated by primary angioplasty.

Postmortem plasma pentraxin 3 is a useful marker of fatal acute coronary syndrome

Pentraxin 3 (PTX3) is an acute-phase protein that belongs to the pentraxin superfamily. Recently, many clinical studies have demonstrated that plasma PTX3 concentrations rapidly increase in patients with the acute coronary syndrome (ACS). The aim of this study was to evaluate the forensic utility of postmortem plasma PTX3 as a marker of fatal ACS. We compared the plasma PTX3 concentration in cadavers with suspected fatal ACS to that exhibited in control cases (e.g., asphyxia and immediate death due to a fatal injury). The ACS groups included a coronary stenosis group, which exhibited apparent coronary stenosis, but an absence of coronary thrombi, a coronary thrombi group with thrombi found in the coronary artery, and a group of myocardial rupture following an acute myocardial infarction. The plasma PTX3 concentration was significantly higher in the coronary thrombi group than the control group and other ACS groups. The postmortem plasma PTX3 concentration was higher than the clinical reference values, which appeared to be caused by a postmortem release from circulating neutrophils. In conclusion, although the clinical reference value cannot be applied to postmortem samples, the postmortem plasma PTX3 concentration may be a useful marker of death occurring immediately after the onset of fatal ACS.

A1319 The responses of the inflammatory marker, pentraxin 3, to dietary sodium and potassium interventions

Objectives: Pentraxin-3 is a sensitive marker of inflammation that plays dual roles, pathogenic and cardioprotective, in the progression of cardiovascular diseases. Inflammation is intimately involved in salt-induced hypertension. We investigated the responses of pentraxin-3 to sodium and potassium supplementation to elucidate the potential role of pentraxin-3 in salt-induced hypertension. Methods: 48 participants were enrolled from northwest China. All subjects were maintained on a 3-day normal diet, which was sequentially followed by a 7-day low sodium diet, a 7-day high sodium diet and a 7-day high sodium plus potassium diet. Plasma concentrations of pentraxin-3 were assessed using ELISA. Results: Plasma pentraxin-3 decreased significantly during the low salt period compared to baseline (0.57 ± 0.19 ng/ml vs. 0.72 ± 0.33 ng/ml, p = 0.012) and increased during the high salt period (0.68 ± 0.26 ng/ml vs. 0.57 ± 0.19 ng/ml, p = 0.037). Potassium supplementation inhibited the salt-induced increase in pentraxin-3 (0.56 ± 0.21 ng/ml vs. 0.68 ± 0.26 ng/ml, p = 0.015). Ln-transformed pentraxin-3 at baseline was inversely correlated with BMI (r = −0.349, p = 0.02), DBP (r = −0.414, p = 0.005), MAP (r = −0.360, p = 0.017). We found a positive correlation between the ln-transformed concentrations of pentraxin-3 and 24-h urinary sodium during low and high Na+ periods (r = 0.269, p = 0.012) and a negative relationship with 24 h urinary potassium excretion during the high salt and high salt plus potassium period (r = − 0.246, p = 0.02). These correlations remained significant after adjusting for confounders. Pentraxin-3 responses were more prominent in salt sensitive subjects than salt- resistant subjects. Conclusion: Dietary salt and potassium interventions significantly altered circulating pentraxin-3.

Aerobic fitness alters the capacity of mononuclear cells to produce pentraxin 3 following maximal exercise.

Pentraxin 3 (PTX3) is a vital regulator of innate immune function. Although plasma PTX3 concentrations are elevated with aerobic fitness, the cellular functions of PTX3 remain unknown in aerobically trained and untrained subjects. Thirty individuals (aerobically trained = 15 and untrained = 15) participated in a maximal exercise protocol to examine ex vivo PTX3 production from isolated peripheral blood mononuclear cells (PBMCs) exposed to LPS or palmitate. The capacity of PTX3 to stimulate inflammatory cytokine production ex vivo was also examined. Elevated plasma PTX3 concentrations prior to exercise were positively associated with the percent change (pre to post exercise) in plasma PTX3 concentrations in all subjects, independent of cardiorespiratory fitness (VO2max). In addition, elevated plasma PTX3 concentrations in aerobically trained subjects at rest predicted changes in the LPS- and palmitate-stimulated PTX3 production from isolated PBMCs following acute exercise. In response to PTX3 simulation, the capacity of PBMCs to produce the anti-inflammatory cytokine IL-10 was decreased following acute exercise in all subject (no changes in IL-6, TGF-β1, and TNF-α observed). However, the percent change in IL-6 production was positively associated with VO2max in all subjects, and in aerobicallytrained subjects only, positively associated with elevated plasma PTX3 concentrations at rest and in response to acute exercise. These results suggest that aerobic training enhances the utilization of plasma PTX3 concentrations to predict the capacity of mononuclear cells to produce PTX3, and potentially, its reciprocal role of PTX3 as an initiator of the innate immune response following maximal exercise.

Plasma pentraxin 3 and glucose kinetics following acute high-intensity interval exercise versus continuous moderate-intensity exercise in healthy men.

Pentraxin 3 (PTX3) is mainly synthesized and released by neutrophils to help regulate innate immunity. While plasma PTX3 concentrations are associated with improved glucose metabolism and overall metabolic health, there is evidence that significant elevations in plasma glucose downregulate circulating levels of PTX3. To examine whether this relationship would be altered in response to exercise, this study investigated the kinetics of the plasma glucose and PTX3 responses following high-intensity interval exercise (HIIE) and continuous moderate-intensity exercise (CMIE). It was hypothesized that the increased concentrations of plasma glucose following HIIE compared with CMIE would be associated with an attenuated plasma PTX3 response. Eight healthy male subjects participated in both HIIE and CMIE protocols administered as a randomized, counterbalanced design. Linear mixed models for repeated measures revealed that the overall plasma glucose response was greater following HIIE compared with CMIE (protocol × time effect: p = 0.037). Although the plasma PTX3 response was higher only at 19 min into HIIE compared with CMIE (protocol × time effect: p = 0.013), no relationships were observed between plasma glucose and PTX3 either at baseline or in response to both exercise protocols, as indicated by the area under the curve "with respect to increase" analysis. Our results indicate that exercise-mediated plasma PTX3 concentrations are independent of the plasma glucose response. In addition, the present study suggests that the neutrophil-mediated innate immune response, as indicated by plasma PTX3 response, may be activated earlier during HIIE compared with CMIE.

The responses of the inflammatory marker, pentraxin 3, to dietary sodium and potassium interventions.

Pentraxin-3 is a sensitive marker of inflammation that plays dual roles, pathogenic and cardioprotective, in the progression of cardiovascular diseases. Inflammation is intimately involved in salt-induced hypertension. We investigated the responses of pentraxin-3 to sodium and potassium supplementation to elucidate the potential role of pentraxin-3 in salt-induced hypertension. A total of 48 participants from northwest China were enrolled. All participants were maintained on a 3-day normal diet, which was sequentially followed by a 7-day low-sodium diet, a 7-day high-sodium diet, and a 7-day high-sodium plus potassium diet. Plasma concentrations of pentraxin-3 were assessed using ELISA. Plasma pentraxin-3 decreased significantly during the low-salt period compared to baseline (0.57±0.19ng/mL vs 0.72±0.33ng/mL, P=.012) and increased during the high-salt period (0.68±0.26ng/mL vs 0.57±0.19ng/mL, P=.037). Potassium supplementation inhibited salt-induced increase in pentraxin-3 (0.56±0.21ng/mL vs 0.68±0.26ng/mL, P=.015). Ln-transformed pentraxin-3 at baseline was inversely correlated with BMI (r=-.349, P=.02), DBP (r=-.414, P=.005), MAP (r=-.360, P=.017). We found a positive correlation between the ln-transformed concentrations of pentraxin-3 and 24-hour urinary sodium during low and high Na+ periods (r=.269, P=.012) and a negative relationship with 24hours urinary potassium excretion during high-salt and high-salt plus potassium periods (r=-.246, P=.02). These correlations remained significant after adjusting for confounders. Pentraxin-3 responses were more prominent in salt-sensitive individuals than salt-resistant individuals. Dietary salt and potassium interventions significantly altered circulating pentraxin-3.

Role of interleukin-6 and pentraxin 3 as an early marker in Peyronie’s disease

Inflammation is mechanistically involved in the development of Peyronie’s disease (PD). The aim of this study is to assess the relevance of serum pentraxin 3 (PTX3) and interleukin-6 (IL-6) concentrations in PD. The study enrolled 40 patients with PD in the acute phase and 40 healthy controls. Plasma PTX3 and IL-6 concentrations were evaluated in 40 patients in the acute phase of PD and 40 healthy controls by enzyme-linked immunosorbent assay. Serum concentrations of both PTX3 and IL-6 were significantly higher in the PD patients than in the control group (p=0.001 and p=0.001, respectively). There was a significant correlation between concentration of PTX3 and painful erections. IL-6 concentrations were significantly higher in patients with erectile dysfunction. IL-6 and PTX3 levels showed no correlation with age, serum C-reactive protein, degree of curvature, and disease duration. IL-6 trans-signaling and PTX3 amplification at the site of inflammation could have a role in pathophysiological mechanisms of PD. Biological drugs may be used for treatment during the acute phase of the disease based on this mechanism.

Association of Plasma Pentraxin-3 Levels on Admission with In-hospital Mortality in Patients with Acute Type A Aortic Dissection

Background:Acute aortic dissection is a life-threatening cardiovascular emergency. Pentraxin-3 (PTX3) is proposed as a prognostic marker and found to be related to worse clinical outcomes in various cardiovascular diseases. This study sought to investigate the association of circulating PTX3 levels with in-hospital mortality in patients with acute Type A aortic dissection (TAAD).Methods:A total of 98 patients with TAAD between January 2012 and December 2015 were enrolled in this study. Plasma concentrations of PTX3 were measured upon admission using a high-sensitivity enzyme-linked immunosorbent assay system. Patients were divided into two groups as patients died during hospitalization (Group 1) and those who survived (Group 2). The clinical, laboratory variables, and imaging findings were analyzed between the two groups, and predictors for in-hospital mortality were evaluated using multivariate analysis.Results:During the hospital stay, 32 (33%) patients died and 66 (67%) survived. The patients who died during hospitalization had significantly higher PTX3 levels on admission compared to those who survived. Pearson's correlation analysis demonstrated that PTX3 correlated positively with high-sensitivity C-reactive protein (hsCRP), maximum white blood cell count, and aortic diameter. Multivariate logistic regression analysis demonstrated that PTX3 levels, coronary involvement, cardiac tamponade, and a conservative treatment strategy are significant independent predictors of in-hospital mortality in patients with TAAD. The receiver operating characteristic curve analysis further illustrated that PTX3 levels on admission were strong predictors of mortality with an area under the curve of 0.89. A PTX3 level ≥5.46 ng/ml showed a sensitivity of 88% and a specificity of 79%, and an hsCRP concentration ≥9.5 mg/L had a sensitivity of 80% and a specificity of 69% for predicting in-hospital mortality.Conclusion:High PTX3 levels on admission are independently associated with the in-hospital mortality in patients with TAAD.

Serum pentraxin 3 is elevated in patients with neurological Wilson's disease

BackgroundWilson's disease (WD) is an autosomal recessive inherited disorder of copper (Cu) metabolism, resulting in pathological accumulation of Cu in many organs and tissues, predominantly in the liver and brain. Cu deposition may lead to neuroinflammation in the brain of WD patients. Pentraxin 3 (PTX3) may play an important role in innate immunity and in WD. We compared plasma PTX3 concentrations in WD patients and healthy controls, and to determine whether PTX3 concentration was associated with neurological disease severity. MethodsThis study included 86 WD patients and 28 controls. Plasma PTX3 and C-reactive protein (CRP) concentration levels were measured using specific enzyme-linked immunosorbent assays. Disease severity was determined using the neurological Global Assessment Scale (GAS) for WD. ResultsPlasma PTX3 levels were significantly higher in patients with neurological WD than in controls. PTX3 levels in WD patients were associated with neurological disease severity. However, there was no correlation between CRP and neurological GAS scores. ConclusionsPTX3 represents a potential biochemical marker of disease severity in patients with neurological WD.

Pentraxin 3 (PTX3) promoter methylation associated with PTX3 plasma levels and neutrophil to lymphocyte ratio in coronary artery disease.

BackgroundPentraxin 3 (PTX3) is expressed in the heart under inflammatory conditions and plays an important role in atherogenesis. Patients with increased PTX3 levels may suffer from higher rates of cardiac events. Regulation of specific genes by promoter methylation is important in atherogenesis. The factors influencing PTX3 levels and the association between epigenetics and PTX3 levels have not been investigated.MethodsBlood samples were collected from 64 patients admitted to the Department of Cardiology, 35 who had coronary artery disease (CAD), and 29 who were CAD-free. Plasma levels of PTX3 were measured by ELISA. PTX3 promoter methylation was evaluated via methyl-specific PCR. The severity of coronary artery lesion was evaluated by angiography.ResultsThe level of PTX3 promoter methylation in the CAD group was 62.69% ± 20.57%, significantly lower than that of the CAD-free group, which was 72.45% ± 11.84% (P = 0.03). Lower PTX3 promoter methylation levels in the CAD group were associated with higher plasma PTX3 concentrations (r = −0.29, P = 0.02). Furthermore, lower PTX3 promoter methylation levels were associated with higher neutrophil to lymphocyte ratio (NLR) in men (r = −0.58, P = 0.002).ConclusionsThe present study provides new evidence that methylation of the PTX3 promoter is associated with PTX3 plasma levels and NLR in coronary artery disease. This study also shows that modification of epigenetics by chronic inflammation might be a significant molecular mechanism in the atherosclerotic processes that influence plasma PTX3 concentrations.

Association of pentraxin 3 with insulin resistance and glucose response following maximal aerobic exercise in obese and normal-mass individuals.

Pentraxin 3 (PTX3), a cardioprotective protein, has recently been shown to be associated with improved insulin resistance (IR) and glucose metabolism. Therefore, the primary purpose of this study was to examine whether or not increased plasma PTX3 following maximal aerobic exercise would differ between obese and normal-mass subjects, and its association with the homeostatic model assessment of insulin resistance (HOMA-IR) and glucose response. Twenty-five untrained obese (n = 13 [6 males and 7 females]) and normal-mass (n = 12 [5 males and 7 females]) subjects performed an acute bout of maximal aerobic exercise to assess maximal oxygen consumption (VO2max). At baseline, plasma PTX3 concentrations are decreased in obese compared with normal-mass subjects and are negatively associated with plasma insulin and HOMA-IR values. In response to maximal exercise, plasma PTX3 responses were similar in obese and normal-mass subjects while the intensity of plasma PTX3 response as indicated by area under the curve analysis (AUCi) was not associated with HOMA-IR or glucose AUCi. However, PTX3 AUCi was positively associated with cardiorespiratory fitness levels (relative VO2max). These findings suggest that PTX3 could serve as a biomarker for both metabolic health, as well as a measurement to monitor the effectiveness of exercise interventions in obesity.