scholarly journals Resistin and Cardiac Arrest—A Prospective Study

2019 ◽  
Vol 9 (1) ◽  
pp. 57
Author(s):  
Raluca M. Tat ◽  
Adela Golea ◽  
Rodica Rahaian ◽  
Ştefan C. Vesa ◽  
Daniela Ionescu
Keyword(s):  
Cardiac Arrest ◽  
Ischemia Reperfusion ◽  
Univariate Analysis ◽  
Laboratory Data ◽  
Early Death ◽  
Serum Levels ◽  
High Serum ◽  
Cardiovascular Comorbidities ◽  
Biological Variables ◽  
The Impact

The systemic response to ischemia-reperfusion that occurs after a cardiac arrest (CA) followed by the return of spontaneous circulation leads to endothelial toxicity and cytokine production, both responsible for the subsequent occurrence of severe cardiocirculatory dysfunction and early death. Resistin is emerging as a biomarker of proinflammatory status and myocardial ischemic injury and as a mediator of endothelial dysfunction. The study aimed to analyze the possible associations between several clinical and biological variables and the serum levels of resistin in CA survivors. Forty patients with out-of-hospital resuscitated CA, were enrolled in the study. Demographic, clinical and laboratory data (including serum resistin measurements at admission and at 6, 12, 24, 48 and 72 h) were recorded. For resistin, we calculated the area under the curve (AUC) using the trapezoidal method with measurements from 0 to 12 h, 0 to 24 h, 0 to 48 h and 0 to 72 h. Fifteen (37.5%) patients died in the first 72 h after CA. Cardiovascular comorbidities were present in 65% of patients. The majority of patients had post-CA shock (29 (72.5%)). Resistin serum levels rose in the first 12–24 h and decreased in the next 48–72 h. In univariate analysis, advanced age, longer duration of resuscitation, high sequential organ failure assessment score, high lactate levels, presence of cardiovascular comorbidities and the post-CA shock were associated with higher resistin levels. In multivariate analysis, post-CA shock or cardiovascular comorbidities were independently associated with higher AUCs for resistin for 0–12 h and 0–24 h. The only identified variable to independently predict higher AUCs for resistin for 0–48 h and 0–72 h was the presence of post-CA shock. Our data demonstrate strong independent correlation between high serum resistin levels, cardiac comorbidities and post-CA shock. The impact of the post-CA shock on serum concentration of resistin was greater than that of cardiac comorbidities.

scholarly journals POS0329 GASTROINTESTINAL INVOLVEMENT IN SYSTEMIC SCLEROSIS: PATHOGENETIC ROLE OF GUT MICROBIOME, CYTOKINES AND ADIPOKINES

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 392.1-392
Author(s):  
E. Pigatto ◽  
M. Schiesaro ◽  
M. Caputo ◽  
M. Beggio ◽  
P. Galozzi ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Gut Microbiome ◽  
Serum Levels ◽  
High Serum ◽  
Healthy Population ◽  
Gastrointestinal Involvement ◽  
Degrading Bacteria ◽  
Gi Symptoms ◽  
Low Levels ◽  
The Impact

Background:Gastrointestinal (GI) involvement is very common in patients with Systemic Sclerosis (SSc). The pathophysiology of GI manifestations has not yet been defined. Cell-mediated immunological reactions appear to lead to endothelial damage resulting in fibrosis. The risk of developing malnutrition reinforces the need to better understand GI pathophysiology in these patients.Objectives:The study aimed to evaluate GI symptoms (GIT 2.0) and malnutrition status (MUST) and to determine specific bacterial changes in gut microbiome by investigating the possible presence of positive hot spots in bacterial species in SSc patients and their potential role in the disease progression. We also evaluated serum levels of adipokines and cytokines involved in the pathogenesis of SSc and their role, in addition to gut microbiome, in predicting the onset of GI involvement and malnutrition in SSc patients.Methods:We enrolled 25 scleroderma patients (EULAR/ACR 2013 criteria). UCLA-SCTC GIT 2.0 questionnaire to evaluate GI symptoms and MUST to investigate the risk of malnutrition were used. Gut microbiome was analyzed and the samples were subjected to extraction for the 16S rRNA gene (Earth Microbiome Project and the NIH-Human Microbiome Project). The microbiome was investigated at phenotypic and genotypic level. Serum levels of cytokines and adipokines (adiponectin and leptin) were evaluated by ELISA.Results:79.9% of patients had GERD and 63.5% abdominal distension at GIT 2.0 questionnaires. 48% of patients had moderate risk of malnutrition (MUST=2) and 12% had high risk (MUST=3). Gut microbioma: 19 patients (76%) had low similarity and 11 (44%) low diversity compared to the healthy population. The prevailing enterotypes of gut microbiome was Bacteroides (80%) and Prevotella (20%). The genotypic evaluation showed a reduced concentration of: gluten-digesting (Lactobacillus); lactose-digesting (Faecalibacterium); vitamin K-producing (Enterococcus, Desulfovibrio and Veillonella); acetaldehyde-degrading bacteria. 24 patients (96%) showed a reduction in bacteria devoted to maintaining weight control (Bifidobacterium and Ruminococcus). The patients had an altered intestinal permeability with less mucolytic bacteria (Bacteroides) and reduced production of LPS (Enterobacter and Escherichia). Low levels of butyrate (Eubacterium and Clostridium), acetate and propionate were found for SCFA-producing bacteria. Potentially pathogenic bacteria were also investigated: Salmonella was found in 14 (56%), Klebsiella in 9 (36%) and Enterococcus Faecalis in 3 (12%) patients. 11 (44%) patients had elevated serum levels of IL10 and IL12; 4 (16%) had high value of leptin. Correlation was found in patients who had a reduced concentration of gluten-digesting bacteria and MUST. Elevated MUST was correlated with serological increase in IL17A and IFN-α. Serum levels of IL12 and IL10 were found to correlate with specific bacteria alterations: high concentration of acetaldehyde-producing bacteria and low levels of acetaldehyde-degrade bacteria (also correlated with high serum levels of IL6), mucolytic bacteria and producers of hydrogen sulphide, acetate and propionate. Finally, reduced levels of mucolytic bacteria and acetate producing bacteria correlated with high serum leptin levels.Conclusion:The relationship between the gut microbiome and SSc seems to be multifactorial. In our study genotypic changes of gut microbioma might play a role in damaging the permeability of the mucosa and increasing risk of malnutrition. The evaluation of gut microbiome and cytokine profile is probably going to be of value in the follow-up of SSc. However, further studies are needed to clarify the impact of GI dysbiosis on the immune system in SSc.References:[1]Patrone V. et al. Gut microbiota profile in systemic sclerosis patients with and without clinical evidence of gastrointestinal involvement, Sci Rep. 2017; 7: 14874Disclosure of Interests:None declared

Abstract 328: Hemodynamic Comparison of Zucker Diabetic Fatty Rats to Their Lean Littermates After Asphyxial Cardiac Arrest

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Claudius Balzer ◽  
Franz Baudenbacher ◽  
Michele M Salzman ◽  
William J Cleveland ◽  
Susan Eagle ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Arrest ◽  
Ejection Fraction ◽  
Ischemia Reperfusion ◽  
Diabetic Rats ◽  
Arterial Blood ◽  
Zucker Diabetic Fatty Rats ◽  
Zdf Rats ◽  
The Impact

Patients with metabolic syndrome are at higher risk for cardiac arrest (CA), and also have worse neurologic outcome after CA related to their comorbidities (e.g., Type 2 Diabetes Mellitus [T2DM]). Using Zucker Diabetic Fatty (ZDF) rats as a new and relevant model with common comorbidities for CA and cardiopulmonary resuscitation (CPR), we hypothesized that T2DM is associated with a lower chance for return of spontaneous circulation (ROSC) and/or a worse outcome regarding heart function after asphyxial CA compared to their lean littermates. Two groups of rats (8 ZDF, 7 lean) were monitored for 37±2 weeks. The rats were anesthetized and intubated; heart rate was monitored by subcutaneous ECG needles. Femoral artery and vein were cannulated for continuous blood pressure measurement and delivery of fluids and medications, respectively. Before ventilation was stopped to initiate asphyxial CA, rocuronium was given. After 8 minutes of CA, ventilation was re-initiated with FiO 2 1.0, epinephrine and sodium-bicarbonate were administered, and pneumatic chest compression were started with 200 compressions per minute. Chest compressions were stopped when a systolic blood pressure of 120 mmHg was achieved. During 4 hours of observation, vital parameters were closely monitored, blood gases were measured, and ejection fraction (EF %) was assessed with ultrasound. Data are mean ± SD. Statistics: Unpaired student’s t-test (two-tailed), α.05. At baseline, ZDF rats showed significantly higher blood glucose levels (504±52 vs 174±14 mg/dl) compared to their lean littermates. All ZDF and lean rats achieved ROSC, and measurements taken directly after ROSC and after the first hour showed no relevant differences. After four hours, there was no difference in heart rate between ZDF and lean rats. However, diabetic rats had a significantly higher mean arterial blood pressure (142±24vs. 107±19 mmHg) and ejection fraction (42±16%vs 20±8%) compared to their lean littermates. The hypothesis that ROSC-rate in diabetic rats would be lower could not be proven. Conversely, the ZDF rats showed a significantly higher blood pressure related to an increased EF%. Further analysis in this study will focus on the impact of T2DM on cardiac and neurological ischemia-reperfusion injury.

scholarly journals A Versatile Macromer-Based Glycosaminoglycan (sHA3) Decorated Biomaterial for Pro-Osteogenic Scavenging of Wnt Antagonists

Pharmaceutics ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 1037
Author(s):  
Mathis Gronbach ◽  
Franziska Mitrach ◽  
Stephanie Möller ◽  
Sandra Rother ◽  
Sabrina Friebe ◽  
...  
Keyword(s):  
Serum Levels ◽  
Bone Defects ◽  
High Serum ◽  
Qualitative And Quantitative Analysis ◽  
Negative Effects ◽  
Bone Defect Healing ◽  
2D System ◽  
Surface Decoration ◽  
The Impact ◽  
Regeneration Of Bone

High serum levels of Wnt antagonists are known to be involved in delayed bone defect healing. Pharmaceutically active implant materials that can modulate the micromilieu of bone defects with regard to Wnt antagonists are therefore considered promising to support defect regeneration. In this study, we show the versatility of a macromer based biomaterial platform to systematically optimize covalent surface decoration with high-sulfated glycosaminoglycans (sHA3) for efficient scavenging of Wnt antagonist sclerostin. Film surfaces representing scaffold implants were cross-copolymerized from three-armed biodegradable macromers and glycidylmethacrylate and covalently decorated with various polyetheramine linkers. The impact of linker properties (size, branching) and density on sHA3 functionalization efficiency and scavenging capacities for sclerostin was tested. The copolymerized 2D system allowed for finding an optimal, cytocompatible formulation for sHA3 functionalization. On these optimized sHA3 decorated films, we showed efficient scavenging of Wnt antagonists DKK1 and sclerostin, whereas Wnt agonist Wnt3a remained in the medium of differentiating SaOS-2 and hMSC. Consequently, qualitative and quantitative analysis of hydroxyapatite staining as a measure for osteogenic differentiation revealed superior mineralization on sHA3 materials. In conclusion, we showed how our versatile material platform enables us to efficiently scavenge and inactivate Wnt antagonists from the osteogenic micromilieu. We consider this a promising approach to reduce the negative effects of Wnt antagonists in regeneration of bone defects via sHA3 decorated macromer based macroporous implants.

Serum levels of macrophage inhibitory cytokine-1 (MIC1) and matrix metallopeptidase-7 (MMP7) as diagnostic and prognostic markers in gastric cancer (GC) patients (pts).

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e14595-e14595
Author(s):  
Manuel Valladares-Ayerbes ◽  
Nuria Tarrío ◽  
Moisés Blanco-Calvo ◽  
Mar Haz-Conde ◽  
Isabel Santamarina Cainzos ◽  
...  
Keyword(s):  
Diagnostic Performance ◽  
Cox Regression ◽  
Univariate Analysis ◽  
Prognostic Significance ◽  
Serum Levels ◽  
High Serum ◽  
Youden Index ◽  
Matrix Remodeling ◽  
Diagnostic Potential ◽  
Increased Risk

e14595 Background: MIC1 and MMP7 are secreted cytokines involved respectively in the modulation of immunological processes and in extracellular matrix remodeling. Their expression were found deregulated in different tumors, including GC. However, few data are available about their serum levels, their diagnostic potential, and their prognostic significance in GC pts. Here, we analyze the diagnostic performance of these markers and we present data linking them with short survival in GC pts. Methods: Serum samples were assayed in duplicate for MIC1 and MMP7 levels by ELISA. The diagnostic performance of markers was assessed by ROC curve analysis and the cut-offs were set using the Youden index approach. The cut-offs for prognostic purposes were determined using X-tile software. Differences in progression free (PFS) and overall survival (OS) were analyzed using Kaplan-Meier curves and logrank test. Cox regression was used to determine the prognostic independence of biomarkers. Results: From November 2006 to July 2010, 52 GC pts and 28 healthy donors were consecutively recruited. The follow-up of pts was performed until their death or the end of study (September 2011). The AUCs for MIC1 and MMP7 were respectively 0.897 and 0.865 (p < 0.001). Using the optimal cut-off to diagnose GC pts, we obtained a 73.08% of sensitivity (Ss) and a 92.86% of specificity (Sp) for MIC1, and a 78.85% of Ss and an 85.71% of Sp for MMP7. In the survival analysis, high serum levels of MIC1 and MMP7 were significantly associated with shorter PFS (p < 0.001) and OS (p < 0.001 and p = 0.003, respectively). In univariate analysis, pts with high serum levels of MIC1 and MMP7 had an increased risk of progression (HR = 3.608, p<0.001 for MIC1; HR = 4.172, p<0.001 for MMP7) and death (HR = 3.843, p=0.001 for MIC1; HR = 2.602, p=0.006 for MMP7). However, MIC1 and MMP7 failed to reach prognostic independence in multivariate analysis. Conclusions: We obtained cut-off values of MIC1 and MMP7 in serum for diagnostic purposes in GC. In addition, we established a correlation between increased levels of MIC1 and MMP7 in serum and shorter PFS and OS in GC. These findings justify studies with a larger number of pts.

Effect of statin and metformin on survival in veterans (V) with B-cell lymphoproliferative disorders (BLD).

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 1602-1602
Author(s):  
Shanthi Srinivas ◽  
Melanie L. Gonzalez ◽  
Sunniya Khan ◽  
Arpita Gandhi ◽  
Barbara Crump ◽  
...  
Keyword(s):  
Rating Scale ◽  
Cox Regression ◽  
Univariate Analysis ◽  
Laboratory Data ◽  
Cox Regression Analysis ◽  
Comorbidity Index ◽  
Beta 2 Microglobulin ◽  
Ecog Ps ◽  
The Impact ◽  
Statin Use

1602 Background: The incidence of BLD has been increasing in V. As many V are on statin and metformin for comorbid conditions, we evaluated the impact of their use on survival. Methods: In an IRB-approved protocol, we reviewed the records of 332 V diagnosed with BLD from January 1997 to Dec 2011 for demographics, height(H),weight(W), BMI,statin and metformin use, clinical and laboratory data and ECOG PS. Comorbidity was assessed using the Charlson Comorbidity Index (CCI),Kaplan-Feinstein Index (KFI) and Cumulative Illness Rating Scale (CIRS). Cox regression analysis was performed using SAS v 9.2. Results: There were 332 V with a median (M) age of 70 years (27-94). The M for H 70 inches (58-78), W 183lbs (99-356.5) and BMI 26.7 kg/m2 (15.54 -48.45). The M for hemoglobin(Hgb) 12.8 g/dl (7.3-17.4), albumin 3.9(1.2-5.4), lactate dehydrogenase( LDH) 183 IU/L (85-1905), beta 2-microglobulin 2.6 mg/dl (0.8-39) . The M for CCI was 4.7 (0.8-12), KFI 2 (0-3), CIRS15 3 (0-6), CIRS16 6(0 -14), CIRS17 1.9(0-6), CIRS18 0(0-3), CIRS19 0(0-3). M survival was 1297days(4-7468).The number of V receiving statin was 167 (51%) and metformin 46 (14%). Statin use was a predictor of survival by both univariate and multivariate analysis but metformin was a predictor only by univariate analysis. Conclusions: Statin use was an independent and significant predictor of survival in this group of V with BLD and needs to be validated in a larger group of patients. [Table: see text]

scholarly journals Featured Article: Pyruvate preserves antiglycation defenses in porcine brain after cardiac arrest

2017 ◽  
Vol 242 (10) ◽  
pp. 1095-1103 ◽  
Author(s):  
Gary F Scott ◽  
Anh Q Nguyen ◽  
Brandon H Cherry ◽  
Roger A Hollrah ◽  
Isabella Salinas ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Glutathione Reductase ◽  
Ischemia Reperfusion ◽  
Protein Glycation ◽  
Carbonyl Stress ◽  
Swine Model ◽  
Glyoxalase 1 ◽  
Cardiocerebral Resuscitation ◽  
The Impact ◽  
The Brain

Cardiac arrest (CA) and cardiocerebral resuscitation (CCR)-induced ischemia–reperfusion imposes oxidative and carbonyl stress that injures the brain. The ischemic shift to anaerobic glycolysis, combined with oxyradical inactivation of glyceraldehyde 3-phosphate dehydrogenase (GAPDH), provokes excessive formation of the powerful glycating agent, methylglyoxal. The glyoxalase (GLO) system, comprising the enzymes glyoxalase 1 (GLO1) and GLO2, utilizes reduced glutathione (GSH) supplied by glutathione reductase (GR) to detoxify methylglyoxal resulting in reduced protein glycation. Pyruvate, a natural antioxidant that augments GSH redox status, could sustain the GLO system in the face of ischemia–reperfusion. This study assessed the impact of CA-CCR on the cerebral GLO system and pyruvate’s ability to preserve this neuroprotective system following CA. Domestic swine were subjected to 10 min CA, 4 min closed-chest CCR, defibrillation and 4 h recovery, or to a non-CA sham protocol. Sodium pyruvate or NaCl control was infused (0.1 mmol/kg/min, intravenous) throughout CCR and the first 60 min recovery. Protein glycation, GLO1 content, and activities of GLO1, GR, and GAPDH were analyzed in frontal cortex biopsied at 4 h recovery. CA-CCR produced marked protein glycation which was attenuated by pyruvate treatment. GLO1, GR, and GAPDH activities fell by 86, 55, and 30%, respectively, after CA-CCR with NaCl infusion. Pyruvate prevented inactivation of all three enzymes. CA-CCR sharply lowered GLO1 monomer content with commensurate formation of higher molecular weight immunoreactivity; pyruvate preserved GLO1 monomers. Thus, ischemia–reperfusion imposed by CA-CCR disabled the brain’s antiglycation defenses. Pyruvate preserved these enzyme systems that protect the brain from glycation stress. Impact statement Recent studies have demonstrated a pivotal role of protein glycation in brain injury. Methylglyoxal, a by-product of glycolysis and a powerful glycating agent in brain, is detoxified by the glutathione-catalyzed glyoxalase (GLO) system, but the impact of cardiac arrest (CA) and cardiocerebral resuscitation (CCR) on the brain’s antiglycation defenses is unknown. This study in a swine model of CA and CCR demonstrated for the first time that the intense cerebral ischemia–reperfusion imposed by CA-resuscitation disabled glyoxalase-1 and glutathione reductase (GR), the source of glutathione for methylglyoxal detoxification. Moreover, intravenous administration of pyruvate, a redox-active intermediary metabolite and antioxidant in brain, prevented inactivation of glyoxalase-1 and GR and blunted protein glycation in cerebral cortex. These findings in a large mammal are first evidence of GLO inactivation and the resultant cerebral protein glycation after CA-resuscitation, and identify novel actions of pyruvate to minimize protein glycation in postischemic brain.

scholarly journals In-hospital Death Following Successful OHCA Resuscitation: Causes of early and late mortality and the impact of withdrawal of care

2020 ◽  
Author(s):  
Shu Li ◽  
Christos Lazaridis ◽  
Fernando D. Goldenberg ◽  
Atman P. Shah ◽  
Katie Tataris ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Hospital Mortality ◽  
Human Study ◽  
Early Death ◽  
Organ Injury ◽  
Neurological Injury ◽  
Hospital Death ◽  
Categorization System ◽  
The Impact ◽  
Hospital Cardiac Arrest

AbstractObjectiveIn-hospital mortality in patients successfully resuscitated following out-of-hospital cardiac arrest (OHCA) is high. The factors and timings of these deaths is not well known. To better understand in hospital post-OHCA mortality we developed a novel categorization system of in hospital death and studied the factors and timings associated with these deaths.MethodsThis was a single-centered retrospective observational human study in adult non-traumatic OHCA patients in a university affiliated hospital. Through an expert consensus process, a novel classification system of hospital death was developed.ResultsTwo hundred and forty-one patients were enrolled in the study. Death was categorized as due to withdrawal of life sustaining treatment (WOLST) 159 (66.0%), recurrent in-hospital cardiac arrest 51 (21.1%), or due to neurological criteria 31 (12.9%). Subcategorization of factors associated with WOLST into 7 categories was done by defined criteria. Inter-reliability of this system was 0.858. 50% of WOLST decisions were due to neurological injury. Early death (≤ 3 days) was associated with recurrent in-hospital cardiac arrest and WOLST in the setting of refractory shock or multi-organ injury. Late in-hospital death (> 3 days) was primarily due to WOLST decisions in the setting of isolated neurological injury.ConclusionsOHCA in hospital mortality occurred in a bimodal pattern with early deaths due to recurrent arrest and multiorgan injury while late deaths were due to isolated neurological injury. The majority of deaths occurred in the setting of WOLST decisions. Further study of the influence of these factors on post OHCA survival are needed.

scholarly journals Clinical characteristics of hospitalized mild/moderate COVID-19 patients with a prolonged negative conversion time of SARS-CoV-2 nucleic acid detection

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ya Yang ◽  
Xiaogang Hu ◽  
Lirong Xiong ◽  
Peishu Fu ◽  
Wei Feng ◽  
...  
Keyword(s):  
Disease Progression ◽  
Clinical Symptoms ◽  
Univariate Analysis ◽  
Laboratory Data ◽  
Global Scale ◽  
Viral Rna ◽  
Nucleic Acid Detection ◽  
Conversion Time ◽  
The Impact ◽  
Negative Conversion

Abstract Background The impact of COVID-19 has been devastating on a global scale. The negative conversion time (NCT) of SARS-CoV-2 RNA is closely related to clinical manifestation and disease progression in COVID-19 patients. Our study aimed to predict factors associated with prolonged NCT of SARS-CoV-2 RNA in mild/moderate COVID-19 patients. Methods The clinical features, laboratory data and treatment outcomes of COVID-19 patients were retrospectively analyzed. Then univariate and multivariate analysis were used to screen out risk factors of influencing prolonged NCT of SARS-CoV-2 RNA. Results Thirty-two hospitalized mild/moderate COVID-19 patients were enrolled. The general clinical symptoms were cough (78.1%), fever (75%), diarrhea (68.8%), expectoration (56.3%), and nausea (37.5%). More than 40% of the patients had decreased erythrocyte, hemoglobin and leucocyte and 93.8% patients were detected in abnormalities of chest CT. The median NCT of SARS-CoV-2 RNA was 19.5 days (IQR: 14.25–25). Univariate analysis found fever, nausea, diarrhea and abnormalities in chest CTs were positively associated with prolonged NCT of viral RNA (P< 0.05). The multivariate Cox proportional hazard model revealed that fever [Exp (B), 0.284; 95% CI, 0.114–0.707; P<0.05] and nausea [Exp (B), 0.257; 95%CI, 0.096–0.689; P<0.05] were two significant independent factors. Conclusions Fever and nausea were two significant independent factors in prolonged NCT of viral RNA in mild/moderate COVID-19 patients, which provided a useful references for disease progression and treatment of COVID-19.

scholarly journals Syncope and Collapse Are Associated with an Increased Risk of Cardiovascular Disease and Mortality in Patients Undergoing Dialysis

2018 ◽  
Vol 15 (10) ◽  
pp. 2082
Author(s):  
Shih-Ting Huang ◽  
Tung-Min Yu ◽  
Tai-Yuan Ke ◽  
Ming-Ju Wu ◽  
Ya-Wen Chuang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiovascular Events ◽  
Incidence Rates ◽  
Major Adverse Cardiovascular Events ◽  
Study Cohort ◽  
Coronary Syndrome ◽  
Cardiovascular Comorbidities ◽  
Increased Risk ◽  
The Impact ◽  
Overall Mortality

Objective: This study explored the impact of syncope and collapse (SC) on cardiovascular events and mortality in patients undergoing dialysis. Methods: Patients undergoing dialysis with SC (n = 3876) were selected as the study cohort and those without SC who were propensity score-matched at a 1:1 ratio were included as controls. Major adverse cardiovascular events (MACEs), including acute coronary syndrome (ACS), arrhythmia or cardiac arrest, stroke, and overall mortality, were evaluated and compared in both cohorts. Results: The mean follow-up periods until the occurrence of ACS, arrhythmia or cardiac arrest, stroke, and overall mortality in the SC cohort were 3.51 ± 2.90, 3.43 ± 2.93, 3.74 ± 2.97, and 3.76 ± 2.98 years, respectively. Compared with the patients without SC, those with SC had higher incidence rates of ACS (30.1 vs. 24.7 events/1000 people/year), arrhythmia or cardiac arrest (6.75 vs. 3.51 events/1000 people/year), and stroke (51.6 vs. 35.7 events/1000 people/year), with higher overall mortality (127.7 vs. 77.9 deaths/1000 people/year). The SC cohort also had higher risks for ACS, arrhythmia or cardiac arrest, stroke, and overall mortality (adjusted hazard ratios: 1.28 (95% confidence interval (CI) = 1.11–1.46), 2.05 (95% CI = 1.50–2.82), 1.48 (95% CI = 1.33–1.66), and 1.79 (95% CI = 1.67–1.92), respectively) than did the non-SC cohort. Conclusion: SC was significantly associated with cardiovascular events and overall mortality in the patients on dialysis. SC may serve as a prodrome for cardiovascular comorbidities, thereby assisting clinicians in identifying high-risk patients.

Elevated Serum Levels of Soluble CD163 in Polymyositis and Dermatomyositis: Associated with Macrophage Infiltration in Muscle Tissue

2015 ◽  
Vol 42 (6) ◽  
pp. 979-987 ◽  
Author(s):  
Qing-Lin Peng ◽  
Yin-Li Zhang ◽  
Xiao-Ming Shu ◽  
Han-Bo Yang ◽  
Lu Zhang ◽  
...  
Keyword(s):  
Muscle Tissue ◽  
Laboratory Data ◽  
Elevated Serum ◽  
Clinical Manifestations ◽  
Serum Levels ◽  
High Serum ◽  
Macrophage Infiltration ◽  
Healthy Controls ◽  
Soluble Cd163 ◽  
Cell Counts

Objective.To investigate serum levels of soluble CD163 (sCD163) in patients with polymyositis (PM) and dermatomyositis (DM), and to correlate these to clinical manifestations and laboratory data.Methods.Serum levels of sCD163 were detected in 24 patients with PM, 84 patients with DM, and 46 healthy controls by using the ELISA method. Immunohistochemistry staining of macrophage infiltration in muscle tissue using anti-CD163 monoclonal antibody was conducted on muscle biopsy specimens from 13 patients with PM and 17 with DM.Results.Serum levels of sCD163 were significantly increased in patients compared with healthy controls (p < 0.001). Patients with interstitial lung disease (ILD) had statistically higher sCD163 levels than patients without ILD (p < 0.001). High serum sCD163 levels were associated with increased incidence of antinuclear antibody (p < 0.05), higher serum levels of immunoglobulin G (p < 0.01) and immunoglobulin A (p < 0.05), and increased erythrocyte sedimentation rates (p < 0.01). Serum sCD163 levels were inversely correlated with CD3+ T cell counts in peripheral blood of patients (r = −0.306, p < 0.01). Cross-sectional assessment and longitudinal study revealed a significant correlation between serum sCD163 levels and disease activity. Patients with high serum sCD163 levels showed a higher incidence of CD163+ macrophage infiltration in muscle tissue than patients with normal sCD163 levels (chi-square value = 10.804, p < 0.01).Conclusion.Serum levels of sCD163 were significantly elevated and correlated with disease severity in patients with PM/DM, suggesting serum sCD163 as a promising biomarker in the disease evaluation of PM/DM. Our finding of elevated serum sCD163 levels associated with muscle macrophage infiltration highlights the role activated macrophage plays in the pathogenesis of PM/DM.

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