Home About us Contact
|
Home About us Contact | ||
|
|
||
Serum CRP Level (serum + crp_level)
Selected AbstractsC-Reactive Protein and Aortic Stiffness in Patients with Idiopathic Dilated CardiomyopathyECHOCARDIOGRAPHY, Issue 1 2007Feridun Kosar M.D. Background: Previous studies have shown an association between C-reactive protein (CRP)and arterial stiffness in most cardiovascular diseases. Increased CRP levels and arterial stiffness have been considered independent predictors of cardiovascular mortality in cardiovascular disease and even in the general population. Objective: The aim of this study was to investigate the relationship between CRP, a marker of systemic inflammation and aortic stiffness in patients with idiopathic dilated cardiomyopathy (DCMP). Methods: Serum CRP levels and aortic stiffness parameters were measured in DCMP patients (n= 37) and age- and gender-matched control subjects (n= 30). High-sensitivity CRP levels were determined by an immunonephelometry assay. Aortic strain (AS) and aortic distensibility (AD) were calculated from the aortic diameters measured using M-mode echocardiography and blood pressure obtained by sphygmomanometry. Results: Serum levels of CRP in DCMP patients were higher than in the control subjects (5.47 ± 2.06 mg/L and 2.35 ± 0.47 mg/L, P < 0.001, respectively). AS and AD were significantly decreased in DCMP patients compared to the controls (P < 0.001 and P < 0.001, respectively). There were positive correlations between CRP, and (r = 0.3.64, P = 0.027) smoking (r = 0.3.56, P = 0.024), and increasing age (r = 0.587, P < 0.001), and negative correlations between CRP, and DBP (r =,0.485, P < 0.001), diameter change (DC; r =,0.493, P < 0.001), AS (r =,0.526, P < 0.001), and AD (r =,0.626, P < 0.001). Conclusion: We have shown that there is a significant relation between high serum CRP levels and impaired aortic stiffness in patients with idiopathic DCMP. These findings may indicate an important role of CRP in the pathogenesis of impaired aortic stiffness in idiopathic DCMP. [source] Quality of life in chronic kidney disease: effects of treatment modality, depression, malnutrition and inflammationINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 4 2007B. Kalender Summary In the present study, our aim is to investigate the effects of the treatment modality, depression, malnutrition and inflammation on quality of life (QoL) in chronic kidney disease (CKD). Twenty-six patients with CKD on conservative management, 68 patients on haemodialysis (HD), 47 patients on continuous ambulatory peritoneal dialysis (CAPD) and 66 healthy controls were enrolled in the study. QoL was measured by means of the Short Form-36 (SF-36) and subscale scores were calculated. All patients were evaluated for the presence of depression using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Axis I Disorders , Clinician Version. The severity of depression was evaluated by means of the Beck Depression Inventory (BDI). Serum C-reactive protein (CRP), ferritin, albumin, haemoglobin and haematocrit (Hct) levels were measured. All the SF-36 subscale scores were lower in the patient groups compared with control group. The SF-36 scores were higher and BDI scores were lower in the CAPD group than CKD and HD groups. In patients with depression, all SF-36 subscale scores were lower than that of the patients without depression. There was a significant negative correlation between all the SF-36 subscale scores and the BDI scores. There was a significant positive correlation between the SF-36 physical and total summary scores and the Hct value and serum albumin levels, but an inverse correlation between the SF-36 physical, mental and total summary scores and the serum CRP level in the HD patients. The authors suggest that the treatment modality, depression, malnutrition and inflammation have an important role on QoL in CKD. [source] Antibody responses to Porphyromonas gingivalis outer membrane protein in the first trimesterAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 2 2009Jun SASAHARA Background:,Porphyromonas gingivalis (Pg) is one of the most harmful periodontal pathogens and it has been reported that Pg is associated with preterm birth (PTB), intrauterine growth retardation (IUGR) and pregnancy-induced hypertension (PIH), discovered by animal experiments and clinical research. The relationship between adverse pregnancy outcomes and maternal antibody response to Pg is controversial. On the other hand, the serum C-reactive protein (CRP) has been recognised as a reliable serum marker of periodontal disease. Aims:, To determine the significance of antibody responses to Pg affecting pregnancy outcomes in the first trimester. Methods:, A case,control study was carried out on women with PTB (n = 58), IUGR (n = 91), PIH (n = 32) and without any complications (control, n = 98). The serum level of the CRP and IgG1 against 40-kDa outer membrane protein of Pg (anti-40-kDa OMP Pg -IgG1) in the first trimester was measured. Results:, The IUGR group, and PTB patients whose placentas were diagnosed as chorioamnionitis or whose vaginal flora included Lactobacilli, showed a lower level of anti-40-kDa OMP Pg -IgG1 than the control group. There was no difference in the serum CRP level between each case group and control group. Conclusions:, These results suggest that a lack of humoral immunity against Pg in early pregnancy is associated with IUGR and some PTB. [source] Interferon-, mediates suppression of C-reactive protein: Explanation for muted C-reactive protein response in lupus flares?ARTHRITIS & RHEUMATISM, Issue 12 2009Helena Enocsson Objective C-reactive protein (CRP) is synthesized by hepatocytes in response to interleukin-6 (IL-6) during inflammation. Despite raised IL-6 levels and extensive systemic inflammation, serum CRP levels remain low during most viral infections and disease flares of systemic lupus erythematosus (SLE). Because both viral infections and SLE are characterized by high levels of interferon-, (IFN,), the aim of this study was to determine whether this cytokine can inhibit the induction of CRP. Methods The interference of all 12 IFN, subtypes with CRP promoter activity induced by IL-6 and IL-1, was studied in a CRP promoter, and luciferase reporter,transfected human hepatoma cell line, Hep-G2. CRP secretion by primary human hepatocytes was analyzed by enzyme-linked immunosorbent assay. Results CRP promoter activity was inhibited by all single IFN, subtypes, as well as by 2 different mixtures of biologically relevant IFN, subtypes. The most prominent effect was seen using a leukocyte-produced mixture of IFN, (56% inhibition at 1,000 IU/ml). The inhibitory effect of IFN, was confirmed in primary human hepatocytes. CRP promoter inhibition was dose dependent and mediated via the type I IFN receptor. Transferrin production and Hep-G2 proliferation/viability were not affected by IFN,. Conclusion The current study demonstrates that IFN, is an inhibitor of CRP promoter activity and CRP secretion. This finding concords with previous observations of up-regulated IFN, and a muted CRP response during SLE disease flares. Given the fundamental role of both IFN, and CRP in the immune response, our results are of importance for understanding the pathogenesis of SLE and may also contribute to understanding the differences in the CRP response between viral and bacterial infections. [source] Association between early systemic inflammatory response, severity of multiorgan dysfunction and death in acute pancreatitis,BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 6 2006R. Mofidi Background: Mortality in patients with acute pancreatitis is associated with the number of failing organs and the severity and reversibility of organ dysfunction. The aim of this study was to assess the significance of early systemic inflammatory response syndrome (SIRS) in the development of multiorgan dysfunction syndrome (MODS) and death from acute pancreatitis. Methods: Data for all patients with a diagnosis of acute pancreatitis between January 2000 and December 2004 were reviewed. Serum C-reactive protein (CRP), Acute Physiology And Chronic Health Evaluation (APACHE) II scores and presence of SIRS were recorded on admission and at 48 h. Marshall organ dysfunction scores were calculated during the first week of presentation. Presence of SIRS and raised serum CRP levels on admission and at 48 h were correlated with the cumulative organ dysfunction scores in the first week. Results: A total of 759 patients with acute pancreatitis were identified, of whom 45 (5·9 per cent) died during the index admission. SIRS was identified in 162 patients on admission and was persistent in 138 at 48 h. The median (range) cumulative Marshall score in patients with persistent SIRS was significantly higher than that in patients in whom SIRS resolved and in those with no SIRS (4 (0,12), 3 (0,7) and 0 (0,9) respectively; P < 0·001). Thirty-five patients (25·4 per cent) with persistent SIRS died from acute pancreatitis, compared with six patients (8 per cent) with transient SIRS and four (0·7 per cent) without SIRS (P < 0·001). No correlation was observed between CRP level on admission and Marshall score (P = 0·810); however, there was a close correlation between CRP level at 48 h and Marshall score (P < 0·001). Conclusion: Persistent SIRS is associated with MODS and death in patients with acute pancreatitis and is an early indicator of the likely severity of acute pancreatitis. Copyright © 2006 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] | ||||||||||