Serum C-reactive protein: a predictor of mortality in continuous ambulatory peritoneal dialysis patients.
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OBJECTIVE: To evaluate the predictive value of a single baseline serum C-reactive protein (sCRP) as a marker of mortality in continuous ambulatory peritoneal dialysis (CAPD) patients. DESIGN: A review of prospectively collected data in a 2-year follow-up study. SETTING: Tertiary medical center. PATIENTS: The study included 106 patients who were stable and had been on CAPD for a minimum of 3 months. MAIN OUTCOME MEASURES: Patient survival rate was the main outcome measure of this study. Other outcome measures were technique survival rate, peritonitis rate, and hospitalized days. Covariables used in the survival analysis were age, sex, the presence of cardiovascular disease or diabetes mellitus, sCRP, serum albumin, hematocrit, cholesterol, HDL-cholesterol, malnutrition by subjective global assessment (SGA), weekly Kt/V urea, and weekly standardized creatinine clearance (SCCr). RESULTS: The 2-year patient survival rate was significantly lower in the increased sCRP group than in the normal sCRP group (66.7% vs 94.1%, p = 0.001), although there was no significant difference in technique failure, peritonitis rate, and hospitalized days between the two groups. By Cox proportional hazards analysis, independent predictors of mortality were: cardiovascular disease (relative risk, RR = 8.96, p < 0.005); increased sCRP level (RR = 1.19, p < 0.05); and high hematocrit (RR = 1.18, p < 0.05). CONCLUSION: Serum CRP at enrollment is an independent predictor of 2-year patient survival in CAPD patients. (+info)
Markers of chronic infection and inflammation. Are they important in cases with chronic coronary heart disease.
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The human cytomegalovirus plays a causal role in atherosclerosis etiology, but it is discussed as controversial. We conducted a case control study to investigate whether previous infection with cytomegalovirus is associated with coronary heart disease and markers of systemic inflammation, because systemic inflammation may play a role in atherosclerosis too. We also studied the correlation between anti-cytomegalovirus antibody titer and coronary artery disease. The study involved 150 cases (45 females, mean age +/- SD is 58.73 +/- 7.68 years) with a documented coronary heart disease and 160 healthy volunteers (50 females, mean age +/- SD is 57.82 +/- 7.68, p > 0.05). Cytomegalovirus serology was performed to determine the presence of specific IgG antibodies and titers of the anti-cytomegalovirus IgG antibodies. In addition, C-Reactive protein levels were determined for each case. The prevalence of specific antibodies to cytomegalovirus was 57.30% for the patients and 56% for the controls (p = 0.39). But higher levels of anti-cytomegalovirus IgG antibody titer (> 1/800) were seen in the patient group (28.6% versus 10%, p = 0.0000). Mean value of C-reactive protein was higher in the patient group (2.99 +/- 0.92 mg/l versus 1.79 +/- 0.51 mg/l, p = 0.0000), and there was a linar correlation with the high antibody titers and the level of C-reactive protein (r = 0.35, p = 0.0000) These findings support that not the seropositivity of the population but rather the titer of anti-cytomegalovirus antibody and the levels of C-reactive protein could predict patients with a high risk of coronary heart disease. (+info)
Diagnostic markers of infection: comparison of procalcitonin with C reactive protein and leucocyte count.
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BACKGROUND: Procalcitonin has been advocated as a marker of bacterial infection. OBJECTIVE: To evaluate diagnostic markers of infection in critically ill children, comparing procalcitonin with C reactive protein and leucocyte count in a paediatric intensive care unit (PICU). METHODS: Procalcitonin, C reactive protein, and leucocyte count were measured in 175 children, median age 16 months, on admission to the PICU. Patients were classified as: non-infected controls (43); viral infection (14); localised bacterial infection without shock (25); bacterial meningitis/encephalitis (10); or septic shock (77). Six children with "presumed septic shock" (without sufficient evidence of infection) were analysed separately. Optimum sensitivity, specificity, predictive values, and area under the receiver operating characteristic (ROC) curve were evaluated. RESULTS: Admission procalcitonin was significantly higher in children with septic shock (median 94.6; range 3.3-759.8 ng/ml), compared with localised bacterial infection (2.9; 0-24.3 ng/ml), viral infection (0.8; 0-4.4 ng/ml), and non-infected controls (0; 0-4.9 ng/ml). Children with bacterial meningitis had a median procalcitonin of 25.5 (7.2-118.4 ng/ml). Area under the ROC curve was 0.96 for procalcitonin, 0.83 for C reactive protein, and 0.51 for leucocyte count. Cut off concentrations for optimum prediction of septic shock were: procalcitonin > 20 ng/ml and C reactive protein > 50 mg/litre. A procalcitonin concentration > 2 ng/ml identified all patients with bacterial meningitis or septic shock. CONCLUSION: In critically ill children the admission procalcitonin concentration is a better diagnostic marker of infection than C reactive protein or leucocyte count. A procalcitonin concentration of 2 ng/ml might be useful in differentiating severe bacterial disease in infants and children. (+info)
Complement and atherogenesis: binding of CRP to degraded, nonoxidized LDL enhances complement activation.
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Complement activation occurs in temporal correlation with the subendothelial deposition of LDL during early atherogenesis, and complement also plays a pathogenetic role in promoting lesion progression. Two lesion components have been identified that may be responsible for complement activation. First, enzymatic degradation of LDL generates a derivative that can spontaneously activate complement, and enzymatically degraded LDL (E-LDL) has been detected in the lesions. Second, C-reactive protein (CRP) colocalizes with complement C5b-9, as evidenced by immunohistological studies of early atherosclerotic lesions, so the possibility exists that this acute phase protein also fulfills a complement-activating function. Here, we report that addition of LDL and CRP to human serum did not result in significant C3 turnover. Addition of E-LDL provoked complement activation, which was markedly enhanced by CRP. Binding of CRP to E-LDL was demonstrated by sucrose flotation experiments. Binding was Ca(2+)-dependent and inhibitable by phosphorylcholine, and the complement-activating property of E-LDL was destroyed by treatment with phospholipase C. These results indicated that CRP binds to phosphorylcholine groups that become exposed in enzymatically degraded LDL particles. Immunohistological studies complemented these findings in showing that CRP colocalizes with E-LDL in early human atherosclerotic lesions. Thus enzymatic, nonoxidative modification of tissue-deposited LDL can be expected to confer CRP-binding capacity onto the molecule. The ensuing enhancement of complement activation may be relevant to the development and progression of the atherosclerotic lesion. (+info)
Inflammatory markers in men with angiographically documented coronary heart disease.
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BACKGROUND: Recent evidence suggests that atherosclerosis is a chronic inflammatory process. In this study, we examined several markers of inflammation in men with coronary heart disease (CHD) and appropriate controls. METHODS: The concentrations of C-reactive protein (CRP), serum amyloid A (SAA), interleukin-6 (IL-6), and soluble intracellular adhesion molecule (sICAM-1) were examined in 100 men with angiographically documented CHD and 100 age-, gender-, and smoking-matched controls with no history of CHD. We assessed the association of these markers with severity of disease as indicated by >50% obstruction in one vessel (n = 30), two vessels (n = 39), or three vessels (n = 31). RESULTS: Significant increases were noted in serum CRP (median for cases vs controls, 3.4 vs 1.5 mg/L; P <0.0001), SAA (5.9 vs 3.7 mg/L; P <0.005), and IL-6 (2.3 vs 1.7 ng/L; P <0. 013) in patients with CHD compared with controls. These differences remained significant after correction for age, smoking, hypertension, diabetes, and lipid and homocysteine concentrations. Plasma sICAM-1 was not significantly different between the two groups (335 vs 339 microg/L). No significant correlation was seen between these markers and the severity of coronary disease. CONCLUSIONS: Concentrations of CRP, SAA, and IL-6 were increased in patients with CHD but failed to correlate with severity of coronary disease. These markers might reflect the diffuse atherosclerotic process in the vascular system rather than the degree of localized obstruction from coronary lesions. (+info)
Markers of systemic inflammation predicting organ failure in community-acquired septic shock.
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To obtain predictors of organ failure (OF), we studied markers of systemic inflammation [circulating levels of interleukin-6 (IL-6), IL-8, soluble IL-2 receptor (sIL-2R), soluble E-selectin and C-reactive protein, and neutrophil and monocyte CD11b expression] and routine blood cell counts in 20 patients with systemic inflammatory response syndrome and positive blood culture. Eight patients with shock due to community-acquired infection developed OF, whereas 11 normotensive patients and one patient with shock did not (NOF group). The first blood sample was collected within 48 h after taking the blood culture (T1). OF patients, as compared with NOF patients, had at T1 a lower monocyte count, a lower platelet count, higher levels of CD11b expression on both neutrophils and monocytes, and higher concentrations of IL-6, IL-8 and sIL-2R. C-reactive protein and soluble E-selectin concentrations did not differ between groups. No parameter alone identified all patients that subsequently developed OF. However, a sepsis-related inflammation severity score (SISS), developed on the basis of the presence or absence of shock and on the levels of markers at T1, identified each patient that developed OF. The maximum SISS value was 7. The range of SISS values in OF patients was 2-5, and that in NOF patients was 0-1. In conclusion, high levels of CD11b expression, depressed platelet and monocyte counts, and high concentrations of IL-6, IL-8 and sIL-2R predict OF in patients with community-acquired septic shock, and the combination of these markers may provide the means to identify sepsis patients who will develop OF. (+info)
Color Doppler ultrasonographic evaluation of osteomyelitis in children.
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We investigated the capability of color Doppler sonography in evaluating acute osteomyelitis in children. Twelve children suspected of having osteomyelitis were evaluated with color Doppler ultrasonography at admission and at regular intervals to observe the inflammatory process of osteomyelitis, determine the response of antibiotic therapy, and predict the need of surgery in these patients. At admission, color Doppler flow within or around the infected periosteum was found in patients with symptoms for 4 days or longer, whereas those with symptoms for less than 4 days showed no color Doppler flow within and around the periosteum. During sonographic follow-up, six cases were found to have increased color Doppler vascular flow within and around the affected periosteum, and two of them had periosteal abscess. They eventually required surgical treatment. Persistent or increased color Doppler flow during follow-up examination correlated with elevated serum levels of C-reactive protein as well. Our study indicated that color Doppler vascular flow within or around the infected periosteum correlated with advanced acute osteomyelitis, and surgery usually was required in these patients. Those with early stage acute osteomyelitis usually showed no vascular flow within or around the infected periosteum. Thus, color Doppler sonography allowed detection of advanced osteomyelitis and revealed the progression of inflammation during antibiotic therapy. Color Doppler ultrasonography might be valuable in determining the efficacy of antibiotic therapy and justifying the need for operation. (+info)
Activation of monocytes, T-lymphocytes and plasma inflammatory markers in angina patients.
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Inflammation and activation of immune cells have important roles in the pathogenesis of atherosclerosis. We analyzed the plasma levels of inflammatory markers and the degree of activation of peripheral blood monocytes and T-lymphocytes isolated from 12 unstable angina, 12 stable angina, and 12 normal subjects. In 20%-33% of patients, monocytes expressed high basal levels of IL-8, tissue factor, IL-1beta, and monocyte chemoattractant protein-1 mRNA. Furthermore, basal mRNA levels of these cytokines showed strong correlation with each other (p < 0.01 in all combination) but not with tumor necrosis factor-alpha or transforming growth factor-beta1. Plasma level of C-reactive protein was highest in the unstable angina patients (1.63+/-0.70 mg/l) and lowest in the control subjects (0.22+/-0.08 mg/l) (P = 0.03). We also observed a high correlation between C-reactive protein level and the occurrence of minor and major coronary events during 6 months of follow-up. Activation status of T-cells, assessed by the percentage of HLA-DR positive cells, was highest in the unstable angina patients (26.8+/-1.4%) compared with that in the control (14.7+/-1.2%) (P = 0.0053). Our data represent the first case showing that the circulating monocytes in angina patients are activated to a state express numerous proatherogenic cytokines. These results may help to diagnose angina patients according to the inflammatory markers and evaluate the prognosis of the disease. (+info)