Maximum C-reactive Protein Level Research Articles

Arginine Catabolic Mobile Element Is Associated With Low Antibiotic Resistance and Low Pathogenicity in Staphylococcus epidermidis From Neonates

The arginine catabolic mobile element (ACME) in Staphylococci encodes several putative virulence factors. ACME appears to have been transferred from Staphylococcus epidermidis into Staphylococcus aureus and is strongly associated with the epidemic and virulent S. aureus USA300. We sought to determine the distribution of ACME in 128 S. epidermidis blood culture isolates from neonates and to assess ACME's impact on antibiotic resistance, biofilm production, invasive capacity, and host inflammatory response. ACME was detected in 15/64 (23%) invasive blood culture isolates and 26/64 (40%) blood culture contaminants (p = 0.02). ACME-positive S. epidermidis isolates displayed less antibiotic resistance (p < 0.001) and were collected from more mature neonates (p = 0.001). Biofilm production was more prevalent among ACME-negative isolates (61/87) compared with ACME positive (18/41; p = 0.004). Among the 64 children considered having an invasive infection, ACME did not influence the maximum C-reactive protein level. In an in vitro whole-blood sepsis model, there were no differences in the inflammatory response between ACME-positive and ACME-negative isolates. We conclude that ACME in S. epidermidis from neonates was associated with less antibiotic resistance and also does not seem to be associated with increased pathogenicity.

Early Fish Oil Supplementation and Organ Failure in Patients With Septic Shock From Abdominal Infections

Fish oil (FO) has immunomodulating effects and may improve organ function and outcome in critically ill patients. This retrospective, propensity-matched cohort study investigates the effects of early intravenous FO supplementation on organ failure in patients with septic shock from abdominal infection. A medical database was retrospectively searched for critically ill patients admitted because of septic shock from abdominal infection (n = 194). Demographic, clinical, and laboratory data; FO supplementation (10 g/d) (n = 42); rate, degree, and number of organ failures assessed by the Sequential Organ Failure Assessment (SOFA) score; and secondary outcome variables were recorded. A propensity score-based model was used to establish 2 comparable groups (FO, n = 29; control, n = 29). Mann-Whitney rank sum test, Fisher exact test, and logistic regression analyses were used to compare variables between groups. There were no differences in the rate of single organ failures, the maximum SOFA score (median [interquartile range (IQR)], 12 [8-15] vs 11 [9-14]; P = .99), or the number of organ failures (median [IQR], 2 [1-3] vs 2 [1-3]; P = .54] between patients receiving FO supplementation and those not receiving supplementation. There were no group differences in the maximum C-reactive protein levels (P = .1), duration of mechanical ventilation (P = .65) or hemofiltration (P = .21), intensive care unit-acquired infections, intensive care unit length of stay (P = .59), and intensive care unit (P = 1) or hospital mortality (P = 1). Early intravenous FO may not decrease the number and degree of organ failures in patients with septic shock from abdominal infection. Future trials are needed before FO supplementation in septic shock from abdominal infection can be recommended.

Early use of beta-blockers attenuates systemic inflammatory response and lung oxygenation impairment after distal type acute aortic dissection

We have reported that serum C-reactive protein (CRP) elevation is an independent predictor of lung oxygenation impairment (LOI) after distal type acute aortic dissection (AAD). Systemic activation of the inflammatory system after aortic injury may play a role in the development of LOI. The aim of this study is to clarify the effect of beta-blockers on systemic inflammation and the development of LOI after distal type AAD. A total of 49 patients, who were admitted with distal type AAD and treated conservatively, were examined. White blood cell (WBC) count, serum CRP level, and arterial blood gases were measured serially. Forty patients received beta-blocker treatment within 24 h of the onset, while 9 patients received no beta-blocker treatment. Maximum WBC count, maximum CRP level, lowest PaO2/FiO2 (P/F) ratio, and patient background were compared between the two groups. There was no difference between the groups according to age, sex, coronary risk factors, blood pressure, serum level of CRP, WBC count, and oxygenation index on admission. Beta-blocker treatment was associated with lower maximum WBC count (P = 0.0028) and lower maximum serum CRP level (P = 0.0004). The minimum P/F ratio was higher in patients with beta-blocker treatment than in those without (P = 0.0076). Multivariate analysis revealed that administration of a beta-blocker was an independent negative determinant of LOI (P/F ratio ≤200 mmHg). In conclusion, early use of beta-blockers prevented excessive inflammation and LOI after distal type AAD, suggesting a pleiotropic effect of beta-blockers on the inflammatory response after AAD.

Abstract 3307: Early Use of Beta-blockers Attenuates Systemic Inflammatory Response and Lung Oxygenation Impairment after Distal Type Acute Aortic Dissection

BACKGROUND: Systemic activation of the inflammatory system after aortic injury may play a role in the development of lung oxygenation impairment (LOI) in patients with acute aortic dissection (AAD). We have reported that serum C-reactive protein (CRP) elevation is an independent predictor of this complication. We evaluated the effect of beta-blocker on systemic inflammation and the development of LOI after distal type AAD. METHODS: A total of 49 patients, who were admitted with distal type AAD and treated conservatively, were examined. Patients were divided into 2 groups according to the presence or absence of beta-blocker treatment, started within 24 hours of the onset. White blood cell (WBC) count, serum CRP level and arterial blood gases were measured serially. Clinical outcome, maximum WBC count, maximum CRP level, and lowest PaO 2 /FiO 2 (P/F) ratio were compared between the two groups. RESULTS: There was no difference between the groups in patients’ backgrounds, blood pressure, serum level of CRP, WBC count and P/F ratio on admission. Beta-blocker treatment was associated with lower maximum WBC count (14,856 ± 3201 vs. 11,687 ± 2610 /mm 3 , p =0.0028) and lower maximum serum CRP level (28.2 ± 20.5 vs. 14.2 ± 5.6 mg/dl, p =0.0004). The minimum P/F ratio was higher in patients with beta-blocker than in those without (140 ± 41 vs. 226 ± 90 mmHg, p =0.0076). Multivariate analysis revealed that administration of a beta-blocker was an independent negative determinant of LOI (P/F ratio ≤ 200 mmHg). CONCLUSIONS: Early use of beta-blockers prevented excessive inflammation and LOI after distal type AAD, suggesting a pleiotropic effect of beta-blockers on the inflammatory response after AAD.

Kinetics of C-Reactive Protein Release in Different Forms of Acute Coronary Syndrome

Better knowledge of C-reactive protein (CRP) kinetics could lead to improved clinical application of this biomarker. We studied 110 patients: 42 had ST-elevation acute myocardial infarction (STEMI), 35 had non-ST-elevation acute myocardial infarction (NSTEMI), and 33 had unstable angina. Patients were admitted to our institution within 6 hours of symptom onset. The levels of CRP, troponin-I, and creatine kinase MB fraction (CK-MB) were measured on admission and every 6 hours during the first 48 h. The CRP level was also measured daily until hospital discharge. The median (interquartile range) CRP level increased relative to baseline from 6 hours after admission, from 5 (2-9) mg/L to 6 (3-10) mg/L (P=.004). Although, CRP levels on admission were similar in all groups, there was a significant difference in peak CRP level: it was 67 (36-112) mg/L in the STEMI group, 29 (20-87) mg/L in the NSTEMI group, and 18 (12-36) mg/L in the unstable angina group. The maximum CRP level was observed 49 (38-53) hours after the onset of symptoms, but occurred later in patients with STEMI. Although there was only a weak non-significant correlation between CRP and troponin levels (r=0.135) at admission, the maximum CRP level was found to be influenced by the degree of myocardial damage (r=0.496; P< .001). The pattern of CRP release observed was clearly different in different forms of acute coronary syndrome. Although the CRP level measured at admission was similar in all patient groups, it was influenced by the degree of early myocardial tissue necrosis. This variation in CRP kinetics should be taken into consideration when designing future studies.

Leptin is a negative acute phase protein in chronic hemodialysis patients

Hypoalbuminemia strongly predicts death in hemodialysis patients and results from both inflammation and malnutrition. One potential link between malnutrition and inflammation is appetite suppression triggered by inflammation. Leptin is secreted by adipose tissue and suppresses appetite, and it is also a positive acute phase protein in the rat. Factored for body weight, leptin is known to be increased in hemodialysis patients, but its relationship to inflammation is unknown. We examined the relationship between spontaneously occurring activation of the acute phase response and leptin levels in 29 chronic hemodialysis patients. Serum samples were obtained three times weekly for six weeks and then monthly from 29 chronic hemodialysis patients, and the levels of the positive acute phase proteins [C-reactive protein (CRP), alpha1-acid glycoprotein (alpha1 AG), serum amyloid A, ceruloplasmin] and the negative acute phase proteins (albumin and transferrin) as well as leptin and interleukin-6 (IL-6) were measured. Positive and negative acute phase proteins were evaluated at the maximum CRP (mean, 9.42 +/- 1.14 mg/dL) and minimum values (mean, 0.41 +/- 0.09 mg/dL). When CRP was elevated, leptin levels were significantly reduced, as were the negative acute phase proteins albumin and transferrin. Serum amyloid A, ceruloplasmin, alpha1 acid glycoprotein, and IL-6 were all significantly increased at the maximum CRP level, compatible with general activation of the acute phase response. The change in leptin correlated negatively with the change in CRP (R = 0.437, P = 0.018), as did changes in albumin (R = 0.620, P < 0.001). Leptin is not increased as a consequence of inflammation in hemodialysis patients, but behaves as a negative rather than as a positive acute phase protein. Inflammation is unlikely to reduce appetite in dialysis patients through a leptin-mediated mechanism.

Acute-phase responses to cardiopulmonary bypass in children weighing less than 10 kilograms

Cardiopulmonary bypass induces a systemic inflammatory response. This study investigated, in a pediatric population, cytokine-induced responses and their potential modification by intraoperative steroid administration. Markers of the acute-phase response were measured perioperatively in 24 children weighing less than 10 kg undergoing cardiac operations. Those having operations with cardiopulmonary bypass were randomized to receive either no steroid (group I, n = 8) or 10 mg/kg methylprednisolone in the pump prime (group II, n = 10); patients undergoing nonbypass procedures were controls (group III, n = 6). In all groups, plasma interleukin-6 level was elevated (p < 0.01) above baseline throughout the post-operative period, peaking earlier in group I. Levels of C-reactive protein peaked at 48 hours, and postoperative core temperature was raised in all groups. Levels of interleukin-6 from 2 to 6 hours and C-reactive protein at 24 hours postoperatively were greater (p < 0.05) in group I than in group II. Maximum interleukin-6 level, C-reactive protein level, and temperature were all significantly greater in group I than in group III. Maximum interleukin-6 level correlated with maximum C-reactive protein level in group I only (rs = 0.76; p < 0.05) and showed no association with temperature. Duration of bypass did not correlate with levels of interleukin-6. This study demonstrated a marked acute-phase response to operation; the greater response to procedures with cardiopulmonary bypass was abrogated by intraoperative steroid administration. The importance of interleukin-6 as an inducer of acute phase proteins after bypass is supported by its association with C-reactive protein levels, but other factors must be important in the induction of pyrexia.

Serum C-reactive protein levels in the management of infection in acute leukaemia

C-reactive protein (CRP) was measured serially in 29 patients with acute leukaemia. Sixty-four febrile episodes (⩾38° C) occurred during 37 periods of neutropenia (<0.5 × 10 9/ l). In all of 41 microbiologically or clinically documented infections the maximum CRP level exceeded 30 mg/l, and in 25 it was greater than 100 mg/l. In no case in which the CRP level remained below 30 mg/l for 48 hr after the onset of fever was any clinical or microbiological evidence of infection obtained. The CRP level during documented infection began to fall 24–48 hr after appropriate treatment was begun. A CRP level above 30 mg/l in neutropenic patients was associated with early recurrence of fever if systemic antibiotics were discontinued. Graft-vs-host disease, without infection, did not result in high levels of CRP.