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F M Brunkhorst

Publications and source records attributed to F M Brunkhorst.

11 recordsLinked to original sources

Procalcitonin, C-reactive protein and APACHE II score for risk evaluation in patients with severe pneumonia.

OBJECTIVE: Procalcitonin (PCT) is a peptide that is found elevated in patients with sepsis and severe infections. In healthy persons PCT serum levels are below 0.1 ng/mL. The aim of this study was to investigate the value of serum PCT determination for risk evaluation in patients with pneumonia. METHODS: We focused on the correlation of PCT with the clinical status of the patient and prognosis of the disease. In a prospective study, in a nonsurgical intensive care unit the following parameters were assessed regularly in 93 patients with documented pneumonia: C-reactive protein (CRP), white blood cell count (WBC), body temperature, PCT and Acute Physiology and Chronic Health Evaluation (APACHE) II score. RESULTS: At the onset of infection 50% of the patients had elevated PCT levels above 2 ng/mL. The model of multivariate analysis of all tested parameters on days 0-5 stratified for clinical outcome (change in clinical classification or death) showed local significance for APACHE II score only. None of the other parameters in this model serves as an isolated indicator for change of clinical status or death. An intra-individual change of body temperature or CRP was never significantly associated with a change in the clinical status of the patient. CONCLUSION: Change in PCT on admission and at the end of the observation period significantly indicated a clinical change.

APACHE↗

[Diagnostic approach to sepsis - state of the art].

Early diagnosis of the different severities of septic inflammation is important for early implementation of specific therapies. Sepsis and severe sepsis are accompanied by clinical and laboratory signs of systemic inflammation. However, patients suffering from non-infectious inflammation may present with similiar signs and symptoms making it difficult to diagnose infection based on clinical findings alone. Bacteriological evidence of sepsis, though definitive and specific, may not be obtainable, is time-consuming and even may not occur concurrently with clinical signs of sepsis. It is therefore important to identify markers, which, by enabling an early diagnosis of sepsis and organ dysfunction, would allow early specific therapeutic interventions. Wheras C-reactive Protein is a more sensitive parameter for the diagnosis of non-systemic infections, Procalcitonin seems to be a useful parameter to improve the diagnosis and monitoring of therapy in patients with severe sepsis and septic shock.

Biomarkers↗

[Sepsis].

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Humans↗

Clinical experiences with a new semi-quantitative solid phase immunoassay for rapid measurement of procalcitonin.

A self-developing solid-phase immunoassay (B.R.A.H.M.S. PCT-Q, B.R.A.H.M.S.-Diagnostica GmbH, Hennigsdorf, Germany) has recently become available for the semi-quantitative and rapid measurement of procalcitonin (PCT). In this study we examined the validity of this assay at daily clinical routine conditions at five different hospitals in a prospective study. After development of the assay (200 microl plasma, 30 minutes incubation), PCT levels were categorized into four groups (< 0.5 microg/l; > or = 0.5-< 2 microg/l; > or = 2-< 10 microg/l; > or = 10 microg/l) according to the provided reference scale. Samples from patients with suspected elevation of PCT of different etiology (n=237) were read by various analyzers and compared with the results of the Lumitest PCT (B.R.A.H.M.S.-Diagnostica GmbH, Hennigsdorf, Germany). A total of 74.7% of measurements were categorized according to the results of the LumitestPCT, 24.5% were read within the next lower or higher category. Using a +/- 10% range at the reference concentrations (20% at 0.5 microg/l), 82.7% of samples were correctly categorized and 16.4% within the next categories. Using a cut-off value of 2.0 microg/l, 92.0% (94.1% for +/- 10%) of the results were correctly categorized. The semi-quantitative solid phase immunoassay allows a rapid, simple and semi-quantitative measurement of plasma PCT. The validity of the test results and its ease of use are sufficient to support acute diagnostic decisions. However, for the follow-up of PCT concentrations and routine daily measurements, the quantitative luminometric assay should be preferred, when available.

Calcitonin↗

Pyrexia, procalcitonin, immune activation and survival in cardiogenic shock: the potential importance of bacterial translocation.

AIMS: Exposure to bacterial endotoxin, perhaps due to bowel congestion or ischaemia and altered gut permeability, may result in immune activation that is characteristic for patients with severe heart failure. It is known that blood procalcitonin rises in response to bacterial endotoxin exposure. METHODS: We measured procalcitonin in a group of 29 patients with acute cardiogenic shock and no sign of infection (all without bacteraemia) and 26 with septic shock. Blood was analysed for procalcitonin, interleukin-6, tumour necrosis factor-alpha (TNF-alpha), c-reactive protein (CRP) and neopterin. Patients were managed conventionally in an intensive care unit with no further experimental procedures. RESULTS: Three cardiogenic (10%) and seven septic shock patients (27%) survived. Most patients with acute heart failure surviving 12 h or more (18 of 20) developed a pyrexia (738.0 degrees C) of unknown origin in the absence of positive cultures, with a rise in procalcitonin (1.4+/-0.8 to 48.0+/-16.2 ng/ml, P<0.001), CRP (76.5+/-16.4 to 154.7+/-22.9 mg/l, P<0.001) and neopterin (20.7+/-3.5 to 41.2+/-6.7 nmol/l, P<0.001). Patients with septic shock had higher initial levels of cytokines, and higher peak levels. Those with heart failure surviving (n=3) and those dying in the first 12 h (n=9) had no rise in cytokine levels. The patients with high procalcitonin had a higher temperature (38.9+/-0.3 vs. 37.3+/-0.23 degrees C, P<0.05), TNF-alpha (43.95+/-9.64 vs. 16.43+/-4.33 pg/ml; P<0.005) and CRP (146.1+/-18.4 vs. 68.2+/-39.6 mg/ml, P<0.005). Peak procalcitonin levels correlated with peak temperature (r=0.74, P<0.001). CONCLUSION: Cardiogenic shock causes a pyrexia of unknown origin in patients surviving for 12 h and that is associated with a rise in procalcitonin levels. This lends support to the hypothesis that patients with cardiogenic shock may be being exposed to bacterial endotoxin at a time when bowel wall congestion and or ischaemia is likely to be present.

Adult↗

Discrimination of infectious and noninfectious causes of early acute respiratory distress syndrome by procalcitonin.

OBJECTIVE: To test the sepsis marker procalcitonin (PCT) for its applicability to discriminate between septic and nonseptic causes of acute respiratory distress syndrome (ARDS). DESIGN: Prospective study, assessing the course of PCT serum levels in early (within 72 hrs after onset) ARDS. The three other inflammation markers neopterin, interleukin-6 (IL-6), and C-reactive protein (CRP) were tested in parallel. SETTING: Twenty-four-bed medical intensive care unit of a 1,990-bed primary hospital, providing health care for an estimated 39,000 patients. PATIENTS: Twenty-seven patients, 18 male and nine female, aged 16-85 yrs, with early ARDS of known cause (17 with septic and ten with nonseptic ARDS) were enrolled in a prospective study between May 1994 and May 1995. INTERVENTIONS: Serum samples were drawn every 4-6 hrs for measurement of PCT, neopterin, IL-6, and CRP concentrations. Blood cultures, tracheal aspirates, and urine samples were obtained every 12-24 hrs. In 24 of 27 patients, bronchoscopic cultures were also obtained. Clinical sepsis criteria as defined by the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference were checked daily. MEASUREMENTS AND MAIN RESULTS: Assessment of inflammation marker serum levels in septic vs. nonseptic ARDS. PCT serum levels were significantly higher (p < .0005) in the patients with septic ARDS than in patients with nonseptic ARDS within 72 hrs after onset of ARDS. There was no overlap between the two groups. Also, neopterin allowed a differentiation (p < .005), although a substantial overlap between serum levels of septic and nonseptic patients was observed. No discrimination could be achieved by determination of CRP and IL-6 levels. CONCLUSION: PCT determination in early ARDS could help to discriminate between septic and nonseptic underlying disease.

APACHE↗

Procalcitonin in the early phase after renal transplantation--will it add to diagnostic accuracy?

The determination of serum procalcitonin (PCT) was tested for its utility in detecting invasive bacterial infection and acute rejection during the first 6 wk after kidney transplantation. Fifty-seven kidney graft recipients were prospectively included in the study. In 13/57 patients, 16 episodes of acute biopsy-proven rejection occurred and were treated with high-dose steroids (n = 14) or with OKT3 (n = 2). Seventeen out of 57 patients experienced 19 invasive bacterial infections; 2/57 had partial graft necrosis due to malperfusion. Twenty-five out of 57 graft recipients experienced an uncomplicated postoperative course. A total of 116 samples were analyzed and the following data obtained: PCT, C-reactive protein (CRP), white blood cell (WBC) count, corresponding body temperature and serum creatinine. Procalcitonin values for patients with rejection did not differ significantly from those of the healthy transplant recipients (p = 0.47). In contrast, PCT was clearly elevated with invasive bacterial infection or partial graft necrosis (p < 0.01). OKT3 treatment of rejection led to a more than 10-fold increase in PCT. C-reactive protein, unlike PCT, was elevated to a variable extent in patients with graft rejection, though CRP values were significantly more elevated in patients with infection than in those with rejection (p < 0.01). The specifity for detection of invasive bacterial infection was 0.7 for PCT and 0.43 for CRP, whereas sensitivity was 0.87 for PCT and 1.0 for CRP. There was no correlation between PCT and serum creatinine (r = 0.06). Haemodialysis did not lower PCT serum concentrations. Procalcitonin values rose postoperatively to peak levels on the first and second days and mostly declined to normals within 1 wk. In conclusion PCT, not being influenced by acute kidney graft rejection but serving as a specific indicator of systemic bacterial infection, could help to discriminate between both types of inflammation.

Bacterial Infections↗

Usefulness of procalcitonin for differentiation between activity of systemic autoimmune disease (systemic lupus erythematosus/systemic antineutrophil cytoplasmic antibody-associated vasculitis) and invasive bacterial infection.

OBJECTIVE: To investigate whether the determination of serum procalcitonin (PCT) in systemic autoimmune disease will help to discriminate invasive infection from highly active underlying disease. METHODS: Three hundred ninety-seven serum samples, from 18 patients with systemic lupus erythematosus (SLE) and 35 patients with systemic antineutrophil cytoplasmic antibody-associated vasculitis (AAV), were analyzed. Clinical disease activity was assessed by the Systemic Lupus Activity Measure in SLE patients and by the Birmingham Vasculitis Activity Score in AAV patients. Procalcitonin concentrations were determined in parallel with concentrations of neopterin, interleukin-6 (IL-6), and C-reactive protein (CRP). Additionally, serum creatinine values were obtained. RESULTS: In 321 of the 324 samples from the 42 patients with autoimmune disease but without systemic infection, serum PCT levels were within the normal range (i.e., <0.5 ng/ml), whereas the values for neopterin, IL-6, and CRP were elevated in patients with active underlying disease. All 16 systemic infections occurred in 11 patients with AAV, and were associated with PCT levels that were markedly elevated, to a mean +/- SD of 1.93 +/- 1.19 ng/ml. No correlation between the degree of renal impairment and PCT concentrations was seen. CONCLUSION: PCT may serve as a useful marker for the detection of systemic bacterial infection in patients with systemic autoimmune disease.

Antibodies, Antineutrophil Cytoplasmic↗