Showing papers on "Procalcitonin published in 1997"

Cytokines, nitrite/nitrate, soluble tumor necrosis factor receptors, and procalcitonin concentrations : comparisons in patients with septic shock, cardiogenic shock, and bacterial pneumonia

Abstract: Objectives To determine and compare the respective concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, soluble TNF receptors, nitrite/nitrate (NO2 sup -/NO3 sup -), and procalcitonin in the plasma of patients with septic shock, cardiogenic shock, and bacterial pneumonia without

The potential role of procalcitonin and interleukin 8 in the prediction of infected necrosis in acute pancreatitis

Abstract: Background— Infection of pancreatic necrosis has a major impact on clinical course, management, and outcome in acute pancreatitis. Currently, guided fine needle aspiration is the only means for an early and accurate diagnosis of infected necrosis. Procalcitonin (PCT), a 116 amino acid propeptide of calcitonin, and interleukin 8 (IL-8), a strong neutrophil activating cytokine, are markers of severe inflammation and sepsis. Aims— To analyse the clinical value of PCT and IL-8 as biochemical parameters for predicting infected necrosis in acute pancreatitis. Patients and methods— Fifty patients with acute pancreatitis entered this prospective study and were stratified into three groups according to morphological and bacteriological findings: 18 patients with oedematous pancreatitis (group I), 14 patients with sterile necrosis (group II), and 18 patients who developed infected necrosis a median of 13.5 days after the onset of symptoms (group III). After admission serum samples were drawn daily for two weeks. Concentrations of PCT and IL-8 were measured by chemoluminescent immunoassays (upper reference range 0.5 ng/ml for PCT and 70 pg/ml for IL-8). The routine parameter C-reactive protein was determined by laser nephelometry (upper reference range 10 mg/l). Results— Median concentrations of PCT and IL-8 were significantly higher in patients with infected necrosis than in those with sterile necrosis during the observation period, whereas there was no difference in C-reactive protein. In oedematous pancreatitis overall median concentrations of all three parameters were low. By receiver operating characteristics best cut off levels for predicting infected necrosis or persisting pancreatic sepsis were 1.8 ng/ml for PCT and 112 pg/ml for IL-8. If these cut off levels were reached on at least two days, sensitivity, specificity, and accuracy for the prediction of infected necrosis were 94%, 91%, and 92% for PCT and 72%, 75%, and 74% for IL-8, respectively. After surgical treatment of infected necrosis median PCT and IL-8 values continued to be significantly higher in patients with persisting pancreatic sepsis (n=11) compared with those having an uneventful postoperative course (n=7). For the preoperative differentiation between infected necrosis and sterile necrosis guided fine needle aspiration was performed in 24 patients with necrotising pancreatitis and reached a diagnostic accuracy of 84% compared with 87% for PCT, and 68% for IL-8. There was no correlation between the aetiology of acute pancreatitis or the extent of necrosis and PCT or IL-8. Conclusion— PCT and IL-8 are found in high concentrations in infected necrosis and associated systemic complications in patients with acute pancreatitis. The course of PCT shows the closest correlation with the presence of infected necrosis. Monitoring of serum PCT is a potential new marker for the non-invasive and accurate prediction of infected necrosis as well as for the selection of patients with persisting septic complications after surgical debridement.

Measurement of Procalcitonin Levels in Children with Bacterial or Viral Meningitis

Abstract: We measured the plasma procalcitonin levels in 59 children who were admitted to the hospital because of bacterial or viral meningitis. Eighteen children with acute bacterial meningitis had elevated procalcitonin levels (mean level, 54.5 micrograms/L; range, 4.8-110 micrograms/L). The procalcitonin levels in 41 children with viral meningitis were low (mean level, 0.32 micrograms/L; range, 0-1.7 micrograms/L; P < .0001). Assay of cerebrospinal fluid (CSF) cells and proteins and serum C-reactive protein showed a zone of overlapping values between the two groups. Procalcitonin was not produced in CSF. Plasma procalcitonin levels decreased rapidly during antibiotic therapy. These data suggest that the measurement of plasma procalcitonin might be of value in the differential diagnosis of meningitis due to either bacteria or viruses.

Procalcitonin : A new indicator of the systemic response to severe infections

Abstract: Severe infection and sepsis with consecutive multiple organ dysfunction or failure (MODS) are major causes of morbidity and mortality in modern intensive care units [1]. Recent advances in our understanding of the pathogenesis of sepsis have made it clear that uncontrolled infections, whether clinically manifest or occult, are not the only cause of systemic inflammation and organ dysfunction. Other stimuli such as pancreatitis [2], major trauma [3], and burns [4] can also trigger an excessive inflammatory response and lead to MODS. As a result, it is now generally accepted that not all patients displaying the clinical signs of sepsis have an underlying infection. It is therefore frequently difficult to distinguish patients with systemic infection from those who appear septic but have no bacteriological or clinical evidence of infection. Common signs of systemic inflammation such as changes in body temperature, leukocytosis, and tachycardia may have an infectious or noninfectious etiology and are neither ,specific nor sensitive for sepsis. Thus, of 61 patients with sepsis (documented infection and at least two signs of remote organ failure), 35 (57%) presented with leukocytosis, 18 (29%) had leukopenia, and eight (14%) had normal leukocyte counts (unpublished data). Likewise, patients with sepsis may present with fever, hypothermia, or normal body temperature. Bacteriological evidence of infection, although considered a gold standard, may have some drawbacks. Negative blood cultures do not exclude sepsis and multiple samples may be required over extended periods before positive cultures emerge [5]. Furthermore, positive or negative cultures may not develop concurrently with clinical signs of sepsis. Because these common clinical and laboratory parameters lack sensitivity and specificity, others are needed to provide an early marker of the infectious etiology of a generalized inflammatory response and thus allow early diagnosis and the application of more specific therapeutic interventions. Furthermore, new parameters also may help identify subgroups of septic patients who may benefit from proor antiinflammatory therapies. One such parameter, procalcitonin, has recently attracted attention as a possible marker of the systemic inflammatory response to infection.

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

Abstract: 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.

Procalcitonin and C-reactive protein levels in neonatal infections.

Abstract: In order to assess the potential fo procalcitonin measurement in the management of neonatal sepsis, daily variations in serum procalcitonin (measured by an immunoluminometric assay) were evaluated in 94 control and infected newborn infants in comparison to C-reactive protein (measured by an immunonephelometric method). High levels of procalcitonin correlated with bacterial invasion and showed no discrepancies with C-reactive protein. procalcitonin increased (up to 400 micrograms l-1 and returned to the normal range (< 0.1 microgram l-1) more quickly than C-reactive protein, suggesting that procalcitonin may be an early marker of favourable outcome. Another finding is a significant procalcitonin peak on the first day of life in the control group, independent of any infectious stimulus. In conclusion, procalcitonin seems to be an interesting marker of neonatal sepsis but additional investigations are needed to understand better its mechanism of synthesis in order to determine its clinical usefulness.

Procalcitonin and its component peptides in systemic inflammation: immunochemical characterization.

Abstract: BACKGROUND The systemic inflammatory response syndrome (SIRS) is a marked, generalized response to a variety of injuries, if infection is implicated, the term "sepsis" is used. Systemic inflammatory response syndrome/sepsis, which is initiated by proinflammatory cytokines, has been found to be associated with increased serum levels of the prohormone of calcitonin, procalcitonin (ProCT) and its aminoterminus peptide (nProCT). The serum levels of ProCT and nProCT are very useful markers for SIRS/sepsis, and may be used to follow the course, the response to therapy, and/or the prognosis. We studied the serum levels and distribution of ProCT and its component peptides in normal persons for comparison with similar immunochemical and separatory studies in patients with neuroendocrine cancer and with SIRS/sepsis of various etiologies. METHODS We studied pooled and extracted serum of 13 normal subjects, and sera of patients with neuroendocrine cancer and SIRS/sepsis, using region-specific immunoassays, gel filtration, and high performance liquid chromatography. RESULTS Normal sera contained small but measurable levels of the intact ProCT molecule, nProCT, a conjoined calcitonin-calcitonin carboxyterminal peptide (CT:CCP-I), CCP-I, free mature CT, and calcitonin gene-related peptide (CGRP). Sera from neuroendocrine cancer usually contained high levels of these peptides. In such cases, free mature CT was always increased, the mean ratio of the intact ProCT to free CT being 168 +/- 68. Gel filtration and HPLC studies of patients with SIRS/sepsis revealed markedly increased levels of ProCT, nProCT, and CT:CCP-I in varying proportions. Mature CT was normal to minimally elevated. The ratio of ProCT to free CT was 2,900 +/- 800. Although serum CGRP is commonly increased in neuroendocrine cancer, it was very low or undetectable in SIRS/sepsis. CONCLUSIONS These studies indicate that ProCT and its component peptides circulate in normal persons. The serum of patients with SIRS/sepsis contains greatly increased levels of ProCT, nProCT and often, CT:CCP-I. However, in this condition, post-translational processing is incomplete, resulting in mature CT levels that are normal or minimally elevated. In contrast, patients with neuroendocrine cancer have considerably high mature CT levels. Interestingly, although serum CGRP levels often are high in neuroendocrine cancer, they are low in SIRS/sepsis. The marked hyperprocalcitonemia of SIRS/sepsis is probably a consequence of the pro-inflammatory cytokine cascade, and appears to be secreted in a constitutive fashion; the cell(s) of origin of this remarkable hypersecretion is unknown. There is a very marked positive correlation between serum levels of ProCT and nProCT, and the lower level of sensitivity for nProCT may make its measurement a more useful marker for early or mild SIRS/sepsis.

Effect of classic heatstroke on serum procalcitonin.

Abstract: OBJECTIVE: Procalcitonin, the precursor peptide of calcitonin, has been shown to be a serum marker of the severity and mortality of several systemic inflammatory response syndromes. This study addressed the correlation of serum procalcitonin with the course of classic (nonexertional) heatstroke. DESIGN: Serum samples were collected prospectively every 6 hrs for 24 hrs. SETTING: Heatstroke treatment unit, Makkah, Saudi Arabia. PATIENTS: A total of 25 patients were admitted during the annual Hajj pilgrimage in 1994. Ten patients evaluated in the same treatment center with minor illnesses and without pyrexia served as controls. INTERVENTIONS: Patients were cooled according to an established evaporation method. MEASUREMENTS AND MAIN RESULTS: Standard critical care parameters including continuous rectal temperature. A rapid immunochemical assay for serum procalcitonin was utilized. The mean serum procalcitonin was elevated 20-fold on admission in patients with heatstroke compared with controls (p 0.5 ng/mL (>0.15 nmol/L) at 6 hrs predicted survival (p = .02). CONCLUSION: Classic heatstroke is associated with increased concentrations of serum procalcitonin, particularly among survivors. Further studies are required to elucidate the source and action(s) of procalcitonin as well as its relationship to cytokine activation. Language: en

Procalcitonin--influence of temperature, storage, anticoagulation and arterial or venous asservation of blood samples on procalcitonin concentrations.

Abstract: In this study we have analysed the influence of temperature and time of storage and of repeated freezing on procalcitonin plasma concentrations ex vivo. We have also analysed the difference of procalcitonin concentrations in arterial or venous blood samples and the influence of different anticoagulation techniques on procalcitonin concentrations (serum, EDTA-, lithium-heparin- or citrate plasma). At room temperature (25 degrees C) a loss of procalcitonin plasma concentrations of 6.4% +/- 2.6% (mean, 2 standard error of the mean) after 3 hours (4.6% +/- 5.2% at 4 degrees C) and 12.3% +/- 3.1% after 24 hours occurred (6.3% +/- 5.0% at 4 degrees C, n = 17 each). Comparing the procalcitonin concentrations of blood samples with different anticoagulants (n = 24 each), there was only a significant difference between procalcitonin concentrations in heparinized plasma and serum (+ 7.6%, difference of the mean). There was no significant influence of the blood sampling technique (arterial or venous line) and of repeated freezing/thawing cycles (up to 3 times) on the procalcitonin concentrations measured. Although the difference of sampling and storage of the blood on procalcitonin concentrations is not significant, multiple factors may act synergistically on the result of procalcitonin measurement. To keep variations of ex vivo conditions as minimal as possible, a standardized technique of anticoagulation, time and temperature of storage is recommended, e.g. the use of EDTA-plasma and storage at room temperature, when samples are measured within 4 hours after blood drawing.

Procalcitonin, a marker of bacterial infection.

Abstract: Catcitonin and its propeptide, procalcitonin (PCT), and other peptide products of the calcitonin gene are known to be elevated in medullary thyroid carcinoma and in several other systemic diseases. But the demonstration of high procalcitonin concentrations without increase of calcitonin in patients with severe bacterial infection is a recent clinical finding in humans [1]. PCT is a 116 amino acid peptide which undergoes post-translational proteolysis into the mature hormone, calcitonin, composed of 32 aminoacids. PCT, which is low or undetectable in serum of healthy subjects, infants or adults, reaches high concentrations in patients with severe bacterial infection, septicemia or meningitis and decreases rapidly after appropriate antibiotic therapy. Moreover, in patients with acute viral infection or with inflammatory diseases, PCT is low. The transformation of procalcitonin into calcitonin occurs in thyroid C cells. Calcitonin and PCT are both elevated in sera of patients with thyroid carcinoma originating in these cells. The type of cells producing PCT during sepsis is not known, but in infected patients with high circulating PCI\" levels, calcitonin is undetectable. Thyroid is not the sole tissue involved in the secretion, since an infection-associated rise of PCT has been shown in a thyroidectomised patient with septicemia [1]. The mechanism of PCT production is unclear. Rapid and substantial release of PCT has been observed in patients with final-stage cancer after intravenous administration of interleukin-2 or TNF [1]. After endotoxin injection, PCT increases at 3-4 h in blood of healthy volunteers and then rises rapidly to a plateau at 6 h and remains elevated until at least 24 h. In the same patients, TNF~ and IL6 peak at 90 min and 3 h and reach baseline concentrations at 6 and 8 h, respectively [2]. Differences in the magnitude of the PCT peaks are observed between the patients, but a marked rise is present in all subjects. However, preliminary studies performed in vitro with endothelial cells, Iymphocytes or macrophages do not reveal PCT secretion after addition of endotoxin to medium. Procalcitonin measurement is actually performed with a immunoluminometric assay (BRAHMS Diagnostica, Berlin). Two monoclonal antibodies bind PCT at two different sites (the calcitonin and the katacalcin segments). This assay, which is specific for the proCT molecule, requires 20 pJ of plasma and can be done within 2 h. Its detection limit is 0.1 txg/1. Interand intra-assay variations at both low and high concentrations are less than 8% and 7%, respectively. Using this assay, plasma proCT levels in healthy adult subjects are < 0.1 lxg/1. Up to now, in the absence of an animal model, only clinical data collected in humans are available. Serum calcitonin-like reactivities have already been reported in various extrathyroid disorders, including bacterial infections, but Infection

Procalcitonin in acute malaria.

Abstract: Procalcitonin, the precursor of calcitonin, is elevated in patients with sepsis and infection (base-line values <0.1 ng/ml). We determined PCT in 38 hospitalised patients with suspected malaria. All of them had signs of infection and had recently returned from Africa. Plasmodium vivax was proven in 15, Plasmodium falciparum in one and an infection with both species was found in another case (n = 17). PCT was determined on admission and the days thereafter. In one patient PCT was determined every 4 hours on the first day. The maxima of the PCT concentration on day 0 and 1 were 5.3 ng/ml with proven Malaria and 0.43 ng/ml without. At the following days we found a decrease to normal values (<0.5 ng/ml) which correlated with the general condition of the patient. At a cut-off point of 2 ng/ml we found a sensitivity of 52%, positive predictive value of 74%, specificity of 86%, negative predictive value of 71%. procalcitonin, malaria

Procalcitonin. A new marker for acute phase reaction in acute pancreatitis

Abstract: Procalcitonin is a protein which is found in elevated concentrations in the blood circulation during systemic bacterial, fungal or protozoal infection. In contrast to classical acute-phase proteins like C-reactive protein or interleukin-6, it is not elevated after operative trauma. In this paper we present current opinions on the assumed induction mechanisms of the protein by cytokines and endotoxin. Furthermore, the clinical value for early detection of systemic infections in abdominal and transplantation surgery is demonstrated by examples from the literature. Our investigation shows that eight patients with necrotizing pancreatitis had a PCT mean value of 6.9 ng/ml on the day of admission. Seven patients with edematous pancreatitis had only a PCT mean value of 0.69 ng/ml. Despite these differences in the mean values, a significant difference between the normal value and the mean value of the group with necrotizing pancreatitis or edematous pancreatitis was not observed due to the wide range of PCT levels in the group of patients with necrotizing pancreatitis. The fact that only a few of the patients had a superinfected necrosis with systemic evasion of bacterias or their toxins may be the reason for this wide range. We suggest that a discrimination between superinfected necrotizing or sterile pancreatitis and edematous pancreatitis by PCT could be possible but more extensive studies with microbiological examination of the necrotic material are required to recognize the subgroups and to establish the real diagnostic efficiency of PCT in clinical practice, especially in the prediction of the outcome of acute pancreatitis.