key: cord-0006521-p4yoozg6
authors: Gendrel, D.; Bohuon, C.
title: Procalcitonin, a marker of bacterial infection
date: 1997
journal: Infection
DOI: 10.1007/bf02113598
sha: 534cef3c19f19ad7c3bb09f1a4934df1f5430c8f
doc_id: 6521
cord_uid: p4yoozg6

nan

Infection the methods employed were unable to discriminate calcitonin and procalcitonin [3, 4] . In these assays, high procalcitonin levels were probably measured as a slight increase of calcitonin, due to a cross-reactivity of the antibodies. Since the publication of our first study, numerous data from other groups have confirmed the evidence that PCT blood concentrations are closely related to severe invasive bacterial infections. When the infection is locoregional or confined to a single organ, without systemic response of the inflammatory reaction, the PCT is low or moderately increased. Melioidosis, a potentially severe infection caused by the gram-negative bacillus Pseudomonas pseudomallei is a good example. PCT has been found to be an excellent marker of disease activity (low in patients with abscess and high at septicemic phase) and a good prognostic indicator [5] . One of the most interesting indications of PCT in clinical practice is the monitoring of critically ill patients with a possibility of sepsis [6] [7] [8] [9] [10] . Very high levels of procalcitonin are a characteristic of septic shock and contrast with the reduced levels observed in cardiogenic shock, while proinflammatory cytokines are elevated in both groups [6] . Procalcitonin allows the differential diagnosis between bacterial and nonbacterial aetiologies of acute situations. In adult respiratory distress syndrome the discrimination in both groups, with or without bacterial etiology, is not possible by C-reactive protein and interleukin 6, since both parameters are increased by non-specific inflammation. In contrast, PCT is elevated only in patients with bacterial etiology, without overlapping with the group of ARDS of toxic origin [7] . A very similar situation is found in acute pancreatitis for biliary versus toxic aetiology: only PCT allows a discrimination but not CRP and IL6 [7] [8] . After major digestive, surgery, the rise of procalcitonin during the daily follow-up of patients is an early indicator of septic complication with a marked increase in non-survivors versus survivors. After transplantation surgery, patients with acute rejection had normal or slightly increased PCT concentrations, while PCT was high in those with bacterial or fungal infections. In all these situations with important inflammatory reaction and increase of proinflammatory cytokines and CRP, a procalcitonin rise is a marker of sepsis [8] [9] [10] . Moreover, in chronic inflammatory diseases, such as Crohn's disease, ulcerative colitis, nephrotic syndrome or juvenile arthritis, procalcitonin is low. But, in acute Plasrnodium falciparum malaria attacks, a disease in which TNF-alpha is produced, PCT reaches high levels [11] . Procalcitonin is useful in young patients to differentiate between viral and bacterial infection. In 18 children with bacterial meningitis, PCT at hospital admission ranged from 4.8 to > 200 ~g/1 and < 1.2 ~g/1 in 45 cases of viral meningitis [12] . Comparing the diagnostic value of different parameters, we have found that sometimes CRP and more often IL 6 values had an important overlapping zone in 22 septicemic children and 51 others infected by viruses, while PCT values were always < 1 p~g/1 in the viral group and only in t/22 in the bacterial group [13] . The delayed diagnosis and treatment of bacterial infection continue to be a major cause of morbidity and mortality in neonates and reliable laboratory tests are needed. Elevated procalcitonin levels are mainly associated with neonatal bacterial sepsis, and decrease rapidly after appropriate antibiotherapy. PCT remains low in viral infections and in bacterial colonization of neonates without invasive infection, and the false-negative results are rare [14] . The main problem for interpretation of high PCT levels in neonatology concerns the cases of some neonates with severe and prolonged hypoxemia or multiorgan failure syndrome and without evidence of infection. The rise of PCT is possibly related to the translocation of enterotoxin from the digestive tract. But high PCT levels were also found in patients with an extended tissue injury, such as burns or severe trauma, and an unknown cellular factor could be involved in PCT production. Further studies are needed to confirm the first results and to determine the cut-off values. We need an animal model to explore the mechanisms of PCT production. But PCT appears to be an early and discriminant marker of severe bacterial infections.

High serum procalcitonin concentrations in patients with sepsis and infection

Procalcitonin increase after endotoxin injection in normal subjects

Increased serum and urinary calcitonin levels in patients with pnlmonary disease

HypercNcitoninemia in fulminant meningococcaemia in children

Serum procalcitonin in melioidosis

Cytokines NO3/NO2, soluble TNF receptors and procalcitonin levels: comparisons in patients with septic shock, cardiogenic shock and bacterial pneumonia

Discrimination of infectious and non-infectious etiologies of adult respiratory distress syndrome with procalcitonin

Stellenwert von PCT zur Diagnose von spezifischen In: fektionen. 28. Gemeinsame Jahrestagung Internistische Intensivmedizin

Procalcitonin als Prognoseparameter bei Peritonitis. 28. Gemeinsame Jahrestagung Internistische Intensivmedizin

Procalcitonin in diagnosis of severe infections

Serum procalcitonin concentrations in acute malaria

Procalcitonin in bacterial and viral meningitis in children

Procalcitonin in sepsis: comparison with IL6 and C-reactive protein in infected children and neonates. 36th ICAAC