• B Korczowski and W Szybist.
• Department of Pediatrics and Pediatric Gastroenterology, District Hospital No. 2, University of Rzeszów, Poland. bartosz@uw.rzeszow.pl
• Acta Paediatr. 2004 Feb 1;93(2):169-73.

AimProcalcitonin (PCT) and C-reactive protein (CRP) are two acute-phase reactants with different clinical features. The study aimed to compare the diagnostic value of admission serum PCT and CRP concentrations as indicators of aetiology and intensity of inflammation in children hospitalized with diarrhoea.MethodsSerum PCT and CRP concentrations were determined on admission in 129 children hospitalized with diarrhoea. They were divided into four groups: group A: 37 children with diarrhoea as one of symptoms of ongoing systemic bacterial infection (sepsis/ meningitis): group B: 36 children with bacterial enterocolitis; group C: 43 children with rotaviral enterocolitis; and group D: 13 children with active inflammatory bowel disease (IBD). For comparison serum PCT and CRP concentrations were determined in 30 healthy controls.ResultsPCT concentration was > 0.5 ng ml(-1) in all 37 (100%) children with diarrhoea and systemic bacterial infection (mean 18.5 +/- 3.2 ng ml(-1)) and CRP was above 2 mg dl(-1) in 33 (89%) of these children (11.7 +/- 1.5 mg dl(-1)). PCT concentration was > or = 0.5 ng ml(-1) in 22 of 36 (61%) children with bacterial enterocolitis (2.2 +/- 0.6 ng ml(-1)), in 3 of 43 (7%) children with rotaviral infection (0.2 +/- 0 ng ml(-1)) and in 3 of 13 (23%) patients with IBD (0.3 +/- 0.1 ng ml(-1)). CRP value was > or =2 mg dl(-1) in 22 (61%) children from group B (5.4 +/- 1.0 mg dl(-1)), in 8 (19%) children from group C (l.3 +/- 0.3 mg dl(-1)) and in 6 (46%) patients from group D (3.3 +/- 0.9 mg dl(-1)). In the control group the PCT (0.1 +/- 0.1 ng ml(-1)) and CRP (0.03 +/- 0.1 mg dl(-1)) levels were low or undetectable.ConclusionIn this study PCT was a more reliable marker than CRP of systemic bacterial infection in children with diarrhoea. PCT was more specific but less sensitive in the differentiation of bacterial and non-bacterial aetiology of inflammation.

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