Decaluwe Hélène, Harrison Lisa M, Mariscalco Michele M, Gendrel Dominique, Bohuon Claude, Tesh Vernon L, Proulx François
Department of Pediatrics, Intensive Care Medicine, Sainte-Justine Hospital, University of Montreal, Canada, H3T-1C5.
Pediatr Res. 2006 Apr;59(4 Pt 1):579-83. doi: 10.1203/01.pdr.0000203100.45658.d5.
Shiga toxin producing Escherichia coli (STEC) are noninvasive enteric pathogens that may cause hemorrhagic colitis (HC) and diarrhea-associated hemolytic uremic syndrome (D+ HUS). We hypothesized that development of D+ HUS is associated with increased serum procalcitonin (PCT) levels. PCT was measured by an immunoluminometric assay in 113 patients. Concentrations of PCT were different in normal controls, disease control groups (rotavirus enteritis, HC due to non-STEC pathogens, chronic renal failure), and children with uncomplicated O157:H7 HC or D+ HUS. Children with D+ HUS showed higher PCT levels than those with uncomplicated O157:H7 HC, and increased concentrations were noted in cases requiring peritoneal dialysis. Severely increased concentrations were observed in children with D+ HUS on d 5 or 6 after the onset of enteritis, whereas serial measurements in those with uncomplicated O157:H7 HC remained within the normal range throughout the first week of illness. PCT was correlated with serum concentrations of lipopolysaccharide (LPS)-binding protein and serum levels of alanine aminotransferase. Using two separate sets of real-time PCR primers, we were unable to detect elevated PCT mRNA transcripts in nonadherent undifferentiated (monocytic) or differentiated (macrophage-like) THP-1 cells stimulated with purified Shiga toxin-1 and/or LPS. Our data show that serum levels of PCT are associated with the severity of illness in children with D+ HUS. Further studies are needed to determine the role of PCT in the pathogenesis of thrombotic microangiopathy associated to childhood D+ HUS.
产志贺毒素大肠杆菌（STEC）是一种非侵袭性肠道病原体，可导致出血性结肠炎（HC）和腹泻相关性溶血尿毒综合征（D + HUS）。我们推测D + HUS的发生与血清降钙素原（PCT）水平升高有关。采用免疫发光分析法对113例患者进行了PCT检测。正常对照组、疾病对照组（轮状病毒肠炎、非STEC病原体所致HC、慢性肾衰竭）以及单纯O157:H7 HC或D + HUS患儿的PCT浓度存在差异。D + HUS患儿的PCT水平高于单纯O157:H7 HC患儿，且在需要腹膜透析的病例中浓度升高。肠炎发病后第5天或第6天，D + HUS患儿的浓度显著升高，而单纯O157:H7 HC患儿在疾病的第一周内连续测量的结果均在正常范围内。PCT与血清脂多糖（LPS）结合蛋白浓度及血清丙氨酸转氨酶水平相关。使用两组不同的实时PCR引物，我们未能在纯化的志贺毒素-1和/或LPS刺激的非贴壁未分化（单核细胞）或分化（巨噬细胞样）THP-1细胞中检测到PCT mRNA转录本升高。我们的数据表明，PCT血清水平与D + HUS患儿的疾病严重程度相关。需要进一步研究以确定PCT在儿童D + HUS相关血栓性微血管病发病机制中的作用。
