Division of Neurogastroenterology & Motility, Department of Pediatric Gastroenterology, Great Ormond Street Hospital and UCL, London, UK.
Neurogastroenterol Motil. 2013 Jan;25(1):70-8.e8-9. doi: 10.1111/nmo.12016. Epub 2012 Oct 3.
Severe pediatric slow transit constipation (STC) is commonly due to intrinsic colonic neuromuscular disease. We sought to correlate neuromuscular histological phenotypes in pediatric STC with colonic manometric phenotypes using high-resolution manometry (HRM). We tested the hypothesis that failure of motor quiescence (FQ) between bisacodyl-induced high amplitude propagating sequences (HAPSs) might predict neuromuscular pathology.
Eighteen children (10 males, median age: 7.5 years) with refractory STC underwent stationary colonic HRM before segmental colonic resection. Six age-matched constipated children with normal colonic transit served as controls. Colonic resection specimens underwent histopathological analysis. Conventional manometric parameters and area under the curve (AUC) during a 1-min period following bisacodyl-induced HAPSs [PBAUC(1) ], as measure of FQ, were calculated.
Numbers of postbisacodyl HAPSs in descending and sigmoid segments were lower in patients than controls (P < 0.01, respectively). Low amplitude propagating sequences (LAPSs) were common prebisacodyl in controls and rare in STC (P < 0.001), whereas postbisacodyl LAPS were more common in STC (P < 0.001). Postbisacodyl, both retrograde propagating contractions and bursts of contractions were present in STC patients only (P < 0.001 and P < 0.01). Postbisacodyl simultaneous pressurization was seen only in STC (P < 0.05 and P < 0.001, in descending and rectosigmoid segments). Histological abnormalities were present in 17/18. Fourteen were neurogenic, one neuro-myogenic, and two myogenic. In segments with HAPS, PBAUC(1) was predictive of colonic neuropathy using a cutoff of 205 mmHg.s(-1) (Sensitivity 100%, specificity 86%, PPV92%, NPV100%).
CONCLUSIONS & INFERENCES: PBAUC(1) is increased in multiple colonic segments in neuropathic pediatric STC and constitutes a sensitive and specific biomarker of neuropathy.
严重的小儿慢传输型便秘（STC）通常是由于内在的结肠神经肌肉疾病引起的。我们试图通过高分辨率测压（HRM）将小儿 STC 的神经肌肉组织表型与结肠测压表型相关联。我们提出了这样一个假设，即在双羟苯氧丁酸诱导的高振幅传播序列（HAPSs）之间，运动静止（FQ）的失败可能预测神经肌肉病理学。
18 名患有难治性 STC 的儿童（男 10 例，中位年龄：7.5 岁）在进行结肠节段切除术前行静止性结肠 HRM。6 名年龄匹配的结肠转运正常的便秘儿童作为对照。结肠切除标本进行组织病理学分析。计算双羟苯氧丁酸诱导 HAPS 后 1 分钟期间的常规测压参数和曲线下面积（AUC）[PBAUC（1）]，作为 FQ 的衡量标准。
与对照组相比，患者降结肠和乙状结肠段的双羟苯氧丁酸诱导的 HAPS 次数较少（分别为 P < 0.01）。对照组双羟苯氧丁酸诱导前存在低振幅传播序列（LAPSs），而 STC 中罕见（P < 0.001），而 STC 中双羟苯氧丁酸诱导后的 LAPSs 更为常见（P < 0.001）。STC 患者仅存在双羟苯氧丁酸诱导后的逆行传播收缩和收缩爆发（P < 0.001 和 P < 0.01）。仅在 STC 中观察到双羟苯氧丁酸诱导后的同时加压（在降结肠和直肠乙状结肠段分别为 P < 0.05 和 P < 0.001）。18 例中有 17 例存在组织学异常。其中 14 例为神经性，1 例为神经肌源性，2 例为肌源性。在存在 HAPS 的节段中，使用 205mmHg·s（1）作为截断值，PBAUC（1）可预测结肠神经病（灵敏度 100%，特异性 86%，PPV92%，NPV100%）。
神经源性小儿 STC 多个结肠节段的 PBAUC（1）增加，是神经病的敏感和特异性生物标志物。
