主胰管的内镜治疗:形态学、测压和临床随访的相关性。

C Renou, P Grandval, E Ville, R Laugier
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引用次数: 44

摘要

背景与目的:在慢性胰腺炎过程中,主胰管压力的逐渐升高是引起疼痛的主要病理生理因素,但到目前为止,在内镜支架置入期间和之后,胰管内压力从未被测量过,并与临床结果相关。因此,这种压力测量可以提供关于支架术有效时间的客观信息。方法:对13例慢性胰腺炎症状患者(男10例,女3例,平均年龄45.1+/-7.9岁)行内镜测压法测量主胰管压力;临床随访29.0+/-16.1个月。治疗前主要解剖改变为主胰管局部狭窄,即直径小于2mm(单独为慢性胰腺炎)10例;慢性胰腺炎合并胰腺分裂3例。内镜下支架治疗狭窄:F支架7例,F支架12例,6例。使用电子装置同时测量十二指肠(零水平)和主胰管内的压力,胰十二指肠梯度被认为是主胰管和十二指肠之间的压力差。结果:内镜下支架置入后导管内压力无明显降低(p = 0.16)。在支架置入结束时血压正常且解剖结果成功的9例患者中,6例在随访期间无痛,3例出现复发性胰腺型疼痛。其余4例患者在整个随访期间均无症状,但支架置入结束时主胰管压力较高,狭窄未完全治愈。结论:支架术结束时的导管内压力与解剖结果是否成功完全相关,但对于解剖结果较差的患者,并不能准确预测其临床预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Endoscopic treatment of the main pancreatic duct: correlations among morphology, manometry, and clinical follow-up.

Background and aim: During the course of chronic pancreatitis, the gradual increase in the main pancreatic duct pressure is the main pathophysiological factor responsible for pain, but up to now, the intra ductal pressure has never been measured during and after endoscopic stenting and correlated with clinical results. Pressure measurements of this kind could thus provide objective information about the useful duration of stenting period.

Methods: Main pancreatic duct pressure was measured by performing endoscopic manometry on 13 chronic pancreatitis symptomatic patients (10 men, 3 women, mean age: 45.1+/-7.9 yr); clinical follow-up was carried out for a period of 29.0+/-16.1 mo. Before treatment, the main anatomical alteration present was a localized stenosis of the main pancreatic duct, i.e., one with a diameter of less than 2 mm (chronic pancreatitis alone), 10 cases; chronic pancreatitis associated with pancreas divisum, 3 cases). Stenosis was treated by endoscopic stenting: 7 F stent (7 cases) and 12 F stent (6 cases). The pressure was measured simultaneously in the duodenum (zero level) and within the main pancreatic duct, using an electronic device, The pancreatico-duodenal gradient was taken to be the difference between the pressure in the main pancreatic duct and the duodenum.

Results: The endoscopic stenting induced a nonsignificant decrease in the intraductal pressure (p = 0.16). Among the 9 patients with a normal pressure at the end of the stenting and a successful anatomical outcome, 6 were painless during the follow-up period whereas 3 presented with recurrent pancreatic-type pain. The remaining 4 patients were symptom-free during the entire follow-up period, although the main pancreatic duct pressure was high at the end of the stenting and the stenosis was not completely cured.

Conclusion: The intraductal pressure at the end of the stenting period was perfectly correlated with the anatomical result, whether or not it was successful, but was not an accurate predictor of a favorable clinical outcome in patients with a poor anatomical result.

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