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远端胃肠道慢性和急性炎症中胃排空障碍的机制。

Mechanisms of gastric emptying disturbances in chronic and acute inflammation of the distal gastrointestinal tract.

机构信息

Israelitic Hospital, D-22297, Hamburg, Germany.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2009 Nov;297(5):G861-8. doi: 10.1152/ajpgi.00145.2009.

Abstract

It is unclear why patients with inflammation of the distal bowel complain of symptoms referable to the upper gastrointestinal tract, specifically to gastric emptying (GE) disturbances. Thus we aimed to determine occurrence and putative pathomechanisms of gastric motor disorders in such patients. Thirteen healthy subjects (CON), 13 patients with Crohn's disease (CD), 10 with ulcerative colitis (UC), and 7 with diverticulitis (DIV) underwent a standardized (13)C-octanoic acid gastric emptying breath test. Plasma glucose, CCK, peptide YY, and glucagon-like peptide-1 (GLP-1) were measured periodically and correlated with GE parameters. Results were given in means +/- SD. Compared with CON, GE half time (T) was prolonged by 50% in CD (115 +/- 55 vs. 182 +/- 95 min, P = 0.037). Six CD, 2 DIV, and 2 UC patients had pathological T (>200 min). Postprandial plasma glucose was increased in all patients but was highest in DIV and correlated with T (r = 0.90, P = 0.006). In CD, mean postprandial CCK levels were increased threefold compared with CON (6.5 +/- 6.7 vs. 2.1 +/- 0.6 pmol/l, P = 0.027) and were correlated with T (r = 0.60, P = 0.041). Compared with CON, GLP-1 levels were increased in UC (25.1 +/- 5.2 vs. 33.5 +/- 13.0 pmol/l, P = 0.046) but markedly decreased in DIV (9.6 +/- 5.2 pmol/l, P < 0.0001). We concluded that a subset of patients with CD, UC, or DIV has delayed GE. GE disturbances are most pronounced in CD and might partly be caused by excessive CCK release. In DIV there might be a pathophysiological link between decreased GLP-1 release, postprandial hyperglycemia, and delayed GE. These explorative data encourage further studies in larger patient groups.

摘要

目前尚不清楚为何患有远端肠道炎症的患者会出现上胃肠道症状,特别是胃排空(GE)障碍。因此,我们旨在确定此类患者中胃运动障碍的发生和可能的发病机制。13 名健康受试者(CON)、13 名克罗恩病(CD)患者、10 名溃疡性结肠炎(UC)患者和 7 名憩室炎(DIV)患者接受了标准化的 13C-辛酸胃排空呼吸试验。定期测量血浆葡萄糖、CCK、肽 YY 和胰高血糖素样肽-1(GLP-1),并与 GE 参数相关联。结果以平均值 +/- SD 表示。与 CON 相比,CD 的 GE 半衰期(T)延长了 50%(115 +/- 55 与 182 +/- 95 min,P = 0.037)。6 名 CD、2 名 DIV 和 2 名 UC 患者的 T 异常(>200 min)。所有患者的餐后血浆葡萄糖均升高,但 DIV 患者的血糖升高最为明显,且与 T 相关(r = 0.90,P = 0.006)。与 CON 相比,CD 患者的平均餐后 CCK 水平增加了三倍(6.5 +/- 6.7 与 2.1 +/- 0.6 pmol/l,P = 0.027),且与 T 相关(r = 0.60,P = 0.041)。与 CON 相比,UC 患者的 GLP-1 水平升高(25.1 +/- 5.2 与 33.5 +/- 13.0 pmol/l,P = 0.046),但 DIV 患者的 GLP-1 水平明显降低(9.6 +/- 5.2 pmol/l,P < 0.0001)。我们得出结论,一部分 CD、UC 或 DIV 患者存在 GE 延迟。GE 障碍在 CD 中最为明显,可能部分是由 CCK 过度释放引起的。在 DIV 中,GLP-1 释放减少、餐后高血糖和 GE 延迟之间可能存在病理生理联系。这些探索性数据鼓励在更大的患者群体中进一步研究。

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