Rottier S J, de Jonge J, Dreuning L C, van Pelt J, van Geloven A A W, Beele X D Y, Huisman P M, Deurholt W Y, Rottier C A, Boermeester M A, Schreurs W H
Department of Surgery, Northwest Clinics, Wilhelminalaan 12, 1815 JD, Alkmaar/Den Helder, Netherlands.
Department of Surgery, Tergooi, Hilversum, Netherlands.
Int J Colorectal Dis. 2019 May;34(5):933-938. doi: 10.1007/s00384-019-03248-8. Epub 2019 Feb 15.
The underling pathophysiological mechanisms that cause the formation of colonic diverticula (diverticulosis) remain unclear. Connective tissue changes due to ageing that cause changes in collagen structure of the colonic wall is one theory. Alpha-1-antitrypsin (A1AT) is a protease inhibitor known to protect connective tissue in other organs. Associations between (carriers of) A1AT deficiency and the development of colonic diverticula will be the main focus of this study.
A multicentre prospective case-controlled study. In total, 230 patients ≥ 60 years with acute abdominal pain undergoing an abdominal computed tomography (CT) will be included. The research group consists of patients with diverticulosis and/or diverticulitis; controls are patients without diverticula (0 to ≤ 5 diverticula). Genotype analysis for A1AT deficiency will be performed.
Hypothetically, connective tissue changes, in particular related to (carriers of) A1AT deficiency, can contribute to the development of diverticula and diverticulitis. We expect to find a higher prevalence of A1AT carriers in patients with diverticulosis compared to patients without diverticulosis. Having diverticulosis does not affect the general health of these individuals per se, when asymptomatic. Once an association is found, present findings can be the basis for a second study to assess the risk of developing acute diverticulitis and its disease course in carriers of A1AT deficiency. Because a large cohort is needed in the latter, we shall first perform a pilot study to investigate the likelihood of the primary hypothesis.
Netherlands Trial register, NTR6251, NL55016.094.15.
导致结肠憩室（憩室病）形成的潜在病理生理机制仍不清楚。一种理论认为，衰老引起的结缔组织变化导致结肠壁胶原结构改变。α-1抗胰蛋白酶（A1AT）是一种已知可保护其他器官结缔组织的蛋白酶抑制剂。本研究的主要重点是A1AT缺乏（携带者）与结肠憩室发展之间的关联。
一项多中心前瞻性病例对照研究。总共将纳入230名年龄≥60岁、因急性腹痛接受腹部计算机断层扫描（CT）的患者。研究组由患有憩室病和/或憩室炎的患者组成；对照组为无憩室（0至≤5个憩室）的患者。将进行A1AT缺乏的基因分型分析。
假设结缔组织变化，特别是与A1AT缺乏（携带者）相关的变化，可能导致憩室和憩室炎的发展。我们预计，与无憩室病的患者相比，憩室病患者中A1AT携带者的患病率更高。当无症状时，患有憩室病本身并不影响这些个体的总体健康。一旦发现关联，目前的研究结果可作为第二项研究的基础，以评估A1AT缺乏携带者发生急性憩室炎的风险及其病程。由于后者需要大量队列，我们将首先进行一项试点研究，以调查原假设的可能性。
荷兰试验注册，NTR6251，NL55016.094.15。
