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首页> 外文期刊>International journal of colorectal disease. >Prevalence of alpha-1-antitrypsin deficiency carriers in a population with and without colonic diverticula. A multicentre prospective case-control study: the ALADDIN study
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Prevalence of alpha-1-antitrypsin deficiency carriers in a population with and without colonic diverticula. A multicentre prospective case-control study: the ALADDIN study

机译：α-1-抗真菌血管缺乏载流子血液缺乏，群体血液缺乏症，没有结肠憩室。 多中心预期案例对照研究：阿拉丁研究

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PurposeThe 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.MethodsA multicentre prospective case-controlled study. In total, 230 patients 60years 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.RationaleHypothetically, 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.Trial registrationNetherlands Trial register, NTR6251, NL55016.094.15
机译：原因是导致结肠憩室（憩室）形成的病理生理机制仍然不清楚。由于老化导致的结缔组织变化，导致结肠墙的胶原蛋白结构的变化是一个理论。 α-1-抗酸酯（A1AT）是已知保护其他器官中的结缔组织的蛋白酶抑制剂。 （携带者）A1AT缺乏和结肠憩室的发展之间的关联将是本研究的主要重点。方法是多期形案例控制的研究。总共230名患者60岁，患有腹部计算断层扫描（CT）的急性腹痛。研究小组由患者组成憩室和/或憩室炎;对照组是没有憩室（0至5个憩室）的患者。将进行A1At缺乏的基因型分析。重整性，结缔组织变化，特别是（载体）A1AT缺乏，可以有助于憩室和憩室炎的发育。与没有憩室症的患者相比，我们预计患者患者A1AT载体的患者患病率更高。在无症状的情况下，憩室不影响这些个人的一般健康状况。一旦发现了一个关联，目前的结果可以是第二次研究以评估A1AT缺乏载流子载体发育急性憩室炎的风险的第二种研究的基础。由于在后者需要大量的队列，我们​​首先将首先执行试点研究以调查主要假设的可能性.Trial RecobernEntherlands试验登记登记册，NTR6251，NL55016.094.15

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