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Colorectal Disease 2020-Jul

Alpha-1-Antitrypsin deficiency (carrier) as possible risk factor for development of colonic diverticula. A multicentre prospective case-control study: The ALADDIN study

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
الدخول التسجيل فى الموقع
يتم حفظ الارتباط في الحافظة
S Rottier
L Dreuning
J van Pelt
A van Geloven
X Beele
P Huisman
W Deurholt
C Rottier
K van Leeuwen
M de Boer

الكلمات الدالة

نبذة مختصرة

Aim: Connective tissue changes due to ageing or diseases leading to changes in the colonic wall is one theory for development of diverticula. Alpha-1 antitrypsin(A1AT), a protease inhibitor that protects connective tissue, possibly plays a role in the aetiology of diverticulosis. The aim of this study was to explore associations between the development of diverticula and A1AT deficiency.

Methods: A multicentre prospective case-control study. A total of 221 patients aged ≥60 years with acute abdominal pain undergoing an abdominal computed tomography (CT) were included and analysed. Patients with diverticula were defined as research group, patients without diverticula as controls. Genotype analysis for A1AT deficiency was performed.

Results: Twenty six of 221 patients (11.8%) were diagnosed with (being carrier of) A1AT deficiency. A non-significant difference in prevalence between patients with and without diverticula was found, 20 of 144 (13.9%) versus 6 of 77 (7.8%), respectively; crude odds ratio 1.9 (CI 0.7-5.0; p=0.186) and after adjustment for confounders an adjusted OR of 1.5 (CI 0.5-4.0; p=0.466). A non-significant difference in 30-day mortality rate from acute diverticulitis between A1AT deficiency patients (or carriers) and those without was observed; 2 of 9 patients (22.2%) with versus 1 of 55 (1.8%) without A1AT deficiency.

Conclusion: We found no convincing evidence that A1AT deficiency plays a role in the aetiology of diverticulitis, although deficient patients and carriers had a higher mortality when experiencing diverticulitis. Diverticulitis is a multifactorial disease and larger numbers may be needed to explore the role of A1AT deficiency among other contributing factors.

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