S J Rottier1,2,3, L C Dreuning2, J van Pelt4, A A W van Geloven2, X D Y Beele5, P M Huisman5, W Y Deurholt6, C A Rottier1, K van Leeuwen7, M de Boer7, G van Mierlo8, M A Boermeester3, W H Schreurs1. 1. Department of Surgery, Northwest Clinics, Alkmaar/Den Helder, The Netherlands. 2. Department of Surgery, Tergooi Hospital, Hilversum, The Netherlands. 3. Department of Surgery, Academic Medical Center, Amsterdam, The Netherlands. 4. Department of Clinical Laboratory, Northwest Clinics, Alkmaar/Den Helder, The Netherlands. 5. Department of Radiology, Tergooi Hospital, Hilversum, The Netherlands. 6. Department of Radiology, Northwest Clinics, Alkmaar/Den Helder, The Netherlands. 7. Department of Molecular and Cellular Hemostasis, Sanquin Blood Supply, Division Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. 8. Department of Immunopathology, Sanquin Blood Supply, Division Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam,, Amsterdam, The Netherlands.
Abstract
AIM: Connective tissue changes due to ageing or diseases leading to changes in the colonic wall are one theory for the 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: This was a multicentre prospective case-control study. A total of 221 patients aged ≥ 60 years with acute abdominal pain undergoing abdominal CT were included and analysed. Patients with diverticula were defined as the research group, patients without diverticula as controls. Genotype analysis for A1AT deficiency was performed. RESULTS: Twenty-six of 221 (11.8%) patients were diagnosed with (being a carrier of) A1AT deficiency. A non-significant difference in prevalence between patients with and without diverticula was found, 20 (13.9%) of 144 vs 6 (7.8%) of 77, respectively, with a crude OR of 1.9 (95% CI 0.7-5.0; P = 0.186) and after adjustment for confounders an adjusted OR of 1.5 (95% CI 0.5-4.0; P = 0.466). A non-significant difference in 30-day mortality rate from acute diverticulitis between A1AT deficient patients (or carriers) and those without was observed: two (22.2%) of nine patients with A1AT deficiency vs 1 (1.8%) of 55 without. 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. Colorectal Disease
AIM: Connective tissue changes due to ageing or diseases leading to changes in the colonic wall are one theory for the 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: This was a multicentre prospective case-control study. A total of 221 patients aged ≥ 60 years with acute abdominal pain undergoing abdominal CT were included and analysed. Patients with diverticula were defined as the research group, patients without diverticula as controls. Genotype analysis for A1AT deficiency was performed. RESULTS: Twenty-six of 221 (11.8%) patients were diagnosed with (being a carrier of) A1AT deficiency. A non-significant difference in prevalence between patients with and without diverticula was found, 20 (13.9%) of 144 vs 6 (7.8%) of 77, respectively, with a crude OR of 1.9 (95% CI 0.7-5.0; P = 0.186) and after adjustment for confounders an adjusted OR of 1.5 (95% CI 0.5-4.0; P = 0.466). A non-significant difference in 30-day mortality rate from acute diverticulitis between A1AT deficient patients (or carriers) and those without was observed: two (22.2%) of nine patients with A1AT deficiency vs 1 (1.8%) of 55 without. 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. Colorectal Disease
Authors: A T P M Claassen; P E C Mourad-Baars; M L Mearin; Y Hilhorst-Hofstee; A Gerritsen van der Hoop Journal: Int J Colorectal Dis Date: 2005-01-28 Impact factor: 2.571
Authors: S J Rottier; J de Jonge; L C Dreuning; J van Pelt; A A W van Geloven; X D Y Beele; P M Huisman; W Y Deurholt; C A Rottier; M A Boermeester; W H Schreurs Journal: Int J Colorectal Dis Date: 2019-02-15 Impact factor: 2.571
Authors: J Granlund; T Svensson; O Olén; F Hjern; N L Pedersen; P K E Magnusson; P Thelin Schmidt Journal: Aliment Pharmacol Ther Date: 2012-03-20 Impact factor: 8.171
Authors: Carlo Nicola De Cecco; Maria Ciolina; Bruno Annibale; Marco Rengo; Davide Bellini; Giuseppe Muscogiuri; Antonello Maruotti; Luca Saba; Franco Iafrate; Andrea Laghi Journal: Eur Radiol Date: 2015-06-24 Impact factor: 5.315