Autschbach Frank, Gassler Nikolaus
University Heidelberg, Institute of Pathology, Heidelberg, Germany.
Eur J Gastroenterol Hepatol. 2007 May;19(5):399-400. doi: 10.1097/MEG.0b013e3280116cb8.
This leading article refers to the paper by Meier-Ruge WA, Muller-Lobeck H, Stoss F, Bruder E. The pathogenesis of idiopathic megacolon. Eur J Gastroenterol Hepatol 2006; 18:1209-1215. We apologise to all concerned for the dissociation between the two papers, which was due to an administrative error. The pathogenesis of idiopathic megacolon is still unclear. Besides abnormalities of the enteric nervous system, alterations in the function of intestinal smooth muscle cells and connective tissue elements might play an important role. A permanent extension of the bowel diameter without concrete hints to its aetiology is termed idiopathic megacolon. Evidence exists that idiopathic megacolon comprises a heterogeneous group of conditions characterized by alterations of the enteric nervous system, smooth muscle cells and/or connective tissue. Innovative molecular techniques are needed to get further insights into the pathogenesis of these intestinal motility disorders.
这篇社论提及了迈尔 - 鲁格WA、米勒 - 洛贝克H、施托斯F、布鲁德E所撰写的论文《特发性巨结肠的发病机制》。《欧洲胃肠病学与肝脏病学杂志》2006年；18:1209 - 1215。我们就两篇论文之间因行政失误导致的脱节向所有相关方表示歉意。特发性巨结肠的发病机制仍不清楚。除了肠神经系统异常外，肠道平滑肌细胞和结缔组织成分功能的改变可能也起重要作用。在没有明确病因线索的情况下，肠直径的永久性增大被称为特发性巨结肠。有证据表明，特发性巨结肠包含一组异质性疾病，其特征为肠神经系统、平滑肌细胞和/或结缔组织的改变。需要创新的分子技术来进一步深入了解这些肠道动力障碍的发病机制。
