Scaioli Eleonora, Colecchia Antonio, Marasco Giovanni, Schiumerini Ramona, Festi Davide
Department of Medical and Surgical Science, Policlinico S.Orsola, University of Bologna, Via Massarenti 9, 40138, Bologna, Italy.
Dig Dis Sci. 2016 Mar;61(3):673-83. doi: 10.1007/s10620-015-3925-0. Epub 2015 Oct 12.
Colonic diverticulosis imposes a significant burden on industrialized societies. The current accepted causes of diverticula formation include low fiber content in the western diet with decreased intestinal content and size of the lumen, leading to the transmission of muscular contraction pressure to the wall of the colon, inducing the formation of diverticula usually at the weakest point of the wall where penetration of the blood vessels occurs. Approximately 20 % of the patients with colonic diverticulosis develop abdominal symptoms (i.e., abdominal pain and discomfort, bloating, constipation, and diarrhea), a condition which is defined as symptomatic uncomplicated diverticular disease (SUDD). The pathogenesis of SUDD symptoms remains uncertain and even less is known about how to adequately manage bowel symptoms. Recently, low-grade inflammation, altered intestinal microbiota, visceral hypersensitivity, and abnormal colonic motility have been identified as factors leading to symptom development, thus changing and improving the therapeutic approach. In this review, a comprehensive search of the literature regarding on SUDD pathogenetic hypotheses and pharmacological strategies was carried out. The pathogenesis of SUDD, although not completely clarified, seems to be related to an interaction between colonic microbiota alterations, and immune, enteric nerve, and muscular system dysfunction (Cuomo et al. in United Eur Gastroenterol J 2:413-442, 2014). Greater understanding of the inflammatory pathways and gut microbiota composition in subjects affected by SUDD has increased therapeutic options, including the use of gut-directed antibiotics, mesalazine, and probiotics (Bianchi et al. in Aliment Pharmacol Ther 33:902-910, 2011; Comparato et al. in Dig Dis Sci 52:2934-2941, 2007; Tursi et al. in Aliment Pharmacol Ther 38:741-751, 2013); however, more research is necessary to validate the safety, effectiveness, and cost-effectiveness of these interventions.
结肠憩室病给工业化社会带来了沉重负担。目前公认的憩室形成原因包括西方饮食中纤维含量低,导致肠内容物和肠腔大小减少,致使肌肉收缩压力传导至结肠壁,通常在血管穿透的肠壁最薄弱点诱发憩室形成。约20%的结肠憩室病患者会出现腹部症状(即腹痛、不适、腹胀、便秘和腹泻),这种情况被定义为有症状的非复杂性憩室病(SUDD)。SUDD症状的发病机制仍不确定,关于如何充分管理肠道症状的了解更少。最近,低度炎症、肠道微生物群改变、内脏超敏反应和结肠运动异常已被确定为导致症状发展的因素,从而改变并改进了治疗方法。在本综述中,对有关SUDD发病机制假说和药物治疗策略的文献进行了全面检索。SUDD的发病机制虽未完全阐明,但似乎与结肠微生物群改变以及免疫、肠神经和肌肉系统功能障碍之间的相互作用有关(Cuomo等人,《联合欧洲胃肠病学杂志》2:413 - 442,2014年)。对受SUDD影响的受试者的炎症途径和肠道微生物群组成有了更深入的了解,增加了治疗选择,包括使用肠道定向抗生素、美沙拉嗪和益生菌(Bianchi等人,《营养药理学与治疗学》33:902 - 910,2011年;Comparato等人,《消化疾病科学》52:2934 - 2941,2007年;Tursi等人,《营养药理学与治疗学》38:741 - 751,2013年);然而,需要更多研究来验证这些干预措施的安全性、有效性和成本效益。