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A Step Forward in the Understanding of Structural and Functional Bowel Damage in Patients with Ulcerative Colitis

机译:溃疡性结肠炎患者对肠道结构和功能损害的认识向前迈进了一步

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The concept that chronically undertreated inflammationcan progress to irreversible bowel damage (stricturesand fistulae leading to surgery) is currently well acceptedin Crohn disease (CD) and has resulted in a therapeuticparadigm shift towards earlier and more aggressive therapiesin order to prevent disease progression [1]. It is,however, unknown whether ulcerative colitis (UC) presentsthe same tendency to progress to irreversible boweldamage or which factors could be associated with thisprogression. Being a “solely” mucosal disease, UC is nottypically accompanied by the stricturing and fistulizingcomplications seen in CD, and there is an intuitive tendencyamong physicians to consider it a less aggressive ordestructive disease as compared to CD [2]. Need for hospitalization and surgery, or development of dysplasia, arethe usual complications of UC. However, long-lastingUC, where recurrent bouts of inflammation are allowedto progress, can potentially have devastating consequencesin colonic and rectal physiology, as supported by someevidence [3]. For example, it is well known that chronicUC can be complicated by benign strictures and colonshortening and narrowing, with nefarious consequenceson colonic motility [4]. Additionally, fibrosis has alsobeen reported to exist in UC, and benign strictures, althoughless common than in CD, are also a possible complicationof the disease [5]. Additional complications ofthe disease that could be considered as progression aredisease-proximal extension (disease progressing fromproctitis or left-sided colitis to more extensive forms ofinflammation) and pseudopolyps [3]. Finally, one of thelargely unexplored consequences of chronic UC relates toits potential to affect anorectal and colonic function. Severerectal inflammation, not adequately and timely treated,can result in rectal narrowing and presacral space widening,with impairment in rectal compliance, resulting indistressful complaints of fecal incontinence, urgency, andtenesmus [6]. Likewise, many studies, mostly performedin the past, have shown that UC is characterized by decreasedcontractility and a reduction in the pressure oramplitude of segmental contractions, which has been hypothesizedto be a consequence of wall stiffness [7]. The functional consequences of these manometric changesare not well clarified and could partly explain the fact thateven patients with mucosal healing may maintain symptomsof altered stool frequency and consistency [8].
机译:长期未充分治疗的炎症可能发展为不可逆的肠损害(导致外科手术的狭窄和瘘管)的概念目前在克罗恩病(CD)中得到了广泛接受,并已导致治疗模式向早期和更具侵略性的治疗转移,以防止疾病进展[1]。但是,溃疡性结肠炎(UC)是否表现出相同的发展为不可逆肠损害的趋势,或者与这种进展有关的因素尚不清楚。作为一种“唯一的”粘膜疾病,UC通常不伴有CD中出现的狭窄和瘘管并发症,而且医师们有一种直观的倾向,即与CD相比,UC是一种侵袭性较小或破坏性较大的疾病[2]。 UC的常见并发症是需要住院和外科手术或发育异常。然而,持久的UC(允许反复发作的炎症进展)可能会在结肠和直肠生理上产生毁灭性的后果,有证据支持[3]。例如,众所周知,慢性UC可能因良性狭窄,结肠缩短和狭窄而变得复杂,对结肠蠕动产生有害的后果[4]。另外,据报道,纤维化在UC中也存在,良性狭窄虽然比CD少见,但也是该病的可能并发症[5]。该疾病的其他并发症可被认为是疾病发展,即疾病近端扩展(疾病从肠炎或左侧结肠炎发展为更广泛的炎症形式)和假息肉[3]。最后,慢性UC的最大未发现后果之一涉及其影响肛肠和结肠功能的潜力。严重的直肠炎如果得不到及时及时的治疗,可能会导致直肠狭窄和pre前间隙变宽,直肠顺应性受损,从而导致大便失禁,尿急和腱鞘炎[6]。同样,许多研究(大多是过去进行的研究)显示,UC的特征是收缩力降低和节段性收缩的压力或幅度降低,这被认为是壁硬度的结果[7]。这些压力变化的功能后果尚不十分清楚,可能部分解释了这样一个事实,即即使粘膜愈合的患者也可能会出现粪便频率和稠度改变的症状[8]。

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