Chronic pouchitis versus recurrent Crohn's disease: a diagnostic challenge.
Chronic pouchitis versus recurrent Crohn's disease: a diagnostic challenge.
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慢性储袋炎与复发性克罗恩病：诊断挑战。
DOI：
10.1007/s10620-013-2816-5
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发表时间：
2013
影响因子：
3.1
通讯作者：
Rubin,DavidT
中科院分区：
文献类型：
--
作者：
Weber,ChristopherR;Rubin,DavidT
多达三分之一的溃疡性结肠炎患者由于治疗难治性或黏膜发育不良或癌的发展将需要全腹结肠切除术。在这些患者中，选择的修复程序是回肠袋-肛门吻合术（IPAA），其中回肠远端形成一个袋并与肛门吻合。这样的小袋形成了一个储存器，当功能正常时，它将在没有结肠的情况下最大限度地减少肠道运动的频率。然而，IPAA的一个常见并发症是眼袋炎症的发展，称为眼袋炎，15%的患者在术后第一年内发生。大多数患有袋炎的患者都能成功地使用抗生素治疗，尽管一部分患者会经历多次复发。一些患者在眼袋近端出现炎症，甚至出现穿透性跨壁并发症，提示克罗恩病的诊断。偶尔，由于复发性克罗恩病，患者会经历多次慢性眼袋炎症。虽然这之前被认为是由于最初对结肠炎的潜在原因的误诊，但最近，这种“转变”被认为是由于术后解剖结构改变导致环境压力的变化。在临床上，早期识别诊断改变的患者是很重要的，以便提供适当的克罗恩病治疗，努力防止眼袋失败，并消除传统肠皮回肠造口术的复发。为了区分慢性抗生素耐药袋炎、袋前回肠炎和克罗恩病，通常进行内窥镜检查和活检。最重要的考虑因素是炎症的分布模式。如果袋表现出慢性但非穿透性损伤的特征，并且袋前回肠和胃肠道的其余部分表现正常，则不太可能诊断为克罗恩病。然而，如果疾病的分布有些斑驳，或者在袋近端粘膜有慢性损伤的模糊证据，诊断并不总是直截了当的。在这种情况下，额外的诊断标记将被证明是非常有用的。鉴别克罗恩病和慢性袋炎的一个可能的组织学标志是幽门腺化生（PGM）[5]。当通常存在于回肠袋内的肠型上皮被类似胃幽门腺的腺体所取代时，PGM就会发生（图1b）。通过常规苏木精和伊红（H&E）染色，这些化生的幽门腺很容易被识别为高柱状细胞，胞浆呈淡粉色，细胞核位于基部，小而暗（图1a，插图）。随着腺体的发育，它们通常在粘膜基部生长成簇状结构。PGM可在许多与重复性溃疡和再生[4]相关的肠道疾病中观察到。大多数克罗恩病患者的回肠活检中都存在PGM，然而，由于PGM是对复发性溃疡的反应，因此它被认为是一种非特异性标志物。其他引起PGM的原因包括肿瘤、放射性肠炎、消化性溃疡、肺结核和耶尔森菌性小肠结肠炎。尽管如此，这些疾病的表现在回肠袋中并不典型，通常可以根据临床理由排除。
Up to one-third of patients with ulcerative colitis will require total abdominal colectomy due to being refractory to therapy or the development of mucosal dysplasia or carcinoma. In these patients, the restorative procedure of choice is ileal pouch-anal anastomosis (IPAA), in which the distal ileum is formed into a pouch and anastomosed to the anus. Such a pouch creates a reservoir, which, when functioning properly, will minimize the frequency of bowel movements in the absence of a colon. One frequent complication of IPAA, however, is the development of pouch inflammation, known as pouchitis, which occurs in 15% of patients in the first post-operative year [6]. The majority of patients with pouchitis are successfully managed with antibiotics, though a portion experience multiple recurrent episodes. Some patients develop inflammation proximal to the pouch or even develop penetrating transmural complications suggesting a diagnosis of Crohn’s disease. Occasionally, patients experience multiple episodes of chronic pouch inflammation due to recurrent Crohn’s disease. Although this was previously believed to be due to an initial misdiagnosis of the underlying cause of colitis, more recently, this ‘‘transformation’’is thought to be due to changing environmental pressure given the altered postsurgical anatomy. Clinically it is important to identify patients with a modification in diagnosis early in order to provide appropriate Crohn’s disease therapy in an effort to prevent pouch failure and to eliminate reversion to traditional enterocutaneous ileostomies. In order to differentiate between chronic antibiotic-resistant pouchitis, prepouch ileitis, and Crohn’s disease, endoscopic examination and biopsies are usually performed. The most important factor to consider is the distribution pattern of inflammation. If the pouch displays features of chronic but nonpenetrating injury, and the pre-pouch ileum and the remainder of the GI tract appear normal, the diagnosis of Crohn’s disease is unlikely. Nevertheless, the diagnosis is not always straightforward if the distribution of disease is somewhat patchy, or if there is equivocal evidence of chronic injury in mucosa proximal to the pouch. Under such circumstances, additional diagnostic markers would prove to be quite useful.One possible histological marker useful in differentiating between Crohn’s disease and chronic pouchitis is pyloric gland metaplasia (PGM)[5]. PGM occurs when intestinal-type epithelium, which is normally present in the ileal pouch, is replaced by glands that resemble gastric pyloric glands (Fig. 1 b). These metaplastic pyloric glands are easily identified by routine hematoxylin and eosin (H&E) staining as tall columnar cells with pale pink cytoplasm and small dark basally situated nuclei (Fig. 1 a, inset). As the glands develop, they normally grow into a clustered architecture at the mucosal base. PGM may be observed in a number of intestinal disorders associated with repetitive ulcerations and regeneration [4]. PGM is present in the majority of ileal biopsies from patients with Crohn’s disease [3], however, since PGM arises in response to recurrent ulceration, it has been considered a non-specific marker. Other causes of PGM include tumors, radiation enteritis, peptic ulceration, tuberculosis, and Yersinia enterocolitis [4]. Nonetheless, these disease manifestations are not typically observed in an ileoanal pouch, and can usually be excluded on clinical grounds [3].