Tonelli P
Azienda Ospedaliera Careggi, II U.O. Chirurgia Generale e Vascolare, Scuola di Specializzazione in Chirurgia Generale dell'Università di Firenze.
Chir Ital. 2000 May-Jun;52(3):243-50.
The aetiopathogenesis of terminal ileitis is still unknown, as is the cause of its spread to the small and large bowel. The aim of this study was to shed light on these unknown aspects of Crohn's disease.
The lack of patency of the ileal branch of the ileocolic lymphatic collector which causes terminal ileitis, usually in the earlier part of life, is likely to occur in the foetus around the 10th week of pregnancy as a result of a minor abnormality of the physiological regression of the vitelline duct. Excessive atrophy of the lymphatic network seems to occur, also affecting the rudimentary lymphatic vessels in the midgut destined to become the terminal ileum. The terminal ileitis spreads to the large bowel in an increasing percentage of cases and is directly related to duration of the disease, causing first ileitis plus right colitis, and then ileitis plus total colitis (which, however, does not include the rectum). It may also include the jejunum, causing skip lesions. This spread of lesions is not due to any genetic predisposition (that is to say, it is not predetermined in empirical terms), but rather to the extent of the lymphatic obstruction caused by the spread of immunocomplexes via the lymphatic network. This is shown by the fact that secondary lesions of the jejunum and large bowel are also typical of lymphoedema and that their spread is segmentary. In the light of these pathogenetic mechanisms, it is reasonable to assume that the spread of the process from the ileum to the colon might be prevented by prompt surgery during the initial phase of the ileitis. If these views are correct, the traditional subdivision of Crohn's disease forms into ileitis, ileocolitis and solitary colitis should be replaced by a very simple scheme showing the spread of the primary ileitis very often to ileocolitis, first confined to the right colon and then total. We cannot include either solitary colitis (not clearly defined in the literature) or anorectal Crohn's disease (whose forms have yet to be fully acknowledged) in this scheme.
末端回肠炎的病因发病机制仍然不明,其蔓延至小肠和大肠的原因也不清楚。本研究的目的是阐明克罗恩病这些未知的方面。
回结肠淋巴管收集器的回肠分支不通畅导致末端回肠炎,通常在生命早期发生,可能是由于卵黄管生理性退化的轻微异常,发生在妊娠第10周左右的胎儿身上。淋巴管网络似乎发生过度萎缩,也影响到中肠中注定要成为末端回肠的原始淋巴管。在越来越多的病例中,末端回肠炎蔓延至大肠,并且与疾病持续时间直接相关,首先导致回肠炎加右结肠炎,然后是回肠炎加全结肠炎(然而,不包括直肠)。它也可能累及空肠,导致跳跃性病变。这种病变的蔓延不是由于任何遗传易感性(也就是说,从经验角度来看不是预先确定的),而是由于免疫复合物通过淋巴管网络扩散导致的淋巴阻塞程度。空肠和大肠的继发性病变也是淋巴水肿的典型表现以及它们的蔓延是节段性的这一事实证明了这一点。鉴于这些发病机制,有理由假设在回肠炎的初始阶段通过及时手术可能预防病情从回肠蔓延至结肠。如果这些观点正确,克罗恩病传统上分为回肠炎、回结肠型和孤立性结肠炎的分类应该被一个非常简单的方案所取代,该方案显示原发性回肠炎常常蔓延至回结肠型,首先局限于右半结肠,然后是全结肠。我们不能将孤立性结肠炎(文献中未明确界定)或肛门克罗恩病(其类型尚未得到充分认可)纳入此方案。