Riddell R H
Scand J Gastroenterol Suppl. 1984;104:137-49.
Now that many of the problems associated with the recognition, classification and terminology of dysplasia in ulcerative colitis have been overcome, the clinical effectiveness of such a classification needs to be investigated. Because dysplasia has been defined as an unequivocally neoplastic transformation of the epithelium which is capable of giving rise to an invasive carcinoma, it follows that in waiting for the development of dysplasia in patients at risk, there will always be an associated and as yet undefined incidence of invasive carcinoma already being present. Nevertheless, it is currently inappropriate to consider proctocolectomy before such changes develop. It is emphasised that waiting for high grade dysplasia to develop may lead to an unacceptably high level of associated invasive carcinoma. Also, because dysplasia is frequently focal, the changes of detecting it on random biopsy are directly proportional to the number of biopsies taken, and if found in flat mucosa it may be difficult to confirm the presence of such dysplasia by re-biopsy. Colectomy at this stage is aimed at cancer prevention rather than early cancer detection. Conversely, targeted biopsies of endoscopically visible plaques, nodules or other abnormalities, which may already be the superficial part of invasive carcinomas, offer the best hope of early detection of carcinoma. However, a proportion of these may have metastasised already; this is much more likely to have occurred if such a lesion is found at the first colonoscopy rather than in a patient in whom several surveillance colonoscopies have been carried out. Finally, the initial stages of many colitic cancers are undetectable endoscopically or radiologically but may be biopsied accidentally. All of these factors suggest that unexpected carcinomas will occur in any long-term prospective study. Surprisingly, most will not be lethal and they can be kept to a minimum if proctocolectomy is considered once unequivocal dysplasia is demonstrated on biopsy, particularly in parts of the world where large bowel cancer is already common. Data are required which assess accurately the risk of an invasive carcinoma being present or developing when epithelium indefinite for dysplasia, low grade dysplasia or high grade dysplasia are present both with and without an endoscopic abnormality being the source of the biopsy, and when such biopsies are obtained at the first or at subsequent colonoscopies. Only then can the risks of colectomy be weighed adequately against the likelihood of carcinoma already being present.(ABSTRACT TRUNCATED AT 400 WORDS)
既然溃疡性结肠炎发育异常的识别、分类及术语相关的诸多问题已被克服,那么这种分类的临床有效性就需要进行研究。由于发育异常已被定义为上皮细胞明确的肿瘤性转化,能够引发浸润性癌,因此在等待有风险患者出现发育异常的过程中,总会存在已经存在的、尚未明确的浸润性癌发生率。然而,在这种变化出现之前就考虑行直肠结肠切除术目前并不合适。需要强调的是,等待高级别发育异常的出现可能会导致与之相关的浸润性癌发生率高到不可接受的程度。此外,由于发育异常常常是局灶性的,通过随机活检检测到它的几率与所取活检样本的数量直接相关,如果在扁平黏膜中发现,通过再次活检可能难以证实这种发育异常的存在。此时进行结肠切除术旨在预防癌症而非早期癌症检测。相反,对内镜可见的斑块、结节或其他异常进行靶向活检,这些可能已经是浸润性癌的浅表部分,为早期发现癌症提供了最大希望。然而,其中一部分可能已经发生转移;如果在首次结肠镜检查时发现这样的病变,而不是在已经进行过多次监测结肠镜检查的患者中发现,发生转移的可能性要大得多。最后,许多结肠炎性癌的初始阶段在内镜或放射检查中无法检测到,但可能会在偶然活检时被发现。所有这些因素表明,在任何长期前瞻性研究中都会出现意外的癌症。令人惊讶的是,大多数不会致命,如果在活检显示明确的发育异常后考虑行直肠结肠切除术,尤其是在大肠癌已经很常见的地区,这些癌症可以保持在最低水平。需要准确评估在有或没有内镜异常作为活检来源的情况下,存在发育异常不明确、低级别发育异常或高级别发育异常的上皮细胞时,以及在首次或后续结肠镜检查时获取此类活检样本时,出现或发生浸润性癌的风险的数据。只有这样,才能充分权衡结肠切除术的风险与已经存在癌症的可能性。(摘要截选至400字)