Gyde S N, Prior P, Allan R N, Stevens A, Jewell D P, Truelove S C, Lofberg R, Brostrom O, Hellers G
Gastroenterology Unit, General Hospital, Birmingham.
Gut. 1988 Feb;29(2):206-17. doi: 10.1136/gut.29.2.206.
A retrospective cohort of 823 patients with ulcerative colitis who resided at the time of diagnosis in one of three defined geographical areas (West Midlands region, Oxford region, England and Stockholm County, Sweden) was assembled. The patients were first seen at named hospitals in these areas and the diagnosis of ulcerative colitis established within five years of onset of symptoms between 1945-1965. All patients were 15 years of age or more at onset of disease and were followed for a minimum of 17 years and a maximum of 38 years. Ninety seven per cent completeness of follow up was achieved. Examining the colorectal cancer risk in the series relative to the risk in the general population by standardised morbidity ratios, there was an eight fold increased risk of cancer in the series as a whole. Dividing the series by extent of colitis, extensive colitis patients showed a 19 fold increase in risk. A four fold increased risk was shown in the remainder of the series (left sided colitis, proctitis and extent unknown). Life table analyses in extensive colitis gave cumulative risks of 7.2% (CI 3.6-10.8) at 20 years from onset of disease and 16.5% (CI 9.0-24.0) at 30 years from onset. No significant effect of age at onset, sex or referral centre could be detected. Examination of the data by interval from onset to cancer and by actual age at development of cancer suggests that patients who develop colorectal cancer will do so in a distribution around 50 years of age independent of duration of disease in adult onset ulcerative colitis (greater than 15 years at onset of disease). An inverse relationship was shown between age at onset of disease and interval from onset of disease to cancer. Further age specific rates for cancer increased up to 50 years and decreased thereafter. These results suggest that extensive colitis patients have a genetic predisposition to colorectal cancer and that longstanding inflammation is not of primary importance in the initiation/promotion of cancer in this disease.
收集了823例溃疡性结肠炎患者的回顾性队列,这些患者在诊断时居住在三个特定地理区域之一(西米德兰兹地区、牛津地区、英格兰和瑞典斯德哥尔摩郡)。患者最初在这些地区的指定医院就诊,溃疡性结肠炎的诊断在1945年至1965年症状出现后的五年内确立。所有患者发病时年龄均在15岁及以上,随访时间最短17年,最长38年。随访的完整性达到了97%。通过标准化发病比来检查该队列中结直肠癌风险相对于一般人群的风险,整个队列中癌症风险增加了8倍。按结肠炎范围对该队列进行划分,广泛性结肠炎患者的风险增加了19倍。该队列其余部分(左侧结肠炎、直肠炎和范围不明)的风险增加了4倍。对广泛性结肠炎进行生命表分析,发病后20年的累积风险为7.2%(95%置信区间3.6 - 10.8),发病后30年为16.5%(95%置信区间9.0 - 24.0)。未检测到发病年龄、性别或转诊中心的显著影响。按发病至癌症的间隔时间以及癌症发生时的实际年龄对数据进行检查表明,患结直肠癌的患者将在50岁左右发病,这与成人发病的溃疡性结肠炎(发病时年龄大于15岁)的病程无关。发病年龄与发病至癌症的间隔时间呈负相关。进一步的特定年龄癌症发病率在50岁之前上升,之后下降。这些结果表明,广泛性结肠炎患者对结直肠癌有遗传易感性,并且长期炎症在该疾病癌症的起始/促进过程中并非首要因素。