Although the increased risk of colorectal neoplasia in patients with both primary sclerosing cholangitis (PSC) and ulcerative colitis (UC; termed PSC-UC) is well documented, the mechanism through which concomitant PSC increases the risk of colorectal neoplasia remains unclear. Given that the risk of colorectal neoplasia in UC is positively correlated with increased histologic inflammation, this study sought to investigate whether increased histologic inflammation could be used to stratify the risk of dysplasia development in patients with PSC-UC. Twenty patients with PSC-UC and dysplasia were compared with 30 control patients with PSC-UC who had no history of neoplasia. For each patient, all surveillance biopsies were scored using a 4-point scoring system: (1) no epithelial neutrophils = 0, (2) cryptitis only = 1, (3) cryptitis plus crypt abscess in <50% of crypts = 2, and (4) crypt abscess in ≥50% of crypts, erosion, neutrophilic exudate, and/or ulceration = 3. A score was designated for each biopsy, and both mean and maximum inflammation scores were calculated from all biopsies taken during each colonoscopy. The inflammation burden score was calculated for each surveillance interval by multiplying the average maximum score between each pair of surveillance episodes by the length of the surveillance interval in years. The average scores derived from all colonoscopies for each patient were used to determine the patient's overall mean, maximum, and inflammation burden scores. In both the dysplasia and control groups, the 3 summative inflammation scores were calculated independently for the entire colon, right colon, and left colon. The dysplasia group consisted of 14 (70%) men and 6 (30%) women, with a mean age of 27 years at UC diagnosis and a long history of pancolitis (mean duration: 17 y). A total of 49 dysplastic lesions were detected in the dysplasia group, and 8 (40%) of the 20 patients had multifocal dysplasia. The majority of dysplastic lesions belonged to nonconventional subtypes (n = 28; 57%) and were located in the right colon (n = 37; 76%). Irrespective of the colon segment, there was no significant difference in the 3 summative inflammation scores between the dysplasia and control groups (P > 0.05). However, in each group, the 3 summative inflammation scores were significantly higher in the right colon than in the left colon (P< 0.05). In conclusion, patients with PSC-UC exhibit increased histologic inflammation in the right colon compared with the left colon, regardless of the presence of dysplasia. Although this may provide an explanation for the predominance of right-sided colorectal neoplasia in patients with PSC-UC, increased histologic inflammation does not reliably predict an elevated risk of dysplasia in patients with PSC-UC. These findings reinforce the current recommendation for annual endoscopic surveillance for all patients with PSC-UC, irrespective of the extent and severity of inflammation.

中文翻译：

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结肠活动性炎症的增加并不是原发性硬化性胆管炎和溃疡性结肠炎患者发育不良风险升高的可靠预测因素。


尽管原发性硬化性胆管炎 (PSC) 和溃疡性结肠炎 (UC；称为 PSC-UC) 患者结直肠肿瘤风险增加已有充分记录，但伴随 PSC 增加结直肠肿瘤风险的机制仍不清楚。鉴于 UC 中结直肠肿瘤的风险与组织学炎症增加呈正相关，本研究旨在探讨组织学炎症增加是否可用于对 PSC-UC 患者发生不典型增生的风险进行分层。将 20 名患有 PSC-UC 和不典型增生的患者与 30 名没有肿瘤病史的 PSC-UC 对照患者进行比较。对于每位患者，所有监测活检均使用 4 点评分系统进行评分：(1) 无上皮中性粒细胞 = 0，(2) 仅隐窝炎 = 1，(3) <50 id=24> 0.05 中隐窝炎加隐窝脓肿。然而，在各组中，右结肠的3个炎症总结评分均显着高于左结肠（P<0.05）。总之，与左结肠相比，PSC-UC 患者的右结肠组织学炎症增加，无论是否存在发育不良。尽管这可能为 PSC-UC 患者右侧结直肠肿瘤占主导地位提供了解释，但组织学炎症增加并不能可靠地预测 PSC-UC 患者异型增生风险升高。这些发现强化了目前对所有 PSC-UC 患者进行年度内镜监测的建议，无论炎症的程度和严重程度如何。