Tobi Martin, Bradley Irwin, Moole Sumana, Talwar Harvinder, McVicker Benita, Kintanar Esperanza, Sochacki Paula, Ben-Josef Edgar
Department of R&D, Detroit VAMC, Detroit Michigan.
St. Lukes Hospital, Duluth, Minnesota.
Gastro Hep Adv. 2022 Nov 9;2(3):362-369. doi: 10.1016/j.gastha.2022.11.001. eCollection 2023.
It has been recently proposed to change the nomenclature of "chronic radiation proctitis" (CRP) to "radiation-associated vascular ectasia" on the basis that signs of inflammation are rarely observed. We herein present data supporting the idea that inflammation is a critical step that initiates the process that culminates in the characteristic changes of CRP.
In support of inflammation in the pathogenesis of CRP, we review the pertinent literature and publish our new results, including the role of amifostine treatment and proinflammatory factors (p38 MAP kinase, VEGF, and CEACAM1).
Immunohistochemistry from anterior rectal wall biopsies obtained in a prospective pilot study demonstrates that expression of VEGF and the downstream vascular effector CEACAM1 were elevated before radiotherapy and declined with time. We also show that MAP Kinase p38 expression usually precede the radiation. Fibrosis scores increase from baseline at 9 and 18 months, while vascular scores decrease at 18 months.
The proposed new nomenclature should be held in obeyance until more supportive data are presented. Possibly, the best way to view CRP is as a continuum that may take one of three forms, inflammation-predominant, vasculopathy-predominant, or mixed.
最近有人提议将“慢性放射性直肠炎”（CRP）的命名改为“放射性相关血管扩张症”，理由是很少观察到炎症迹象。我们在此提供数据支持炎症是引发最终导致CRP特征性变化过程的关键步骤这一观点。
为支持CRP发病机制中的炎症，我们回顾相关文献并公布我们的新结果，包括氨磷汀治疗及促炎因子（p38丝裂原活化蛋白激酶、血管内皮生长因子和癌胚抗原相关细胞黏附分子1）的作用。
在前瞻性初步研究中获取的直肠前壁活检组织的免疫组化结果显示，血管内皮生长因子及下游血管效应分子癌胚抗原相关细胞黏附分子1的表达在放疗前升高，并随时间下降。我们还表明，丝裂原活化蛋白激酶p38的表达通常先于放疗出现。纤维化评分在9个月和18个月时从基线开始增加，而血管评分在18个月时下降。
在有更多支持性数据之前，应暂缓采用提议的新命名。或许，看待CRP的最佳方式是将其视为一个连续统一体，可能呈现三种形式之一：以炎症为主、以血管病变为主或混合型。
