摘要
AIG患者胃部可伴发多种息肉/隆起样病变,包括增生性息肉、泌酸黏膜假性息肉或残存胃底腺黏膜岛、肠型腺瘤/异型增生、幽门腺腺瘤、神经内分泌肿瘤和腺癌等[3,5,15]。增生性息肉是最为常见的良性病变,本中心回顾性分析了胃增生性息肉及非息肉背景胃黏膜的特征,根据增生性息肉患者背景胃底体部黏膜的表现,将增生性息肉分为A型增生性息肉(背景胃底体黏膜呈现AIG表现)、B型增生性息肉(背景胃底体腺黏膜呈现Hp相关性胃炎表现)和其他型增生性息肉(即非A且非B)三种,对比研究发现A型增生性息肉表现出相对独特的临床病理学特征[16]:以多发性息肉为主,息肉在胃内的分布以近端胃为主,且多呈现胃内多区域分布,息肉体积更大、多表现为有蒂或亚蒂型息肉;组织病理学上A型增生性息肉伴发更多癌前病变及癌变灶,推测相比其他类型增生性息肉,A型增生性息肉可能是一种相对独特的疾病,临床应增强对其的认识。
AIG胃底体黏膜可观察到ECL细胞单纯性、线性、微结节样(图6A、6B)、腺瘤样和异型增生灶(图6C、6D)等各级别增生,直至肿瘤细胞团直径≥500μm时可诊断(微小)神经内分泌肿瘤(类癌)[17](图6E、6F)。神经内分泌细胞的单纯性增生指腺体内单个神经内分泌细胞的增多;线性增生指≥5个内分泌细胞呈链状排列且每毫米两条链;微结节样增生指腺体内形成由>5个的内分泌细胞组成的结节,但不超过腺体直径(一般为100～150μm);腺瘤样增生指存在≥5个相互融合的结节;异型增生灶指内分泌细胞结节扩大并融合,直径<500μm(一般为150～500μm),细胞可有一定异型性,并可有微小浸润或新生的间质。需要注意的是,肠上皮化生腺管内的神经内分泌细胞增多不作为评价对象[11]。若肿瘤性神经内分泌细胞微巢(一般直径>100μm)侵及至黏膜下层,不考虑细胞团直径大小,亦可诊断为神经内分泌肿瘤。AIG背景基础上发生的神经内分泌肿瘤称之为胃I型神经内分泌肿瘤。研究结果显示在内镜筛查的AIG患者中胃I型神经内分泌肿瘤的检出率约0.4%～7.0%[18]。胃Ⅰ型神经内分泌肿瘤占胃神经内分泌肿瘤70%～80%,多发较常见,多表现为Grade 1[19]。
文献报道AIG患者有发生胃癌的风险,AIG的胃癌的发生率为1%～3%[20],一项大型系统性综述报道恶性贫血患者胃癌的总发病率约为0.27%/人年,胃癌相对风险接近健康人群的7倍[18]。多项研究报道了AIG相关性胃（早）癌的临床病理特征：中老年女性较为多见，病变主要位于胃上部区域，多呈现为隆起型病变，癌组织病理学上以分化型（乳头状或管状）腺癌多见，黏液表型以胃型或胃肠混合型多见[20-24]；此外AIG患者罹患多发性（同时性或异时性）胃癌的比例显著高于非AIG患者[22,24]。但近期有长期随访研究认为，AIG尤其是未感染过Hp的AIG患者，罹患胃癌的风险并不增加[13,25]，AIG合并胃癌可能与既往或现症Hp感染密切相关[13]。因此AIG与胃癌的关系需要进一步研究证实。
参考文献 (请在框内滑动浏览)
[1] Strickland RG,Mackay IR.A reappraisal of the nature and significance of chronic atrophic gastritis[J].Am J Dig Dis,1973,18(5):426-440.
[2] Di Sabatino A,Lenti MV,Giuffrida P,et al.New insights into immune mechanisms underlying autoimmune diseases of the gastrointestinal tract[J].Autoimmun Rev,2015,14(12):1161-1169.
[3] Park JY,Cornish TC,Lam-Himlin D,et al.Gastric lesions in patients with autoimmune metaplastic atrophic gastritis(AMAG) in a tertiary care setting[J].Am J Surg Pathol,2010,34(11):1591-1598.
[4] Miceli E,Lenti MV,Padula D,et al.Common features of patients with autoimmune atrophic gastritis[J].Clin Gastroenterol Hepatol,2012,10(7):812-814.
[5] Zhang H,Jin Z,Cui R,et al.Autoimmune metaplastic atrophic gastritis in chinese:a study of 320 patients at a large tertiary medical center[J].Scand J Gastroenterol,2017,52(2):150-156.
[6] Lenti MV,Miceli E,Cococcia S,et al.Determinants of diagnostic delay in autoimmune atrophic gastritis[J].Aliment Pharmacol Ther,2019,50(2):167-175.
[7] Kamada T,Watanabe H,Furuta T,et al.Diagnostic criteria and endoscopic and histological findings of autoimmune gastritis in Japan[J].J Gastroenterol,2023,58(3):185-195.
[8]中华医学会消化病学分会,中华医学会消化病学分会消化系统肿瘤协作组.中国慢性胃炎诊治指南(2022年,上海)[J].中华消化杂志,2023,43(3):145-175.
[9] Dixon MF,Genta RM,Yardley JH,et al.Classification and grading of gastritis.The updated Sydney System.International Workshop on the Histopathology of Gastritis,Houston 1994[J].Am J Surg Pathol,1996,20(10):1161-1181.
[10]Massironi S,Zilli A,Elvevi A,et al.The changing face of chronic autoimmune atrophic gastritis:an updated comprehensive perspective[J].Autoimmun Rev,2019,18(3):215-222.
[11]Kushima R,Kotera T,Terao S.Histopathological Finding of Autoimmune Gastritis[J].Stomach and Intestine(Tokyo),2024,59(1):23-33.
[12]Bettington M,Brown I.Autoimmune gastritis:novel clues to histological diagnosis[J].Pathology,2013,45(2):145-149.
[13]Rugge M,Bricca L,Guzzinati S,et al.Autoimmune gastritis:long-term natural history in naive Helicobacter pylori-negative patients[J].Gut.2023,72(1):30-38.
[14]Solcia E,Fiocca R,Villani L,et al.Hyperplastic,dysplastic,and neoplastic enterochromaffin-like-cell proliferations of the gastric mucosa:classification and histogenesis[J].Am J Surg Pathol,1995,19(Suppl 1):S1-S7.
[15]Terao S,Suzuki S,Yaita H,et al.Multicenter study of autoimmune gastritis in Japan:Clinical and endoscopic characteristics[J].Dig Endosc,2020,32(3):364-372.
[16]Zhang H,Nie X,Song Z,et al.Hyperplastic polyps arising in autoimmune metaplastic atrophic gastritis patients:is this a distinct clinicopathological entity?[J].Scand J Gastroenterol,2018,53(10-11):1186-1193.
[17]Rindi G,Inzani F,Solcia E.Pathology of gastrointestinal disorders[J].Endocrinol Metab Clin North Am,2010,39(4):713-727.
[18]Vannella L.Systematic review:gastric cancer incidence in pernicious anaemia[J].Aliment Pharmacol Ther,2013,37(4):375-382.
[19]Grozinsky-Glasberg S,Alexandraki KI,Angelousi A,et al.Gastric Carcinoids[J].Endocrinol Metab Clin North Am,2018,47(3):645-660.
[20]Yaita H,Kurahara K,Oshiro Y,et al.Clinicopathological Features of Gastric Cancer in Patients with Autoimmune Gastritis[J].Stomach and Intestine(Tokyo),2019,54(7):1025-1034.
[21]Kitamura S,Muguruma N,Okamoto K,et al.Clinicopathological characteristics of early gastric cancer associated with autoimmune gastritis[J].JGH Open 2021,5(10):1210-1215.
[22]Nomura K,Kikuchi D,Kawai Y,et al.Clinicopathological Features of Early Gastric Cancer Complicated by Autoimmune Gastritis[J].Dig Dis,2024,42(5):407-413.
[23]Arai J,Niikura R,Hayakawa Y,et al.Clinicopathological Features of Gastric Cancer with Autoimmune Gastritis[J].Biomedicines,2022,10(4):884.
[24]Kang D,Lim CH,Kim JS,et al.Impact of Autoimmune Gastritis on Occurrence of Metachronous Gastric Neoplasms after Endoscopic Resection for Gastric Neoplasms[J].Cancers(Basel),2023,15(19):4859.
[25]Miceli E,Lenti MV,Gentile A,et al.Long-Term Natural History of Autoimmune Gastritis:Results From a Prospective Monocentric Series[J].Am J Gastroenterol,2024,119(5):837-845.
[26]Terao S,Suzuki S,Nishizawa A,et al.Comprehensive Understanding of Clinical,Laboratory,Endoscopic,and Pathologic Findings of Autoimmune Gastritis Based on Its Stage[J].Stomach and Intestine(Tokyo),2024,59(1):10-21.
[27]Chmiela M,Gonciarz W.Molecular mimicry in Helicobacter pylori infections[J].World J Gastroenterol,2017,23(22):3964-3977.
[28]中华医学会消化内镜学分会病理学组.胃黏膜幽门螺杆菌感染病理组织学专家共识[J].中华消化内镜杂志,2023,40(8):589-594.
[29]Saito M,Morioka M,Wakasa K,et al.In Japanese patients with type A gastritis with pernicious anemia the condition is very poorly associated with Helicobacter pylori infection[J].J Infect Chemother,2013,19(2):208-210.
[30]张贺军,金珠,崔荣丽,等.296例自身免疫性萎缩性胃炎的临床特征[C].第十四届全国消化系病学术会议论文集,2014:61.
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