腸化生(腸上皮化生)監測

胃部的腸化生(IM)是發展成腸型胃癌的一危險因素。豈因為胃內酸性降低,伴隨胃粘膜改變其外觀偏向腸粘膜。腸化生常發生於幽門螺桿菌感染的患者、吸煙者和酒精飲用者,以及缺乏必需維生素(包括常見於新鮮蔬果中的維生素C)的人身上[1]。膽汁反流也是導致腸化生的危險因素之一。當幽門螺桿菌存在時,需要使用根除治療法來治療,良好的證據顯示這有助於IM的消退[2]。應鼓勵患者戒菸,減少酒精攝入,同時,有證據證明抗氧化劑(新鮮水果和蔬菜和維生素C)可以預防和逆轉IM。

持續監控

胃腸化生(GIM)的患者罹患胃癌的風險可能比一般人高出10倍[3]。 GIM被認為是惡化前病症,可能是對環境刺激如幽門螺桿菌感染、吸煙和高鹽飲食的適應性反應的結果[3]。英國有2項回溯性研究中評估了監測的潛在益處[4,5]。根據研究結果,胃癌的發病率高達11%[5]。內窺鏡監測與早期癌症檢測皆和提高生存率相關[4,5]。此外,GIM和高度不典型增生(HGD)的患者有很高的罹患常見或少見惡性腫瘤的風險[5]。在回顧性[6,7]和前瞻性[8-10]研究皆是。

歐洲對GIM和HGD患者的研究顯示,內窺鏡監測的癌症檢出率為33%〜85%。一項對GIM患者管理的評估顯示,建議對於大多數美國患者,進展為癌症的風險低,並且在臨床上除非其他的胃癌危險因子同時存在(如胃癌家族史和亞洲血統),否則並不需要監測[11]。最近的歐洲普查聲明建議,如果在GIM患者中檢測到低度異型增生,應在1年內使用進行斷層定位切片策略重複進行EGD監測[12]。最理想的後續內窺鏡監測頻率目前尚未知。當兩個連續內窺鏡檢查都沒有發現異常增生時,可能會暫停監測。確診的HGD患者應進行手術或內鏡切除術,因為這些患者罹患共存浸潤性腺癌的機率很高。 25%的HGD患者在一年內會發展為腺癌[13]。如果確診為幽門螺桿菌感染,應進行根除治療。對於診斷為GIM確診後,是否應該對疑似幽門螺桿菌進行治療,目前仍然存在爭議。

參考文獻

  1. You WC, Zhang L, Gail MH, et al. Gastric dysplasia and gastric cancer: Helicobacter pylori, serum vitamin C, and other risk factors. J Natl Cancer Inst 2000;92:1607–12.
  2. Sung JJ, Lin SR, Ching JY, et al Atrophy and intestinal metaplasia one year after cure of H. pylori infection: a prospective, randomized study. Gastroenterology 2000;119:7–14.
  3. Vannella L, Lahner E, Osborn J, et al. Risk factors for progression to gastric neoplastic lesions in patients with atrophic gastritis. Aliment Pharmacol Ther 2010;31:1042-50.
  4. den Hoed CM, Holster IL, Capelle LG, et al. Follow-up of premalignant lesions in patients at risk for progression to gastric cancer. Endoscopy 2013;45:249-56.
  5. Whiting JL, Sigurdsson A, Rowlands DC, et al. The long term results of endoscopic surveillance of premalignant gastric lesions. Gut 2002;50:378-81.
  6. Di Gregorio C, Morandi P, Fante R, et al. Gastric dysplasia. A follow-up study. Am J Gastroenterol 1993;88:1714-9.
  7. Lansdown M, Quirke P, Dixon MF, et al. High grade dysplasia of the gastric mucosa: a marker for gastric carcinoma. Gut 1990;31:977-83.
  8. Farinati F, Rugge M, Di Mario F, et al. Early and advanced gastric cancer in the follow-up of moderate and severe gastric dysplasia patients. A prospective study. I.G.G.E.D.–Interdisciplinary Group on Gastric Epithelial Dysplasia. Endoscopy 1993;25:261-4.
  9. Fertitta AM, Comin U, Terruzzi V, et al. Clinical significance of gastric dysplasia: a multicenter follow-up study. Gastrointestinal Endoscopic Pathology Study Group. Endoscopy 1993;25:265-8.
  10. Rugge M, Leandro G, Farinati F, et al. Gastric epithelial dysplasia. How clinicopathologic background relates to management. Cancer 1995;76:376-82.
  11. Fennerty MB. Gastric intestinal metaplasia on routine endoscopic biopsy. Gastroenterology 2003;125:586-90.
  12. Dinis-Ribeiro M, Areia M, de Vries AC, et al. Management of precancerous conditions and lesions in the stomach (MAPS): guideline from the European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter Study Group (EHSG), European Society of Pathology (ESP), and the Sociedade Portuguesa de Endoscopia Digestiva (SPED). Endoscopy 2012;44:74-94.
  13. Cassaro M, Rugge M, Gutierrez O, et al. Topographic patterns of intestinal metaplasia and gastric cancer. Am J Gastroenterol 2000;95: 1431-8. 54. Toh BH, va.
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