Mehmet IBİS, Mevlut KURT, Fatih SAYGİLİ, Ramazan YİLDİZ, Ibrahim Koral ONAL, Nasser ALİZADEH

Helicobacter Pylori and Gastric Precancerous Lesions: An update

Mide kanseri birkaç dekad boyunca konak onkogenleri ve tümör supresör genlerde meydana gelen değişikliklerle ilişkili olarak gastrit-metaplazidisplazi-kanser sıralaması olarak bilinen birçok-basamaklı-süreç içerisinde gelişir. Helikobakter Pilori (H. pilori) enfeksiyonu mide kanseri ile ilişkisi en net olan risk faktörü olup eliminasyonu bu malign hastalığın insidansını düşürmek açısından en çok umut vaad eden stratejidir. Buna rağmen H. Pilori eradikasyonunun gastrik preneoplastik lezyonların regresyonunu indüklemesi üzerine yapılan çalışmaların sonuçları tartışmalıdır. Tartışmalar genellikle çalışmalarda alınan biyopsi sayısı, bulguların histolojik klasifikasyon metodu, örneklem sayısı ve takip süresi gibi parametrelerdeki heterojeniteden kaynaklanmaktadır. Ek olarak H. Pilori dışında bazı muhtemel veya iyi tanımlanmış faktörler gastrik prekanseröz lezyonların progresyonunu etkileyebilir. Son olarak, "dönüşü olmayan bir nokta" nın gerçekten var olması tartışmalı bulguları kısmen izah edebilir. Burada bir indeks vaka sunmakta, H. Pilori'nin gastrik karsinogenezdeki rolüne dair bilgileri gözden geçirmekte ve ardından H. Pilori eradikasyonunun gastrik prekanseröz lezyonların regresyonu açısından faydasını değerlendirmek üzere güncel çalışmalardan elde edilen bilgileri takdim etmekteyiz

Helikobakter Pilori ve Midenin Prekanseröz Lezyonları: Bir Güncelleme

Gastric cancer (GC) develops through a multistep process known as the gastritis-atrophy-metaplasia-dysplasia-cancer sequence associated with alterations in the expression of host oncogenes and tumor suppressor genes after several decades. Helicobacter pylori (H. pylori) infection is the most consistent risk factor for GC, and its elimination is, therefore, the most promising strategy to reduce the incidence of this malignant disorder. However, the results of the relevant studies are controversial as to whether the H. Pylori eradication effectively induces the regression of gastric preneoplastic lesions. The inconsistencies are likely due to the heterogeneity in studies with respect to the number of biopsy samples taken, the method of histologic classification of findings, sample size, and the duration of the follow-up. Additionally some probable or well-defined factors other than H. Pylori may influence the progression of gastric preneoplastic lesions. Lastly, the real existence of a "point of no return" may partially explain the controversial findings. Here, we present an index case, and review data about the role of H. pylori during gastric carcinogenesis, and subsequently discuss information available from recent studies to evaluate the benefit of the H. pylori eradication for the regression of gastric precancerous lesions

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