胃镜结果显示萎缩性胃炎、肠化生和非典型增生的致癌风险大约有多少？

在门诊时候，不少患者胃镜诊断为萎缩性胃炎，然后百度了一些知识，就寝食难安，以为自己得癌症的风险非常高！下面用数据介绍萎缩性胃炎相关的的知识，也简单描述了肠化生和非典型增生的致癌风险，供大家参考。

第一部分：基础知识：

萎缩性胃炎主要在由Hp感染或自身免疫等原因引起的慢性炎症的情况下，胃黏膜固有腺体萎缩，伴有或不伴有肠化生。无论病因如何，萎缩性胃炎的诊断均应通过组织病理学确诊，也就是发现黏膜固有腺体萎缩才能确诊。

第二部分：萎缩性胃炎成为胃癌的风险：

在胃镜筛查的人群中，萎缩性胃炎的风险并不低，文献数据通常在20-50%之间。

韩国的一项大样本的临床研究显示，在进行胃镜筛查的10185人中，有3714人患有萎缩性胃炎，占比36.5%，在随访中，没有萎缩性改变的患者，出现胃癌的风险是0.1%，轻度萎缩性胃炎的患者，出现胃癌的可能性是1.6%，中度萎缩性胃炎的患者，出现胃癌的风险是5.2%，重度萎缩性胃炎的患者，出现胃癌的风险是12%。

从萎缩性胃炎到确诊胃癌的时间，轻度的患者是6.6±2.7年，中度是5.8±3.4年，重度是4.9±2.4年，所以通常即使诊断萎缩性胃炎，到确诊胃癌通常都在2年以上。

因此，轻度萎缩性胃炎的患者，其实风险不高，不用太过于担心。

第三部分：肠化生和非典型增生形成胃癌的风险：

荷兰的一项研究，纳入了92250位合并胃部癌前病变的患者，在诊断5年内的随访中，发现萎缩性胃炎的患者每年出现胃癌的风险是0.1%，肠化生的风险是每年0.25%，轻到中度非典型增生每年出现胃癌的风险是0.6%，重度非典型增生的患者每年的风险是6%。

因此，通常来说非典型增生的风险高于肠化生高于萎缩性胃炎。从目前的数据看，只要不是中度和重度的萎缩性胃炎，出现胃癌的风险并不高。

第四部分：萎缩性胃炎的患者，后续如何治疗和监测？

（1）如何治疗？

所有萎缩性胃炎患者需要检测幽门螺杆菌（HP）的感染情况。如果为阳性，应进行幽门螺杆菌治疗，并需要确认成功根除。（ 注意，萎缩性胃炎中有一小部分是自身免疫性萎缩性胃炎，需要消化科专科处理）

（2）内镜复查的间隔？

慢性萎缩性胃炎患者的最佳内镜监测间隔应基于对个体的风险评估，并由共同决策确定。简单的说，就是没有完全一致的时间。

我国指南对内镜监测建议：

对累及全胃的重度慢性萎缩性胃炎（OLGA系统和OLGIM系统分期为Ⅲ和Ⅳ期），每1~2年复查高清内镜；

轻中度、局限于胃窦的慢性萎缩性胃炎建议每３年复查胃镜。

（3）慢性萎缩性胃炎和贫血的关系

一旦确诊慢性萎缩性胃炎，应当评估是否存在铁和维生素B12缺乏，是否引起贫血。同样，对于原因不明的铁或维生素B12缺乏患者，在诊断和鉴别诊断时应考虑萎缩性胃炎。

总结：萎缩性胃炎出现胃癌的风险升高，和胃炎的严重程度相关，肠上皮化生和非典型增生导致的胃癌风险也出现明显升高，尤其是重度非典型增生，风险相当高，需要积极处理。

1. Risk Factors for Gastric Tumorigenesis in Underlying Gastric Mucosal Atrophy

Gut Liver . 2017 Sep 15;11(5):612-619. doi: 10.5009/gnl16488

Background/aims: Atrophic gastritis is considered a premalignant lesion. We aimed to evaluate the risk factors for gastric tumorigenesis in underlying mucosal atrophy.

Methods: A total of 10,185 subjects who underwent upper gastrointestinal endoscopy between 2003 and 2004 were enrolled in this retrospective cohort study. Follow-up endoscopy was performed between 2005 and 2014. Atrophic gastritis and intestinal metaplasia were assessed by endoscopy using the Kimura-Takemoto classification. Helicobacter pylori infection was evaluated based on serum immunoglobulin G antibody levels, the rapid urease test, or the urea breath test.

Results: Atrophic gastritis was confirmed in 3,714 patients at baseline; 2,144 patients were followed up for 6.9 years, and 1,138 exhibited increased atrophy. A total of 69 subjects were diagnosed with gastric neoplasm during follow-up (35 adenoma and 34 carcinoma). Age ≥55 years (hazard ratio [HR], 1.234), alcohol consumption (HR, 1.001), and H. pylori infection (HR, 1.580) were associated with increased mucosal atrophy. The risk factors for gastric neoplasm in underlying mucosal atrophy were age ≥55 years (HR, 2.582), alcohol consumption (HR, 1.003), extent of mucosal atrophy (HR, 2.285 in C3-O1; HR, 4.187 in O2-O3), and intestinal metaplasia (HR, 2.655).

Conclusions: Extent of atrophy, intestinal metaplasia, and alcohol consumption are significant risk factors for gastric neoplasm in underlying mucosal atrophy.

2.Gastric cancer risk in patients with premalignant gastric lesions: a nationwide cohort study in the Netherlands Gastroenterology 2008 Apr;134(4):945-52.

Background ＆ aims: A cascade of precursor lesions (eg, atrophic gastritis, intestinal metaplasia, and dysplasia) precedes most gastric adenocarcinomas. Quantification of gastric cancer risk in patients with premalignant gastric lesions is unclear, however. Consequently, endoscopic surveillance is controversial, especially in Western populations.

Methods: To analyze current surveillance practice and gastric cancer risk in patients with premalignant gastric lesions, all patients with a first diagnosis between 1991 and 2004 were identified in the Dutch nationwide histopathology registry (PALGA); follow-up data were evaluated until December 2005.

Results: In total, 22,365 (24%) patients were diagnosed with atrophic gastritis, 61,707 (67%) with intestinal metaplasia, 7616 (8%) with mild-to-moderate dysplasia, and 562 (0.6%) with severe dysplasia. Patients with a diagnosis of atrophic gastritis, intestinal metaplasia, or mild-to-moderate dysplasia received re-evaluation in 26%, 28%, and 38% of cases, respectively, compared with 61% after a diagnosis of severe dysplasia (P ＜ .001). The annual incidence of gastric cancer was 0.1% for patients with atrophic gastritis, 0.25% for intestinal metaplasia, 0.6% for mild-to-moderate dysplasia, and 6% for severe dysplasia within 5 years after diagnosis. Risk factors for gastric cancer development were increasing severity of premalignant gastric lesions at initial diagnosis (eg, severe dysplasia, hazard ratio 40.14, 95% confidence interval 32.2-50.1), increased age (eg, 75-84 years, hazard ratio 3.75, 95% confidence interval 2.8-5.1), and male gender (hazard ratio 1.50, 95% CI 1.3-1.7).

Conclusions: Patients with premalignant gastric lesions are at considerable risk of gastric cancer. As current surveillance of these patients is inconsistent with their cancer risk, development of guidelines is indicated.