豫西地区胃黏膜不典型增生和肠化生的临床流行病学调查

目的：探讨近4年豫西地区胃黏膜不典型增生和肠化生的相关临床流行病学资料的特点及变化趋势。方法：选取2007年1月-2010年6月我院胃镜室行内镜检查的21932例患者为研究对象,对胃黏膜不典型增生和肠化生患者的一般临床资料和病理资料进行回顾性分析。结果：胃黏膜不典型增生和不典型增生伴肠化生有随年龄增加检出率增高的趋势,且不典型增生程度随年龄增加而程度增高。重度不典型增生≥60岁患者比例高于轻、中度不典型增生,（P〈0.05）,中度不典型增生≥60岁患者比例高于轻度不典型增生;中度肠化生≥60岁患者比例高于轻度肠化生患者（P〈0.05）。贲门部不典型增生和肠化生中≥60岁患者比例高于胃角和胃体部（P〈0.05）,幽门螺杆菌检出率均较单纯慢性浅表性胃炎组高,（P〈0.05）差异有统计学意义。结论：胃黏膜不典型增生和肠化生的发生与年龄和幽门螺杆菌感染有关,常发生于贲门部。     

胃癌及癌前病变与幽门螺杆菌感染相关性的临床分析

目的:测定幽门螺杆菌在萎缩肠化生胃炎,异型增生及胃癌中感染情况,探讨Hp与它们的相关性。方法:萎缩肠化生胃炎(A组)患者342例,异型增生(B组)229例,胃癌患者(C组)298例,采用Hp抗体ELISA法检测血清抗Hp-IgG抗体。结果:肠化生患者较非肠化生胃黏膜中的Hp感染多见。异型增生和胃癌的Hp感染率均高于萎缩性胃炎组(P<0.05),异型增生和胃癌两者间的Hp感染率亦存在差异(P<0.05)。幽门螺杆菌感染的萎缩肠化生胃炎及异性增生较非幽门螺杆菌感染者发生癌变的差异性显著,P<0.05;幽门螺杆菌感染的胃癌5年生存期显著短于非感染者,P<0.05。结论:Hp感染与萎缩肠化生胃炎,异型增生及胃癌有密切相关性,并缩短萎缩肠化生胃炎,异型增生癌变时间,缩短胃癌5年生存时间。     

胃癌癌前病变端粒酶活性检测的临床意义

目的通过检测胃黏膜不同病理类型的端粒酶活性,探讨胃癌发生发展进程中端粒酶活性的变化规律及胃癌癌前病变端粒酶活性检测的临床意义.方法采用TRAP-PCR银染定性及TRAP-PCR-EILIA定量法,对浅表性胃炎、肠上皮化生、不典型增生、胃癌的胃黏膜活检组织的端粒酶活性进行检测.结果端粒酶阳性率及活性水平胃癌＞不典型增生＞肠上皮化生＞浅表性胃炎,肠上皮化生、不典型增生、胃癌分别与浅表性胃炎比较,差异有高度显著性(P＜0.01),胃癌与肠上皮化生、不典型增生分别比较,差异有高度显著性(P＜0.01);不完全结肠型肠化生的端粒酶活性水平高于完全结肠型、完全小肠型、不完全小肠型等肠化生(P=0.0105),中度不典型增生的端粒酶活性水平高于轻度不典型增生(P=0.0302).结论端粒酶的活化、活性上调是胃癌癌变过程中的早期事件,胃癌癌前病变肠化生、不典型增生端粒酶活性上调者可能更具恶变倾向,临床上对指导其治疗和评价预后有一定意义.     

根除HP感染对胃黏膜炎症和肠腺化生的影响

目的:探讨根除幽门螺杆菌(helicobacter pylori,HP)感染对胃黏膜炎症和肠腺化生(intestinal meta-plasia,IM)的意义。方法:随访119例10年前HP感染的患者,其中62例行根除HP治疗(治疗组),57例中断治疗或仅接受对症治疗(对照组),对比其前后HP感染情况、胃黏膜炎症及肠腺化生(IM)的变化情况。结果:10年后对照组中45/57例HP呈阳性(78.94%);治疗组中15例HP呈阳性(24.19%),胃炎活动性检出率明显减少与对照组持续HP感染者比较,差异有显著性(P<0.01),肠腺化生(IM)的程度也显著减轻(P<0.05)。结论:HP感染与胃黏膜活动性炎症关系非常密切,根除HP可以减轻胃黏膜的炎症和肠腺化生(IM)程度。     

幽门螺杆菌感染的胃黏膜上皮细皮细胞环氧合酶-2表达及意义

目的探讨幽门螺杆菌(Hp)感染的胃黏膜上皮细胞环氧合酶-2(COX-2)的表达及其在胃黏膜癌变过程中的意义.方法采用快速尿素酶试验和组织学碱性品红染色法检测胃黏膜Hp 感染状况;应用免疫组化法检测胃黏膜上皮细胞COX-2表达状况.结果 32例胃癌中,COX-2表达阳性22例(68.7%).12例Hp阴性的胃黏膜中,有1例(8.3%)COX-2低表达;10例Hp阳性正常胃黏膜中,仅1例(10.0%)COX-2低表达;9例Hp阳性的胃黏膜充血水肿糜烂者中,有5例(55.6%)COX-2表达阳性,与Hp阴性者和Hp阳性正常胃黏膜者比较,差异有统计学意义(P<0.05);10例Hp阳性的轻度萎缩性胃炎伴轻度肠化生者中,COX-2表达阳性5例(50.0%);10例Hp阳性的中重度萎缩性胃炎伴中重度肠化生者中,COX-2表达阳性8例(80.0%);8例Hp阳性的中重度不典型增生者中,COX-2表达阳性6例(75.0%).中重度萎缩性胃炎伴中重度肠化生和不典型增生者的COX-2表达高于轻度萎缩性胃炎伴轻度肠化生者(P<0.05).结论 Hp感染诱导慢性浅表性胃炎黏膜上皮细胞的COX-2表达与黏膜损伤形成有关;根据胃癌发生模式,COX-2表达上调与Hp感染胃黏膜癌变发生相关,且可能在癌前病变形成早期阶段起作用.     

幽门螺杆菌感染与胃癌前病变及胃癌的相关性研究

 目的　从病理形态学方面探讨幽门螺杆菌 ( Helicobacter pylori,Hp)感染与胃粘膜癌前病变和胃癌的关系。方法　采用 HE、Warthin- Starry及 HID- AB( p H2 .5) - PAS染色法 ,对 1 51例胃镜活检及手术切除胃标本中慢性萎缩性胃炎 ( CAG)、胃上皮不典型增生 ( gastric epithelialdysplasia,GED)、肠上皮化生 ( intestinal metaplasia,IM)及胃癌 ( Ca)组织中 Hp的感染状况进行观察 ,并对 Hp的感染与各病变间的关系进行对比研究。结果　本组病例胃粘膜 Hp检出率为 66.2 %( 1 0 0 /1 51 )。 Hp的感染主要见于胃贲门以外部位 ,尤其胃窦部多见 ,但 Hp感染与 CAG、IMI、 型及弥漫型胃癌的发生无明显关系 ( ( P>0 .0 5) ,与 GED(尤其 GED 、 级 )、IM 型和肠型胃癌的发生显著相关 ( P<0 .0 5)。结论　Hp感染是导致胃粘膜 型肠上皮化生、中度和重度不典型增生及肠型胃癌的重要致病因素 ,应引起高度重视.     

胃癌高发区幽门螺杆菌感染与胃黏膜肠化生关系的研究

目的:探讨陕北胃癌高发区幽门螺杆菌(HP)感染与胃黏膜肠化生之间的关系.方法:收集两次普查中行胃镜检查的病例共487例,把慢性胃炎病例(479例)分为无肠化生及轻、中、重度肠化生4组,检测、比较各组之间HP的感染率.结果:无肠化生及轻、中、重度肠化生组HP感染率分别为55.87%、80.52%、76.56%、67.74%.轻、中度肠化生组HP感染率明显高于无肠化生组(P值均＜0.05).其余各组之间HP感染率比较无显著性差异(P值均＞0.05).结论:陕北胃癌高发区轻、中度肠化生与HP感染密切相关.     

慢性萎缩性胃炎的中医中药康复治疗

慢性胃炎包括浅表性胃炎和萎缩性胃炎。其中慢性萎缩性胃炎伴有胃黏膜肠上皮化生或中度、重度不典型细胞增生及幽门螺杆菌（HP）感染。由于胃酸分泌缺乏,胃排空时间延长,为致病菌或致癌物质的接触提供了有利的环境,致使病人常会集中表现胃部各种痛、胀等不适症状,     

能否早期发现胃癌？

近几年来，很多学者对幽门螺杆菌与胃癌的关系作了很多研究，并提出了较为一致的结论，即幽门螺杆菌感染在胃癌的发生中起一定的作用：幽门螺杆菌感染一慢性胃炎一胃黏膜萎缩一肠上皮化生一不典型增生一胃癌这一模式已被部分学者所认同。     

根除HP感染对胃黏膜炎症和肠腺化生的影响

目的：探讨根除幽门螺杆菌（helicobacter pylori,HP）感染对胃黏膜炎症和肠腺化生（intestinal meta-plasia,IM）的意义。方法：随访119例10年前HP感染的患者,其中62例行根除HP治疗（治疗组）,57例中断治疗或仅接受对症治疗（对照组）,对比其前后HP感染情况、胃黏膜炎症及肠腺化生（IM）的变化情况。结果：10年后对照组中45/57例HP呈阳性（78.94%）;治疗组中15例HP呈阳性（24.19%）,胃炎活动性检出率明显减少与对照组持续HP感染者比较,差异有显著性（P〈0.01）,肠腺化生（IM）的程度也显著减轻（P〈0.05）。结论：HP感染与胃黏膜活动性炎症关系非常密切,根除HP可以减轻胃黏膜的炎症和肠腺化生（IM）程度。     

Intestinal metaplasia is the probable common precursor of adenocarcinoma in barrett esophagus and adenocarcinoma of the gastric cardia

BACKGROUND: Intestinal metaplasia in the tubular esophagus is the recognized precancerous lesion of adenocarcinoma in Barrett esophagus. However, it is not yet clear whether adenocarcinoma of the gastric cardia arises from the same premalignant lesion, i.e., intestinal metaplasia of the gastric cardia. The purpose of this study was to compare adenocarcinomas in Barrett esophagus and adenocarcinomas of the gastric cardia at an early stage, when it was more likely that intestinal metaplasia had not been completely overgrown by the tumor. METHODS: The authors compared the epidemiologic, clinical, and pathologic features of early stage adenocarcinoma in Barrett esophagus and adenocarcinoma of the gastric cardia from 42 patients who underwent resection surgery. The presence of intestinal metaplasia was assessed in the resected specimens by using Alcian blue (pH 2.5) staining. RESULTS: Intestinal metaplasia was detected in the mucosa adjacent to neoplasia in 25 of 26 patients with adenocarcinoma in Barrett esophagus and in 11 of 16 (69%) patients with adenocarcinoma of the gastric cardia. Patient and tumor characteristics and survival were comparable in both groups. CONCLUSIONS: Intestinal metaplasia is a very common finding in the mucosa adjacent to early stage adenocarcinoma of the gastric cardia. Adenocarcinoma in Barrett esophagus and adenocarcinoma of the gastric cardia may represent the same disease; the former arises from longer segments of intestinal metaplasia and the latter from intestinal metaplasia of the cardia.     

The mucosa of the gastric remnant harboring malignancy. Histologic findings in the biopsy specimens of 504 asymptomatic patients 15 to 46 years after partial gastrectomy with emphasis on nonmalignant lesions

Endoscopic bioptic screening of 504 asymptomatic postgastrectomy patients, 15 to 46 years after initial surgery, revealed ten gastric stump cancers of which six turned out to be early cancers; three of the early carcinomas were found during follow-up after prior severe dysplasia. At first endoscopy mild dysplasia was found in 58, moderate dysplasia in 11, and severe dysplasia in none of the patients. Follow-up biopsies in 177 patients showed mild dysplasia in 30, moderate dysplasia in six, and severe dysplasia in six patients. Regression of severe dysplasia was not observed. Both progression and regression of mild and moderate dysplasia occurred. At the first endoscopy the frequency of atrophy, intestinal metaplasia, cystic dilatation of glands, and foveolar hyperplasia in the stomal biopsy specimens was 45%, 35%, 54%, and 47%, respectively; during follow-up, 47%, 48%, 56%, and 56% respectively. These four lesions were significantly more frequent in the biopsy specimens of patients with gastric carcinoma or dysplasia than in the other patients and they were present in the environment of the tumor in all the surgical specimens of the six early cancers detected by the screening. Preoperatively a combination of these four lesions could be demonstrated in only those early gastric cancer patients, in whom more than eight stomal biopsy specimens were taken. Of 34 patients with severe atrophy in three or more stomal biopsy specimens taken at the same time, two manifested early stump cancer during follow-up. Severe dysplasia is a marker of malignancy and demands close follow-up; the value of mild and moderate dysplasia is less clear. The combination of atrophy, especially severe atrophy, intestinal metaplasia, cystic dilatation, and foveolar hyperplasia in the biopsy specimens of a single patient may also point to increased cancer risk. It is advisable to obtain multiple biopsy specimens of the anastomosis, also because early gastric cancer may occur without a suspect macroscopic appearance.     

胃癌前病变AgNOR面积及形态与其DNA含量的对照研究

本文应用计算机图象分析系统对１０例肠化、３０例不同程度异型增生的胃粘膜，１０例正常胃粘膜和１０例高分化腺癌细胞核内ＡｇＮＯＲ蛋白的面积及其颗粒的形状进行了定量，并测定了其ＤＮＡ含量，结果显示，随胃粘膜病变程度的加重，其核内ＡｇＮＯＲ蛋白与ＤＮＡ含量依次增加，而ＡｇＮＯＲ颗粒的形状因子呈递减趋势。ＡｇＮＯＲ蛋白面积／核和其颗粒的形状因子与ＤＮＡ含量均有良好的线性相关关系，前者为正相关（ｒ＝０．９９Ｐ＜０．００１），后者为负相关（ｒ＝－０．９５２Ｐ＜０．００１）。我们认为，ＡｇＮＯＲ面积及其颗粒的形状可以反映出胃粘膜的病变程度。可作为胃癌前病变诊断及病情监测的有用指标。     

Gastric carcinoma: pathology findings in a multiethnic population

OBJECTIVES: To assess the pathology of gastric carcinoma and to determine whether carcinoma of the cardia occurs more often among whites than among other ethnic groups in Hawaii. This study focuses on demographic differences in subsite locations and histologic types of gastric carcinoma. METHODS: We reviewed 532 sequential gastric carcinomas accessioned between 1993 and 1999 in the Hawaii Tumor Registry. Pathology reports and slides were reviewed by the study pathologist. RESULTS: Carcinoma of the cardia occurred in 51 (15.8%) of 323 males compared with 18 (8.6%) of 209 females (P = 0.02, after age adjustment). The age-adjusted percent of cardia cases was 41.8% for Hawaiian white males compared with 13.4% for men of all other ethnic groups (P = 0.0002). The age-adjusted percent of cardia cases was 22.4% for Hawaiian white females compared with 7.3% for females of other groups. (P = 0.08). At all age levels, females had more frequent diffuse carcinomas and less frequent intestinal type gastric carcinomas than men. The age-adjusted percent with diffuse carcinoma was 35.3% for females and 13.7% for males (P < 0.0001). Also, the sex-adjusted percent with diffuse carcinoma was 26.0% for patients younger than 75 years of age compared with 17.0% for patients 75 years or older (P = 0.01). Conversely, the sex-adjusted percent with intestinal carcinoma was 67.9% for patients younger than 75 years of age compared with 77.1% for patients 75 years or older (P = 0.02). The proportion of cases showing precursor lesions (intestinal metaplasia or superficial gastritis) increased progressively with the distance of the carcinoma from the cardia. CONCLUSIONS: Carcinoma of the cardia is predominantly a tumor of white males and is not associated with the multifocal gastritis characteristically found with carcinoma distal to the cardia. Diffuse gastric carcinoma shows no ethnic predilection, but expression of this phenotype is clearly related to the age and gender of the patient.     

Cigarette smoking and other risk factors for progression of precancerous stomach lesions.

BACKGROUND: Stomach cancer is generally thought to evolve through a series of gastric mucosal changes, but the determinants of the precancerous lesions are not well understood. PURPOSE: Our purpose was to assess risk factors for intestinal metaplasia and gastric dysplasia arising from chronic atrophic gastritis in a general population at high risk for stomach cancer. METHODS: A population-based gastroscopic screening of more than 3000 residents was conducted in a county in China with one of the world's highest rates of stomach cancer. Information on the lifestyle and other characteristics of the participants was obtained by interview, and responses were compared between those in whom the most advanced gastric lesion was dysplasia or intestinal metaplasia versus those with chronic atrophic gastritis. RESULTS: Cigarette smoking was found to nearly double the risk of transition to dysplasia and to be a mild risk factor for intestinal metaplasia. Smoking accounted almost entirely for the 55% higher prevalence of dysplasia among men than among women. Risk of transition to dysplasia had a weak association with several dietary factors and was increased among those participants with a family history of stomach cancer and with blood type A. CONCLUSIONS: The findings provide strong evidence for a role of tobacco consumption and offer clues to other environmental and genetic factors involved in the process of gastric carcinogenesis.     

Occurrence of intestinal metaplasia of the stomach in Thai patients with gastritis, benign ulcer, and gastric cancer

Pathological sections of gastrectomized specimens of 74 patients with benign gastric ulcer and 79 with gastric cancer were reviewed. Intestinal metaplasia was found in 26 specimens with benign ulcer (35.1%) and in 43 with cancer (54.4%), a difference that is statistically significant. Further analysis of age groups showed that rate of occurrence of metaplasia in cancer patients older than 60 years was 70.3%, which was significantly higher than that of their younger counterparts (40.5%) and of patients with benign ulcer of either age group. A survey was also conducted by taking biopsies of mucosa of antrum and body of the stomach of 250 patients who underwent gastroscopic examinations. Acute and chronic gastritis was found in 22 and 156 patients, respectively. Intestinal metaplasia was found to be associated with acute gastritis in 2 (9.1%) and with chronic gastritis in 25 (16%) patients. In conclusion, intestinal metaplasia was associated with higher proportion than it was with benign gastric ulcer and gastritis among Thai patients.     

幽门螺杆菌感染和环氧合酶-2表达在胃癌发生中的作用

目的探讨幽门螺杆菌 (Hp) 感染和环氧合酶-2(COX-2)表达在胃癌发生中的作用.方法 138例胃镜活检标本包括慢性非萎缩性胃炎30例,慢性萎缩性胃炎85例(其中伴有中度以上肠化生45例,中、重度异型增生12例),和胃癌23例.快速尿素酶试验和组织学改良Giemsa染色联合检测Hp,免疫组化检查COX-1和COX-2表达.结果胃癌的Hp阳性率为69.6%,显著高于慢性非萎缩性胃炎的36.7%(P<0.05).慢性非萎缩性胃炎、慢性萎缩性胃炎、肠化生、异型增生和胃癌的COX-2表达率分别为10.0%、37.6%、37.8%、41.7%和69.6%,而不同胃黏膜病变中COX-1表达无明显差异.慢性萎缩性胃炎、肠化生和异型增生中Hp阳性病例的COX-2表达显著高于Hp阴性病例(P<0.01).结论 Hp感染及其诱导的COX-2表达可能是胃癌发生的早期事件之一.     

Claudin-4, mitogen-activated protein kinase kinase 4, and stratifin are markers of gastric adenocarcinoma precursor lesions.

Approximately 23,000 new gastric cancer cases and 12,000 associated deaths occur annually in the United States. Intestinal metaplasia and gastric epithelial dysplasia are precursor lesions to gastric adenocarcinoma, but are not readily detectable clinically, radiographically, or endoscopically. A noninvasive method of precursor detection would require the ability to distinguish precursor lesions from adjacent normal mucosa. In search of such markers, tissue microarrays were prepared for 133 patients of resected gastric adenocarcinoma. Tissue microarrays contained primary cancer, normal stomach, intestinal metaplasia, and gastric epithelial dysplasia and were probed with antibodies against nine potential markers that were either identified in a database of genes overexpressed in gastric adenocarcinoma or were already of interest to our laboratory: claudin-4, mitogen-activated protein kinase kinase 4 (MKK4), 14-3-3sigma (stratifin), S100A4, mesothelin, fascin, topoisomerase IIalpha, HER-2/neu, and epithelial growth factor receptor. Three markers discriminated gastric adenocarcinoma precursor lesions from normal gastric mucosa. Claudin-4 expression was present in 36 intestinal metaplasia lesions (100%) and 14 gastric epithelial dysplasia lesions (100%), but in only 16 normal stomach samples (15%). MKK4 expression was present in 24 intestinal metaplasia lesions (89%) and 12 gastric epithelial dysplasia lesions (100%), but in only 6 normal stomach samples (8%). Stratifin expression was present in 29 intestinal metaplasia lesions (97%) and 8 gastric epithelial dysplasia lesions (100%), but in only 2 normal stomach samples (3%). Sensitivity and specificity for detection of the precursor lesion intestinal metaplasia were 100% and 85%, respectively, for claudin-4; 89% and 92%, respectively, for MKK4; and 97% and 97%, respectively, for stratifin. In primary cancers, 123 of 125 (98.4%) were positive for claudin-4, 116 of 126 (94%) for MKK4, and 111 of 120 (92%) for stratifin. In conclusion, claudin-4, MKK4, and stratifin immunolabeling detects precursor lesions of gastric adenocarcinoma that are otherwise clinically, radiographically, and endoscopically inapparent. These findings may prove useful in the diagnosis and therapeutic targeting of gastric adenocarcinoma precursor lesions.