重视几类难辨性胃癌的识别和检漏

胃癌是中国最常见的恶性肿瘤,但临床上包括进展期胃癌在内的误判和漏诊情况严重,特别是浅表扩散型早期胃癌、弥漫浸润型胃癌（皮革胃）和形似胃炎样胃癌。本文介绍这几种胃癌的特点及提高诊断正确性的方法和经验。     

提高胃癌的内镜识别和检漏能力

胃癌是我国最常见的恶性肿瘤之一,目前临床上存在着严重的胃癌漏诊和误判。改变这种状况的关键是提高内镜下对胃癌特别是早期胃癌,也包括皮革胃等进展期胃癌的识别能力。强调临床随访复查是减少胃癌漏诊的重要方法,注重肿瘤标记物在胃癌检漏中的作用。内镜下尤其应该重视浅凹型早期胃癌、浅表扩散型早期胃癌、形似胃炎样胃癌、弥漫浸润型胃癌(皮革胃)的诊断,警惕盲目使用质子泵抑制剂的抑酸治疗,可能导致溃疡型胃癌的"假性愈合"。加强内镜操作规范、病灶识别能力及随访复查制度等方面的改进,才能不断减少胃癌的漏诊和误判,逐步提高胃癌的诊断水平。     

经内镜金属支架治疗胃出口梗阻的应用进展

胃出口梗阻包括远端胃、十二指肠和近端空肠梗阻，患者多表现为恶心、呕吐、营养不良和脱水，常见的病因包括胃癌、胰腺癌、淋巴瘤、壶腹癌、胆管癌、十二指肠和空肠转移性肿瘤以及外压性肿瘤。约85％的胰腺癌患者和40％的胃癌患者在诊断时已无法获得根治性切除，15％～20％无法切除的胰腺癌病例最终出现胃出口梗阻症状，进展期胃癌患者出现胃出口梗阻的几率更高。     

进展期胃癌患者术后肝转移的相关因素分析

目的 探讨影响进展期胃癌患者术后肝转移的相关因素.方法 选择进展期胃癌患者共166例,根据患者术后3年内有无并发肝转移将其分为进展期胃癌伴肝转移组(肝转移组)及进展期胃癌未伴肝转移组(对照组).观察患者性别、年龄、肿瘤发生部位(贲门胃底、胃体、胃窦幽门处)、大体类型(局限溃疡型、浸润型、隆起型)、组织学分型(黏液腺癌、低分化腺癌、未分化腺癌、乳头状/管状腺癌、印戒细胞癌)、浸润深度(T1、T2、T3、T4)、合并淋巴结转移情况(N0、N1、N2、N3)、临床病理分期(Ⅰ、Ⅱ、Ⅲ、Ⅳ期)、肿瘤直径、甲胎蛋白、癌胚抗原等与胃癌转移的相关性.结果 进展期胃癌术后仍然存在着较高的术后复发率(24.7％),单因素分析显示大体类型、组织学分型、肿瘤直径、浸润深度、合并淋巴结转移、临床病理分期以及癌胚抗原等均与进展期胃癌患者肝转移有关.进展期胃癌术后Logistic多因素回归分析中肿瘤直径、浸润深度及临床病理分期是影响进展期胃癌术后复发的独立危险因素.结论 肿瘤直径、浸润深度及临床病理分期是影响进展期胃癌术后复发的独立危险因素,可以作为评价胃癌术后肝转移的相关危险因素.     

浅表扩散型早期胃癌的内镜及临床特点分析

目的探讨浅表扩散型早期胃癌的内镜下形态表现及病理特征。方法收集4年间经手术病理证实的早期胃癌患者466例,其中病灶最长径≥5 cm的浅表扩散型早期胃癌患者26例,回顾性分析其临床资料、内镜下形态、手术记录及术后病理结果,并与普通型早期胃癌进行比较。结果 466例早期胃癌患者中,有26例患者为浅表扩散型,占早期胃癌患者的5.58%。其临床表现以中上腹疼痛居多(80.77%,21/26),内镜下检查病灶累及一个以上胃区者15例(57.69%),镜下形态主要为溃疡增殖型(46.15%,12/26)。手术切除胃癌标本中浅表凹陷型占38.46%,而病理上低分化型及未分化型占61.54%;胃癌灶黏膜下层浸润率及淋巴结转移率都较普通型EGC高(65.38%vs 39.77%,P<0.01;38.46%vs 12.27%,P<0.01)。结论浅表扩散型早期胃癌病灶范围广,边界不易判断;黏膜下层浸润率及淋巴结转移率较高,因此应强调术前癌灶范围的正确界定、手术中病灶的完整切除及区域淋巴结的扩大清扫。     

胃癌自然过程中的胃上皮异型增生:多中心前瞻性随访研究

胃癌有两种类型:即肠型和弥漫型,两者的流行病学、临床、病理及生物学特点均不相同;它们的癌前病变也可能不同:肠型胃癌的癌前病变比较明确,为Ⅰ型(或腺瘤型)异型增生,而弥漫型胃癌的不太明确,可能为Ⅱ型起源于非肠化腺体的异型增生。良好的内镜活检及常规的HE染色迄今仍为主要的和最有效的诊断异型增生的措施。胃上皮异型增生(GED)常在浅表型或进展期胃癌的附近发现,在临床实践中,     

早期胃癌内镜形态学诊断进展

早期胃癌内镜形态学诊断进展殷泙综述许幼如审校根据日本东京癌诊断中心１８年（１９７２～１９８９年）发现的胃癌其形态学变化是Ⅰ型早期胃癌减少；Ⅱａ型早期胃癌，小胃癌，进展期胃癌形似Ⅱｃ型早期胃癌，以及早期皮革样胃型胃癌增加。而这些变化是由于早期胃癌诊断技...     

新世纪里胃癌的发病率能进一步降低吗？

胃癌是最常见的肿瘤之一。胃癌的发病率和死亡率在世界各国分布不均。胃癌的发生与幽门螺杆菌（Hp）感染、基因和环境因素有关。Hp感染是启动肠型胃腺癌发生的扳机。东亚和东欧地区胃癌的发病率较高，而非洲地区Hp感染率虽很高，但胃癌的发病率却很低。早期胃癌的5年生存率明显高于进展期胃癌。提高早期胃癌的诊断率对人类战胜胃癌至关重要。近年来胃癌发病率有下降趋势，随着人民生活水平的提高和科学技术的发展，新世纪胃癌的发病率可能会进一步降低。     

胃癌手术切缘癌残留临床分析（附53例报告）

目的 分析胃癌切除术切缘癌残留的原因及预防手段，减少胃癌术后癌残留的发生率，以提高胃癌的手术效果。方法 采用回顾性分析方法，统计我院近20年胃癌手术病例932例，其中发生癌残留53例。结果 胃癌切除术后癌残留率为5．6％，根治性手术为2．9％，姑息性手术为12．8％。远端胃切除为3．2％，近端胃切除为17．1％。近端胃切除癌残留率明显高于远端胃切除，同时提示胃癌术后发生癌残留与肿瘤的大小、分化程度及浸润深度有关。结论浸润型进展期癌，癌肿直径大干5cm，分化较低及癌肿浸及浆膜者，易发生癌残留。     

胃液紫外光吸收光谱对胃癌诊断价值的初步探讨

目的 探讨胃液高效液相紫外光吸收光谱诊断胃癌的价值。方法 以市郊和液相方法分析了１４４例胃内良恶性病变患者的胃液并以紫外光检测器检测，其中进展其胃癌３７例，萎缩性胃炎３０例，消化性溃疡３０例，慢性浅表性胃炎４７例。结果 进展期胃癌与胃内良性病变患者胃液的高效液相紫外光吸收光谱明显不同，胃癌患者峰位数明显多于胃内良性病变患者，这表明进展期胃癌与胃内良性病变患者胃液的成分明显存在差异。经单因素方差分析     

From gastric inflammation to gastric cancer

The majority of gastric adenocarcinomas are related to chronic inflammation induced by Helicobacter pylori infection. For intestinal-type gastric cancer, a multistep process of mucosal alterations leading from gastritis via glandular atrophy, intestinal metaplasia and dysplasia to invasive carcinoma is well recognized. Ongoing clinical studies focus on a 'point of no return'. It is defined as a situation when certain alterations are no longer reversible by H. pylori eradication and progression to gastric cancer may continue. H. pylori affects the mucosal as well as the systemic immune response by secretion of cytokines and the recruitment of distinct inflammatory cells. The immune response is characterized by a balance between a Th1-dominated response and the recruitment of antigen-specific regulatory T cells that allow the bacteria to persist in human gastric mucosa. Besides immune-mediated effects, H. pylori induces cellular alterations as well as genetic alterations in genes that are essential for the epigenetic integrity and mucosal homeostasis. These genetic alterations during gastric cancer development are in focus of intensive research and should ultimately allow the identification of risk factors involved in gastric carcinogenesis. The detection of individuals at high risk for gastric cancer would help to design appropriate strategies for prevention and surveillance.     

Familial gastric cancer

BACKGROUND: Familial aggregation of gastric cancer has pointed out to a possible hereditary and genetic factor involved in the carcinogenesis of this disease. The diffuse type gastric cancer patients are frequently younger and the tumor has locally infiltrative growth pattern early in its development. Observation of families with frequent early onset gastric cancer has led to the identification of a novel gene implicated in gastric cancer susceptibility: CDH1/E-cadherin. Diffuse familiar gastric cancer is defined as any family presenting: two first-degree relatives with diffuse gastric cancer, one of them with age under 50 years or at least 3 first-degree relatives irrespective age of onset. CASE REPORT: The family reported by us does not fit in any of the classification proposed. The precise identification of these families by clinical and molecular tools is of great importance. The case reported is an example of a family that probably is a form of hereditary gastric cancer not yet fully understood. CONCLUSION: Soon there will be new criteria, possibly including genetic and molecular characteristics.     

A p53 genetic polymorphism of gastric cancer： Difference between early gastric cancer and advanced gastric cancer

INTRODUCTIONGastric cancer is one of the most common malignancies worldwide,although the overall incidence of gastric cancer has been decreasing over the past few decades.Chronic H pylori infection and dietary factors,such as those high in salt or nitrate…