He-Ne激光对慢性萎缩性胃炎大鼠胃黏膜的影响

为探讨He-Ne激光对慢性萎缩性胃炎(CAG)大鼠胃黏膜的影响,将52只成年雄性Wistar大鼠随机分成正常组、非治疗组及各激光治疗组。应用2%水杨酸钠和30%酒精的混合溶液灌胃8周,刺激大鼠胃黏膜,并结合劳累、饥饱失常等多因素方法建立大鼠CAG模型,各治疗组在造模完成后,分别给予不同剂量(6.24J·cm-2,4.80J·cm-2,3.36J·cm-2)的He-Ne激光照射,每日一次,连续20d,观察各组大鼠胃黏膜的变化。发现3.36J·cm-2的He-Ne激光组与非治疗组比较,胃黏膜变厚(P<0.01),炎细胞减少(P<0.05),细胞形态、结构、体积、均恢复或接近正常;CyclinD1的阳性表达率较高(P<0.05)。表明3.36J·cm-2的He-Ne激光照射能够促进CAG大鼠的胃黏膜功能恢复,疗效显著。     

红外线、He-Ne激光照射对CAG大鼠胃酸的影响

目的:探讨红外线、He-Ne激光对慢性萎缩性胃炎(CAG)大鼠胃酸的影响.方法:将63只成年雄性Wistar大鼠随机分成正常组、模型组,红外线组及各激光照射组.应用2%水杨酸钠和30%酒精的混合溶液灌胃8周,刺激大鼠胃粘膜,并结合劳累、饥饱失常等多因素方法建立大鼠CAG模型,照射组在建模完成后,分别给予红外线、不同剂量的He-Ne激光照射,每日一次.照射20天后,观察各组大鼠胃酸的变化.结果:红外线组及3.36 J/cm2的He-Ne激光组与模型组比较,胃酸分泌明显增多.结论:红外线及3.36J/cm2的He-Ne激光照射能够促进CAG大鼠的胃酸分泌,对大鼠CAG有较好的治疗作用.     

不同年龄组人群胃粘膜病变的观察(3258例胃非恶性肿瘤标本的分析研究)

本文对我国3258例非胃恶性肿瘤标本不同年龄组人群的胃粘膜良性病变进行了观察,发现CSG、CAG、IM、ATP(异型增生)、胃和十二指肠溃疡的检出率均随年龄增长有增高的趋势,高发年龄除CSG为30～39岁外,余者均为40～49岁,此与我国胃癌高发年龄(50～59岁)相比均提前10～20年,符合文献上记载从癌前状态发展为癌前病变直至癌的所需时间。各种病变检出率为IM1914例(58.75%)、CAG1850例(56.78%)、CSG1356例(41.62%)、GU1335例(40.98%)、DU 1221例(37.48%)。ATP1113例(34.16%)。在CAG中IM和ATP均高,在伴ATP中,肠化型CAG(37.35%)又高于非肠化型(5.72%),因此伴异型肠化的萎缩性胃炎可能与我国胃癌高发密切相关。     

云母对大鼠慢性萎缩性胃炎的预防作用及机制研究

目的：研究云母对大鼠慢性萎缩性胃炎的预防作用并探讨其机制。 〖HTH〗方法：以60%的乙醇、20 mmol/L 的去氧胆酸钠和0.1%的氨水在24周建立SD大鼠慢性萎缩性胃炎模型。在造模的同时用云母进行预防实验。实验终期观察鼠胃黏膜大体观及各项病理学指标，并检测血清表皮生长因子和生长激素浓度。 〖HTH〗结果：云母预防组胃黏膜腺体排列规则，无明显的萎缩现象；胃窦部的胃黏膜炎症级别低于模型组（P<0.01）；胃黏膜腺体厚度(L1)和黏膜肌层厚度(L2)之比(L1/L2) 高于模型组（P<0.01）；单位长度内胃黏膜腺体数目高于模型组（P<0.01）。与正常组无明显差别（P>0.05）。胃窦部黏膜增殖细胞核抗原表达阳性的高度及血清表皮生长因子浓度高于模型组(P<0.01，P<0.05),而生长激素浓度与模型组无明显差别。 〖HTH〗结论： 云母对大鼠慢性萎缩性胃炎的形成有预防作用。减少损伤因子的破坏作用、促进胃黏膜细胞增殖及内源性的表皮生长因子分泌，可能是其重要作用机制。     

红外线对CAG大鼠治疗作用的病理学研究

目的:观察红外线对实验性大鼠慢性萎缩性胃炎的治疗作用.方法:采用水杨酸钠、酒精灌胃,刺激大鼠胃粘膜,并结合劳累、饥饱失常等多因素方法连续造模8周,建立慢性萎缩性胃炎(CAG)大鼠模型..红外线治疗采用220V,200W的红外线灯,垂直照射大鼠胃部投影区,1次/日,10min/次,连续照射20天.光镜下观察胃粘膜的炎症程度及壁细胞的形态、结构等,用测微器测量胃粘膜厚度.结果:模型组大鼠体质量明显减轻(P＜0.01),胃粘膜变薄(P＜0.01).光镜下可见胃粘膜层腺体萎缩,炎细胞浸润,部分标本伴有肠上皮化生.红外线治疗组大鼠胃粘膜增厚,与正常对照组比较差异显著(P＜0.01).炎细胞明显减少(P＜0.05),细胞形态、结构、体积均恢复或接近正常.结论:红外线是一种治疗大鼠慢性萎缩性胃炎的有效途径.     

不同胃黏膜病变患者的血清胃蛋白酶原变化

目的：探讨胃溃疡、十二指肠球部溃疡、非萎缩性胃炎、萎缩性胃炎、胃癌患者胃蛋白酶原(pepsinogen,PG)Ⅰ、PGⅡ水平和PGⅠ/PGⅡ比值变化。方法：选择2015年1月至2015年10月因消化道症状行胃镜检查的门诊及住院患者共133例,根据胃镜检查及组织病理学结果,将受检者分为5组。非萎缩性胃炎组42例、萎缩性胃炎组33例、胃溃疡组20例、十二指肠球部溃疡组23例、胃癌组15例、比较各组血清PGⅠ、PGⅡ水平。结果：与非萎缩性胃炎组相比,胃溃疡、十二指肠球部溃疡患者PGI明显升高(P<0.05),胃溃疡PGII明显升高(P<0.05),萎缩性胃炎组、胃癌组血清PGⅠ及PGⅠ/PGⅡ水平降低(P<0.05)。结论：血清PGⅠ、PGⅡ水平以及PGⅠ/PGⅡ比值对提高消化性溃疡、胃癌前病变及胃癌的诊断有重要的临床价值。     

Comparative proteomics analysis of chronic atrophic gastritis: changes of protein expression in chronic atrophic gastritis with out Helicobacter pylori infection

Chronic atrophic gastritis (CAG) is a very common gastritis and one of the major precursor lesions of gastric cancer, one of the most common cancers worldwide. The molecular mechanism underlying CAG is unclear, but its elucidation is essential for the prevention and early detection of gastric cancer and appropriate intervention. A combination of two-dimensional gel electrophoresis and mass spectrometry was used in the present study to analyze the differentially expressed proteins. Samples from 21 patients (9 females and 12 males; mean age: 61.8 years) were used. We identified 18 differentially expressed proteins in CAG compared with matched normal mucosa. Eight proteins were up-regulated and 10 down-regulated in CAG when compared with the same amounts of proteins in individually matched normal gastric mucosa. Two novel proteins, proteasome activator subunit 1 (PSME1), which was down-regulated in CAG, and ribosomal protein S12 (RPS12), which was up-regulated in CAG, were further investigated. Their expression was validated by Western blot and RT-PCR in 15 CAG samples matched with normal mucosa. The expression level of RPS12 was significantly higher in CAG than in matched normal gastric mucosa (P < 0.05). In contrast, the expression level of PSME1 in CAG was significantly lower than in matched normal gastric mucosa (P < 0.05). This study clearly demonstrated that there are some changes in protein expression between CAG and normal mucosa. In these changes, down-regulation of PSME1 and up-regulation of RPS12 could be involved in the development of CAG. Thus, the differentially expressed proteins might play important roles in CAG as functional molecules.     

养胃冲剂对大鼠慢性萎缩性胃炎胃黏膜的保护作用

目的　观察养胃冲剂对慢性萎缩性胃炎组织病理学变化的影响。方法　施行胃 肠吻合术建立慢性萎缩性胃炎 ,连续灌胃给药 3个月后 ,大体观察并作石蜡切片 ,HE染色后在显微镜下观察并拍照。结果　养胃冲剂能明显改善胃上皮损伤程度、减少炎症浸润范围 ,缩小胃小凹的宽度 ,与模型组比较有明显差异 (P <0 0 5) ,与阳性对照组无差别 (P >0 0 5)。结论　养胃冲剂通过减轻胃黏膜炎症反应、逆转肠上皮化生能有效的修复损伤的胃黏膜 ,从而改善胃黏膜萎缩     

胃蛋白酶原Ⅰ、Ⅱ测定在胃癌早期诊断中的研究

研究血清胃蛋白酶原Ⅰ、Ⅱ含量变化与胃癌发生的关系,探讨血清胃蛋白酶原Ⅰ、Ⅱ作为胃癌早期诊断标志物的可行性.应用化学发光法测定非萎缩性胃炎、慢性萎缩性胃炎、胃癌患者的血清胃蛋白酶原Ⅰ、Ⅱ的含量并计算其比值的变化.结果显示:与非萎缩性胃炎组相比,萎缩性胃炎和胃癌组血清胃蛋白酶原Ⅰ水平下降,差异均有统计学意义(P<0.05)...     

益气清热活血方治疗慢性萎缩性胃炎及其 癌前期病变的临床研究

目的 观察益气清热活血方治疗慢性萎缩性胃炎及其癌前期病变的临床效果。方法 选取2015年12月~2017年11月在我院诊治的110例慢性萎缩性胃炎及其癌前期病变患者为研究对象,随机分为对照组和治疗组,各55例。对照组采用胃复春片治疗,治疗组在此基础上采用益气清热活血方治疗,对比两组患者临床症状评分、胃黏膜EGF,EGFR、TGF-a水平、黏膜萎缩、IM和Dys积分。结果 治疗组总有效率90.90%,高于对照组的72.72%,差异有统计学意义（P＜0.05）;治疗后两组患者胃痛、嗳气、乏力、口苦等临床症状评分降低,与治疗前对比,差异有统计学意义（P＜0.05）,且治疗组降低高于对照组,差异有统计学意义（P＜0.05）;治疗后两组患者胃黏膜EGF,EGFR、TGF-a表达量均下降,与治疗前对比,差异有统计学意义（P＜0.05）,且治疗组降低程度低于对照组,差异有统计学意义（P＜0.05）;治疗后两组患者黏膜萎缩、IM和Dys积分下降,与治疗前对比,差异有统计学意义（P＜0.05）,治疗组降低程度优于对照组,差异有统计学意义（P＜0.05）;两组患者均未发生严重不良反应。结论 益气清热活血方治疗慢性萎缩性胃炎及其癌前期病变效果显著,可提高治疗有效率,改善临床症状,减轻病变组织的增值,对患者的康复具有重要的作用。     

慢性萎缩性胃炎患者Hp 感染与TGF-β、IL-6 和TNF-αRII 的表达研究

目的:探讨慢性萎缩性胃炎患者幽门螺旋杆菌感染与胃黏膜中转化生长因子茁受体域、白介素6 和肿瘤坏死因子琢的表达情况。方法:选取76例慢性萎缩性胃炎(CAG)患者胃黏膜病变组织的胃镜活检标本,采取PCR 荧光法检测Hp 感染情况,免疫组化法检测TGF-βRⅡ、IL-6 和TNF-α在胃小凹上皮和间质炎细胞中的表达。结果:慢性炎症程度在Hp感染阳性组和阴性组中差异有统计学意义(P<0.05);间质炎细胞中IL-6的表达在Hp感染阳性组和阴性组中差异有统计学意义(P<0.05);TGF-βRⅡ、TNF-α的表达在Hp感染阳性组和阴性组中无显著性差异(P>0.05);间质炎细胞中IL-6与慢性炎症程度呈正相关关系(r=0.249,P=0.03);萎缩程度与肠上皮化生严重程度、上皮内瘤变程度呈正相关关系(r=0.697,0.366)。结论:IL-6在间质炎性细胞中的表达与Hp相关性CAG患者的慢性炎症程度有关,慢性萎缩程度促进肠上皮化生和上皮内瘤变的发生。     

胃癌组织cyclinE和p21~(WAF1/CIP1)蛋白表达的意义

目的 :探讨cyclinE和p2 1WAF1/CIP1蛋白在胃癌发生发展中的作用及其表达的意义。方法 :采用免疫组化S P法检测正常胃黏膜、萎缩性胃炎伴肠上皮化生、萎缩性胃炎伴不典型增生各 2 0例和 78例胃腺癌组织中cyclinE和 p2 1WAF1/CIP1蛋白表达。结果 :cyclinE蛋白阳性表达在胃癌组高于正常胃黏膜、萎缩性胃炎伴肠上皮化生组 ,而 p2 1WAF1/CIP1蛋白表达则相反 ,差异均有显著性 (P <0 0 5 ) ;cyclinE、p2 1WAF1/CIP1蛋白表达与胃癌细胞分化程度相关 (P <0 0 5 ) ;有肝转移的胃癌组cyclinE阳性表达率高于无肝转移组 (P <0 0 5 ) ;有淋巴结转移组 p2 1WAF1/CIP1蛋白表达率低于无淋巴结转移组 (P <0 0 5 )。结论 :cyclinE蛋白高表达与 p2 1WAF1/CIP1蛋白失表达可能参与胃癌的发生发展过程 ,检测cyclinE和p2 1WAF1/CIP1蛋白作为反映胃癌病理学特点的参考指标可能有一定意义     

Effect of Helicobacter pylori infection on epidermal growth factor receptor (EGFR) expression and cell proliferation of gastric epithelial mucosa: correlation to macroscopic and microscopic diagnosis

Our aim was to compare the expression of EGFR and proliferative cell nuclear antigen (PCNA) in different histological and endoscopic diagnostic groups, in cases of Helicobacter pylori infection, in vivo. Paraffin embedded human gastric biopsy samples (86) were analysed by EGFR and PCNA immunohistochemistry and classified both on the basis of histology and endoscopic findings. In normal epithelia (NE), a positive correlation was found between PCNA and EGFR and in H. pylori-negative gastritis with and without intestinal metaplasia (P < 0.01). On the other hand, a negative correlation was detected between the two immunohistochemical findings in H. pylori-associated gastritis with intestinal metaplasia (HPGIM) and in the atrophic gastritis (AG) group. In HPGIM the percentage of EGFR-positive cells was significantly lower (32.4 +/- 30.4) when compared to either the NE (50.3 +/- 23.7) or H. pylori-negative gastritis with intestinal metaplasia (HNGIM) (48.3 +/- 23.7). In AG, EGFR was significantly lower when compared to the NE (P < 0.05). Based on the endoscopic findings, a significant decrease of EGFR expression was found in gastric ulcer cases as compared to NE, gastritis or erosion cases (P < 0.01). PCNA showed no significant alterations between the NE and gastritis, AG groups. The presence of H. pylori has an inverse effect on PCNA and EGFR expression in HPGIM.     

Expression of glycoprotein hormone alpha-subunit by endocrine cells of the oxyntic mucosa is associated with hypergastrinemia

Previous studies have shown that hyperplastic endocrine cells of the oxyntic mucosa in patients with atrophic gastritis may express immunoreactivity for the alpha-subunit of human chorionic gonadotropin (alpha-HCG, common to all glycoprotein hormones). Since this endocrine proliferation is regarded as dependent on the trophic effect of the concomitant hypergastrinemia, the relation between immunohistochemical expression of alpha-HCG by oxyntic endocrine cells and serum levels of gastrin were investigated. The study was performed on endoscopic gastric biopsies of the oxyntic mucosa from 49 patients subdivided into the following groups: A) with histologically normal mucosa and normogastrinemia (22 cases), B) with atrophic gastritis and normogastrinemia (12 cases), C) with normal mucosa and hypergastrinemia (Zollinger-Ellison syndrome, retained antrum) (7 cases) and D) with atrophic gastritis and hypergastrinemia (with or without pernicious anemia) (8 cases). The alpha-HCG immunoreactive cells were found in all hypergastrinemic patients (groups C and D), regardless of the concomitant pathological condition of the mucosa. These cells accounted for 7.8% to 44.7% of the number of Grimelius argyrophil cells in consecutive serial sections. In contrast, alpha-HCG-containing cells were exceptional or absent in most normogastrinemic patients. Their number was sizable in only two cases of group A and three cases of group B, where it ranged from 2.5% to 14.8% of the number of argyrophil cells. It was concluded that expression of alpha-HCG is another feature of oxyntic endocrine cells associated with hypergastrinemia in addition to those previously recognized such as development of hyperplasia and/or carcinoid tumors.     

胃黏膜线粒体DNA不稳定与白细胞介素8活性的关系

目的　评价胃黏膜线粒体DNA不稳定 (mtMSI)与组织白细胞介素 8(IL 8)活性的关系。方法　采用聚合酶链反应 单链构象多态性分析 (PCR SSCP)方法检测mtMSI;组织IL 8含量测定采用ELISA方法。结果　 3 0例胃癌检出mtMSI 11例 ( 3 6 7% ) ,15例肠化胃黏膜组织中有 2例为mtMSI,10例异型增生黏膜组织有 2例为mtMSI,10例萎缩性胃炎黏膜组织有 1例检出mtMSI。胃黏膜细胞IL 8水平在mtMSI阳性组 [( 76 8± 3 8)pg/mg]显著高于mtMSI阴性组 [( 48 3± 3 6)pg/mg ,P <0 0 5 ]。结论　胃黏膜细胞mtMSI可能与IL 8释放有关 ,并参与了胃癌的发生     

Absence of pepsinogen A3 gene expression in the gastric mucosa of patients with gastric cancer.

AIMS--To investigate the expression of pepsinogen A3 (Pg3) encoding genes in the gastric mucosa of normal controls and subjects with atrophic gastritis and gastric cancer. METHODS--One hundred and fifty nine patients underwent upper gastrointestinal endoscopy with sampling of gastric biopsy specimens and serum. Pg3 isoproteins were determined by electrophoresis in serum and gastric mucosal biopsy specimens. Pg3 encoding genes were assessed by PCR in DNA obtained from peripheral blood. RESULTS--One hundred and one subjects (82 normal histology/chronic gastritis, 17 atrophic gastritis, two gastric cancer) showed a pepsinogen phenotype with presence of Pg3 and a corresponding pepsinogen genotype with presence of Pg3 encoding genes. Fifty eight subjects showed a phenotype lacking Pg3. In 39 of them (23 normal histology/chronic gastritis, 11 atrophic gastritis, five gastric cancer), a corresponding genotype without Pg3 encoding genes was found. However, in the remaining 19 subjects (4 normal histology/chronic gastritis, nine atrophic gastritis, six gastric cancer); Pg3 encoding genes were demonstrable in the absence of Pg3 production. CONCLUSIONS--Unexpressed Pg3 encoding genes can be shown in many cases of atrophic gastritis and gastric cancer, but rarely in healthy controls and subjects with superficial gastritis. The correlation of atrophic gastritis and gastric cancer with a pepsinogen phenotype lacking Pg3 can be explained by loss of expression of Pg3 encoding genes throughout the complete gastric mucosa. The mechanism of such loss and the importance as a marker for premalignant degeneration have to be elucidated.     

MUC1 gene polymorphism in the gastric carcinogenesis pathway.

MUC1 like most mucin genes shows extensive length polymorphism in the central core region. In a previous study it was shown that individuals with small MUC1 alleles/genotypes have an increased risk for development of gastric carcinoma. Our aim was to see if MUC1 gene polymorphism was involved in susceptibility for the development of conditions that precede gastric carcinoma: chronic atrophic gastritis (CAG) and intestinal metaplasia (IM). We evaluated MUC1 polymorphism in a population of 174 individuals with chronic gastritis (CG) displaying (CAG) and/or intestinal metaplasia (IM). The population of patients with CG shows MUC1 allele frequencies significantly different from the gastric carcinoma patients and blood donors population. A significantly lower frequency of CAG and IM was observed in MUC1 VNTR heterozygotic patients. Within the group of patients with IM, MUC1 large VNTR homozygotes show a significantly higher frequency of complete IM while small VNTR homozygotes show a significantly higher frequency of incomplete IM. These findings show that MUC1 polymorphism may define different susceptibility backgrounds for the development of conditions that precede gastric carcinoma: chronic atrophic gastritis (CAG) and intestinal metaplasia (IM).     

PGⅠ、PGⅡ、G 17和Hp IgG抗体筛查慢性萎缩性胃炎和胃癌的价值

分析胃蛋白酶Ⅰ（PGⅠ）、胃蛋白酶Ⅱ（PGⅡ）、胃泌素 17（G 17）和幽门螺杆菌（Hp IgG）抗体筛查对慢性萎缩性胃炎和胃癌的诊断价值。方法：以2014年5月至2015年5月胃部不适来我院就诊的90例患者为研究对象,根据病理诊断结果分为正常对照组（包括慢性非萎缩性胃炎）、慢性萎缩性胃炎组和胃癌组,每组各30例,比较三组患者PGⅠ、PGⅡ、G 17水平及Hp IgG抗体阳性检出率。结果：胃癌组患者的PGⅠ、PGⅡ水平低于对照组和慢性萎缩性胃炎组,且慢性萎缩性胃炎组患者上述指标低于对照组;胃癌组G 17水平高于慢性萎缩性胃炎组和对照组,而慢性萎缩性胃炎组和对照组无明显差异;三组间Hp IgG抗体阳性率有明显差别,胃癌组显著高于对照组和慢性萎缩性胃炎组;Hp感染患者的PGⅠ和PGⅡ水平低于未感染Hp者,而G 17水平高于未感染Hp者;胃癌患者的PGⅠ、PGⅡ水平与年龄、病理分期和转移显著负相关,与分化程度显著正相关,而G 17水平及Hp IgG抗体阳性率与年龄、病理分期和转移显著正相关,而与分化程度显著负相关。结论： PGⅠ、PGⅡ和Hp IgG抗体筛查对慢性萎缩性胃炎和胃癌均有很好的诊断价值,而对胃癌的诊断价值更好,G17对胃癌的诊断价值远远好于慢性萎缩性胃炎;且PGⅠ、PGⅡ、G17水平及Hp IgG抗体阳性检出率与胃癌患者的临床病理特征密切相关。     

Twenty-four-month oral carcinogenicity study of ebrotidine in rats

Three groups of Sprague-Dawley CD rats (males and females) were initially administered p.o. with ebrotidine, a novel H2-receptor antagonist, mixed with the diet, at 50, 200, and 500 mg/kg/d, respectively. Two concurrent control groups of animals were used. After 13 months, initial 200 mg/kg was lowered to 150 mg/kg, and a new group was administered with 300 mg/kg, due to the body weight reduction observed in the top dose group. After 24 months, survivors were killed and necropsied, and a histopathological study was performed. The frequencies of the different tumour types that were found were not raised due to the treatment. Lower frequencies of some types of pituitary and mammary gland tumours, in the groups treated with the higher doses, were the only statistically significant changes. Among the non-neoplastic effects, a lower body weight increment and food consumption (500 and 300 mg/kg, both sexes), lower survival (500 mg/kg, males), presence of lipoid pneumonia (500 mg/kg, only in males, and 300 mg/kg, both sexes), and lithiasis in urinary system (500 mg/kg) were observed. No changes in gastric mucosa (the main target organ) were attributable to ebrotidine. Regarding the non-neoplastic effects, 150 mg/kg was the no observed adverse effect level. According to the previous results of the carcinogenicity study in mice, conjointly with those of the study in rats reported here, there is no evidence of carcinogenic risk either in males or in females in these species.     

联合检测胃蛋白酶原、胃泌素-17及CEA、CA19-9在胃癌诊断中的应用

目的 探讨胃蛋白酶原Ⅰ、Ⅱ(PG Ⅰ、PGⅡ)及PG Ⅰ/PGⅡ的比值(PGR)、胃泌素-17(G-17)和CEA、CA19-9几项指标联合检测在胃癌诊断中的临床价值.方法 选择瑞金医院卢湾分院经胃镜检查确诊的185例胃疾病患者为研究对象,以组织病理学检查结果将受检者分为3组,即浅表性胃炎组85例、萎缩性胃炎组50例、胃癌组50例.采用时间分辨荧光免疫分析法检测PG Ⅰ和PGⅡ,然后计算出PGR的值,采用放射免疫分析法检测G-17,采用电化学发光免疫分析法检测CEA及CA19-9.比较不同分组间各指标的差异,最后绘制各指标检查胃癌及胃炎的ROC曲线.结果 在PG Ⅰ、G-17、CEA及CA19-9这四项指标中,浅表性胃炎组和萎缩性胃炎组与胃癌组的差异均有统计学意义(P＜0.05),而浅表性胃炎组与萎缩性胃炎组的差异均无统计学意义(P＞0.05).在PGⅡ和PGR这两项指标中,各组间的差异均无统计学意义(P＞0.05).将PG Ⅰ、G-17及CEA、CA19-9单独测定对胃癌的诊断价值的结果与联合测定对胃癌的诊断价值的结果进行比较并用ROC曲线进行分析,线下面积分别为0.742、0.699、0.614、0.520和0.850.结论 PG Ⅰ、G-17及CEA、CA19-9联合检测可提高胃癌的诊出率,对胃癌的诊断具有较为重要的临床意义.