Effect of Helicobacter pylori infection on gastric epithelial proliferation in progression from normal mucosa to gastric carcinoma

AIM To study the effect of Helicobacter pylori ( H. pylori ) infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma. METHODS Gastric biopsy specimens from normal controls ( n =11), superficial gastritis ( n =32), atrophic gastritis with intestinal metaplasia ( n =83), dysplasia ( n =25) and gastric carcinoma ( n =10) were studied by immunohistochemical staining of proliferating cell nuclear antigen (PCNA). RESULTS The gastric epithelial proliferation, expressed as PCNA labeling index (LI)%, was progressively increased in successive stages from normal mucosa to gastric carcinoma regardless of H. pylori status. There was significant difference in PCNA LI% among all groups ( P <0 01). The analysis pursuing the effect of H. pylori infection on gastric epithelial proliferation in the progression from normal mucosa to gastric carcinoma showed that in superficial gastritis and mild atrophic gastritis groups, PCNA LI% in H. pylori positive patients were 13 14±1 6 and 19 68±2 22 respectively, significantly higher than 6 95±0 78 and 11 34±1 89 in H. pylori negative patients ( P <0 01); but there was no such difference in other groups ( P >0 05). CONCLUSION H. pylori infection causes increased gastric epithelial proliferation in the stages of superficial and mild atrophic gastritis and may play a part in triggering gastric carcinogenesis.

Multiple genetic alterations and behavior of cellular biology in gastric cancer and other gastric mucosal lesions:H.pylori infection,histological types and staging

AIM To investigate the expression of multiplegenes and the behavior of cellular biology ingastric cancer（GC）and other gastric mucosallesions and their relations to Helicobacter pylori（H.pylori）infection,tumor staging andhistological subtypes.METHODS Three hundred and twenty-sevenspecimens of gastric mucosa obtained viaendoscopy or surgical resection,and ABCimmunohistochemical staining were used todetect the expression of p53,p16,Bcl-2 andCOX-2 proteins.H.pylori was determined byrapid urea test combined with pathologicalstaining or14C urea breath test.Cellular image analysis was performed in 66 patients withintestinal metaplasia（IM）and/or dysplasia（Dys）.In 30 of them,both cancer and theparacancerous tissues were obtained at the timeof surgery.Histological pattern,tumor staging,lymph node metastasis,grading ofdifferentiation and other clinical data werestudied in the medical records.RESULTS p16 expression of IM or Dys wassignificantly lower in positive H.pylori chronicatrophic gastritis（CAG）than those withnegative H.pylori（CAG:54.8% vs 88.0%,IM:34.4% vs 69.6%,Dys:23.8% vs 53.6%,allP【0.05）,Bcl-2 or COX-2 expression of IM orDys in positive H.pylori cases was significantlyhigher than that without H.pylori（Bcl-2:68.8%vs23.9%,90.5% vs 60.7%;COX-2:50.0% vs10.8%,61.8% vs 17.8%;all P【0.05）.Themean number of most parameters of cellularimage analysis in positive H.pylori group wassignificantly higher than that in negative H.pylori group（Ellipser:53±14,40±12μm,Area1:748±572,302±202 μm2,Area2:3050±1661,1681±1990 μm2,all P【0.05;Ellipseb:79±23,58±15 μm,Ratio1:22%±5%,13%±4%,Ratio2:79%±17%,53%±20%,all P【0.01）.There was significant correlation between Bcl-2and histologic pattern of gastric carcinoma,andbetween COX-2 and tumor staging or lymph nodemetastasis（Bcl-2:75.0% vs 16.7%;COX-2:76.0% vs 20.0%,79.2% vs 16.7%;allP【0.05）.CONCLUSION p1l6, Bcl-2, and COX-2 but not p53 gene may play a role in the early genesis/ progression of gastric carcinoma and are associated with H. pylori infection. p53 gene is relatively late event in gastric tumorigenesis and mainly relates to its progression. There is more cellular-biological behavior of malignant tumor in gastric mucosal lesions with H. pylori infection. Aberrant Bcl-2 protein expression appears to be preferentially associated with the intestinal type cancer. COX-2 seems to be related to tumor staging and lymph node metastasis.

Protection of gastric mucosa from ethanol induced injury by recombinant epidermal growth factor in rats

AIM To determine whether recombinant human epidermal growth factor (rhEGF) can protect gastric mucosa against ethanol induced injury in rats. METHOD Fifty four SD rats weighing 200g - 500g each were divided into six groups after fasting for 24 hours. Three groups received different doses of oral rhEGF (30, 60 and 120μg·kg -1 ·d -1 ), one group was given cimetidine, one subcutaneous rhEGF (rhEGFⅣ) and one received saline as control. RESULTS Acute gastric dilatation developed in the control and cimetidine groups and bloody gastric juice was found in the control group. The ulcer index was 58 in control group, 53 in rhEGFⅠ, 46 in rhEGFⅡ ( P <0 01) , 11 in rhEGFⅢ ( P <0 01) , 19 in rhEGFⅣ ( P <0 01) , and 39 in cimetidine group ( P <0 05) . CONCLUSION rhEGF protected gastric mucosa against ethanol induced damage. The effect was dose dependent with blood levels of epidermal growth factor (EGF) at a dosage range of 60μg·kg -1 ·d -1 -120μg·kg -1 ·d -1 . It was more effective by injection than via oral route at the same dosage.

Profiling cellular bioenergetics, glutathione levels, and caspase activities in stomach biopsies of patients with upper gastrointestinal symptoms

AIM: To measure biochemical parameters in stomach biopsies and test their suitability as diagnostic biomarkers for gastritis and precancerous lesions.METHODS: Biopsies were obtained from the stomachs of two groups of patients(n = 40) undergoing fiberoptic endoscopy due to upper gastrointestinal symptoms. In the first group(n = 17), only the corpus region was examined. Biopsies were processed for microscopic examination and measurement of mitochondrial O2 consumption(cellular respiration), cellular adenosine triphosphate(ATP), glutathione(GSH), and caspase activity. In the second group of patients(n = 23), both corpus and antral regions were studied. Some biopsies were processed for microscopic examination, while the others were used for measurements of cellular respiration and GSH level.RESULTS: Microscopic examinations of gastric corpus biopsies from 17 patients revealed normal mucosae in 8 patients, superficial gastritis in 7 patients, and chronic atrophic gastritis in 1 patient. In patients with normal histology, the rate(mean ± SD) of cellular respiration was 0.17 ± 0.02 μmol/L O2 min-1 mg-1, ATP content was 487 ± 493 pmol/mg, and GSH was 469 ± 98 pmol/mg. Caspase activity was detected in 3 out of 8 specimens. The values of ATP and caspase activity were highly variable. The presence of superficial gastritis had insignificant effects on the measured biomarkers. In the patient with atrophic gastritis, cellular respiration was high andATP was relatively low, suggesting uncoupling oxidative phosphorylation. In the second cohort of patients, the examined biopsies showed either normal or superficial gastritis. The rate of cellular respiration(O2. μmol/L min-1 mg-1) was slightly higher in the corpus than the antrum(0.18 ± 0.05 vs 0.15 ± 0.04, P = 0.019). The value of GSH was about the same in both tissues(310 ± 135 vs 322 ± 155, P = 0.692).CONCLUSION: The corpus mucosa was metabolically more active than the antrum tissue. The data in this study will help in understanding the pathophysiology of gastric mucosa.

Study on the pathogenetic effect of salted pork from a high risk area of stomach cancer in China

AIM To study the pathogenetic effect of salted pork (SP) (special food in Zhuanghe City, a high risk area of stomach cancer in northern China) on stomach cancer, and provide scientific basis for primary prevention of stomach cancer in this high risk area. METHODS The study consisted of three parts. The first part was to study the mutagenicity of SP. The Ames test and micro nuclei assay of V 79 cell were employed in this part. The second part was to study the effect of SP on the gastric mucosa of residents in Zhuanghe area who had consumed SP for more than 10 years and the dose effect relations between SP and pathological changes of gastric mucosa. A total of 300 cases were analysed. The third part was to study the mucosal lesions of experimental dogs by gastroscopy and mucosal biopsy. Six healthy male dogs were chosen, three were fed with SP, and the others served as control. RESULTS In this study, the results showed that the extract of SP could lead to mutation of Salmonella typhimurium TA 98 and induce the increase of micro nuclei rate (MNR) and micro nuclei cell rate (MNCR) of V 79 at a dose range of 20～80μl/ml. There were dose effect relations between SP, MNR, MNCR. Pathological changes of gastric mucosa of local residents who had consumed SP showed significant difference from those of the control group. In people who had consumed SP for 10 years, mucosal lesions including necrosis and erosion were found; in those who consumed SP for 10～20 years, hyperplasia and dysplasia were also seen besides the above lesions and those for 20～30 years, severe dysplasia and even malignant changes could be observed. SP had damaging effect on the gastric mucosa of dogs fed with SP. The mucosal lesions became more severe with increasing feeding time. CONCLUSION SP is a strong mutagen and long term exposure to SP may result in repeated gastric mucosal damage and repair, and finally leading to severe dysplasia and malignancy.

Efficacy of mucosa-submucosa clip closure method after gastric endoscopic submucosal dissection

BACKGROUND We recently developed a new endoscopic closure technique using only conventional endo-clips for colorectal lesions.Little is known about the feasibility of the endoscopic mucosa-submucosa clip closure method for gastric lesions.AIM To elucidate the efficacy of the endoscopic mucosa-submucosa clip closure method after gastric endoscopic submucosal dissection(ESD).METHODS Twenty-two patients who underwent gastric ESD and mucosa-submucosa clip closure were included in this study.In this method,endo-clips are placed at the edges of a mucosal defect.Additional endo-clips are then applied in the same way to facilitate reduction of the defect size.Additional endo-clips are applied to both sides of the mucosal defect.Complete closure can be achieved.We have also developed a“location score”and“closure difficulty index”for assessment purposes.RESULTS Complete closure was achieved in 68.2%of the patients(15/22).The location score in the failure group was significantly larger than that in the complete closure group(P=0.023).The closure difficulty index in the failure group was significantly higher than that in the complete closure group(P=0.007).When the cutoff value of the closure difficulty index was set at 99,the high closure difficulty index predicted failure with a sensitivity of 57.1%,specificity of 100%,and accuracy of 86.3%.CONCLUSION The endoscopic mucosa-submucosa clip closure method was unreliable after gastric ESD,especially in cases with a high closure difficulty index.

穴位埋线辅助四联疗法治疗脾胃虚弱型慢性萎缩性胃炎伴Hp感染临床研究

目的:观察穴位埋线辅助四联疗法治疗脾胃虚弱型慢性萎缩性胃炎(CAG)伴幽门螺杆菌(Hp)感染的临床疗效。方法:选取112例脾胃虚弱型CAG伴Hp感染患者,采用随机数字表法分为对照组(予四联疗法治疗)和观察组(予穴位埋线辅助四联疗法治疗)各56例。治疗结束后,2组均随访5个月。比较2组临床疗效、胃黏膜功能指标[胃泌素17(G-17)、胃蛋白酶原Ⅰ(PGⅠ)]、健康调查简表(SF-36)评分、中医证候积分、病理评分、不良反应发生率及复发率。结果:总有效率观察组96.43%,高于对照组80.36%(P<0.05)。治疗后3个月,2组血清G-17、PGⅠ水平均较治疗前升高(P<0.05),观察组上述2项指标水平均高于对照组(P<0.05)。治疗后1个月、3个月,2组SF-36评分均较治疗前升高(P<0.05),观察组SF-36评分均高于同期对照组(P<0.05)。治疗后3个月,2组中医证候积分均较治疗前降低(P<0.05),观察组中医证候积分低于对照组(P<0.05)。治疗后5个月,2组病理评分均较治疗前下降(P<0.05),观察组病理评分低于对照组(P<0.05)。不良反应发生率观察组8.93%,与对照组3.57%比较,差异无统计学意义(P>0.05)。治疗后5个月,复发率观察组1.85%,低于对照组15.56%(P<0.05)。结论:穴位埋线辅助四联疗法治疗脾胃虚弱型CAG伴Hp感染,可减轻患者的临床症状,改善胃黏膜功能,提高生活质量,降低复发率,且安全性好。

人胃粘膜肥大细胞的分布与超微结构

光镜观察了25例人胃底部组织甲苯胺蓝染色切片的粘膜肥大细胞的分布.电镜观察了5例人胃底活检材料内粘膜肥大细胞的超微结构.结果:人胃粘膜肥大细胞主要分布在粘膜的浅层和中层,与壁细胞的分布有密切的位置关系;人胃粘膜肥大细胞超微结构可分为T型与TC型两种,与啮齿类动物消化道T型和TC型肥大细胞的分布有所不同.结论:人胃粘膜肥大细胞释放的组胺可能刺激邻近的壁细胞分泌胃酸.

猴头菌提取物对大鼠胃粘膜损伤保护作用的研究

用三种不同主式得到的猴头菌提取物(猴头菌子实体粗多糖、猴头菌菌丝体粗多糖、猴头菌菌丝体全提物)对乙醇致大鼠胃粘膜损伤的治疗作用进行研究。结果表明,当以等原生药量计时,子实休机多糖疗效最明显,菌丝体全提物次之,菌丝体粗多糖较差,溃疡抑制率分别达70.8％、51.4％和41.5％;当以等多糖含量计时,则三个样品的疗效接近,溃疡抑制率达到60％左右。这进一步证实猴头菌多糖是猴头菌保护大鼠胃粘膜的主要活性物质。

中医药对慢性萎缩性胃炎伴胃粘膜不典型增生患者的临床及实验研究

以疏肝健脾、温胃健脾、养阴益胃、清利健脾4型复方煎剂治疗慢性萎缩性胃炎伴不典型增生,在取得临床疗效的基础上,做了不同药物浓度对不典型增生细胞的细胞培养。结果显示,4型系列复方对不典型增生的抑制率均>70％以上。

海螵蛸多糖对小鼠胃黏膜保护作用的研究

目的:用海螵蛸中提取的多糖盐洗组分(CBP-s)预处理小鼠后,用无水乙醇灌胃处理,观察小鼠胃黏膜的损伤程度,探究其保护胃黏膜的机制。方法:用CBP-s分别预处理小鼠3d和5d,再用无水乙醇诱导其胃黏膜损伤,测定溃疡指数、胃内容物pH值,以及胃黏膜的一氧化氮(NO)、谷胱甘肽(GSH)、丙二醛(MDA)和过氧化物歧化酶(SOD)等指标。结果:100、200和400mg/kg CBP-s预处理3 d和5 d的小鼠溃疡指数下降;100、200和400mg/kg CBP-s预处理3d和5d,胃内容物pH值分别是3.09±0.20、3.43±0.23、3.32±0.15、3.34±0.25、3.38±0.15、3.68±0.24;400mg/kg CBP-s预处理3d和5d,胃黏膜的MDA含量较造模组都有显著下降[(125.41±28.79)vs(145.80± 26.13);(153.88±21.19)vs(127.14±5.68)nmol/g,P<0.05];除了100mg/kg预处理3d组,各剂量组均能显著提高GSH和NO的含量[GSH:(282.93±32.33),(293.57±20.76),(260.79±39.23),(253.71±21.11),(359.38±10.89)mg/g,P<0.05];NO:(23.40±4.41),(25.83±4.89),(21.60±3.05),(22.75±2.44)μmol/g,P<0.05];各组的SOD活性均有显著上升[(30.61±6.37),(45.35±1.90),(47.12±4.68),(36.48±5.64),(41.38±8.23),(39.42±8.76)U/mg,P<0.05]。结论:CBP-s对乙醇诱导的小鼠胃黏膜具有细胞保护作用。

+Gz值暴露后大鼠胃十二指肠粘膜及生长抑素含量的变化

目的观察+Gz值暴露对大鼠胃十二指肠生长抑素(SS)含量的影响及其意义。方法40只雄性Wister大鼠随机分成4组:对照组,+5Gz值组,+10Gz值组,重复暴露组。对照组不受加速度作用,+5Gz值组,+10Gz值组各连续暴露5min,重复暴露组亦为连续暴露:+5Gz值2min,+10Gz值2min,+5Gz值2min。每组下离心机后即时乙醚麻醉取胃窦、十二指肠粘膜组织,用放免法测定粘膜SS含量。结果1)对照组、+5Gz值组胃、十二指肠粘膜光滑,完整;+10Gz值组肉眼见胃窦、十二指肠粘膜散在小出血斑;重复暴露组胃底、胃窦、十二指肠粘膜均可见散在出血斑及小溃疡,光镜下见粘膜下血管充血、粘膜上皮的完整性破坏,糜烂及溃疡形成。2)+Gz值暴露使胃窦、十二指肠粘膜SS含量显著升高(P<0.01)。结论+Gz值暴露使胃窦、十二指肠粘膜SS含量显著升高。SS含量显著升高可能在胃粘膜保护方面起重要作用。

大鼠胃窦粘膜5-羟色胺免疫反应阳性细胞的体视学研究

本文用免疫组织化学PAP法显示SD大鼠胃窦部含5-HT的细胞,并用Weibel体视学方法对其进行定量分析。结果如下:大鼠胃窦部免疫反应阳性细胞仅存在于腺上皮和胃小凹上皮中。该细胞在胃窦粘膜中的体积密度(V_v)为0.0038±0.0004,面数密度(N_A)为42.86±3.20个/mm^2,数密度(N_V)为2627.11±200.42个/mm^3。该细胞的分布有明显的区域性差异。从胃小弯至胃大弯部,细胞密度逐渐降低。小弯区密度最高,两侧壁密度次之;胃大弯区密度最低。大部分5-HT免疫反应阳性细胞位于粘膜深1/3段,该段密度最高,粘膜中1/3段密度次之,粘膜浅1/3段密度最低。此外,本文还对5-HT免疫反应阳性细胞的形态,进行了较详细的观察。

cagA基因对胃粘膜上皮细胞增殖和凋亡的影响

目的 观察不同基因型Hp感染对胃上皮细胞增殖和凋亡的影响,进而探讨Hp增加胃癌发生危险性的机制。 方法 研究对象为19例Hp阴性的慢性浅表性胃炎和37例Hp阳性的慢性浅表性胃炎患者,应用ki-67免疫组化技术评价胃幽门窦上皮细胞增生,用切口末端标记法(TUNEL)检测胃上皮细胞凋亡,应用聚合酶链反应(PCR)技术检测Hp的cagA基因。 结果 Hp阳性患者的增殖指数(LI)和凋亡指数(AI)显著高于Hp阴性者(17±4对7.3±3.3和11.3±3.8对6.6±1.2,P<0.01),cagA^+或cagA^-Hp患者的LI和AI均显著高于Hp^-患者,cagA^+Hp患者(n=27)的LI明显高于cagA^-Hp患者(n=10)(18.6±5.8对13.8±4.2,P<0.05),而AI则明显低于cagA^-Hp患者(8.9±3.2对12.2±4.6,P<0.01),LI和AI与胃粘膜炎症程度无明显关系。 结论 Hp感染诱导胃上皮细胞过度增殖和凋亡,cagA^+Hp与cagA^-Hp促增殖和凋亡作用的能力明显不同。

无损光学法测量人胃粘膜/粘膜下层组织的光衰减特性

研究了人正常胃粘膜及粘膜下层组织对640 nm,690 nm,740 nm,790 nm,840 nm和890 nm波长的钛宝石激光的光衰减特性以及光学穿透深度,实验采用激光斜入射式空间分辨反射光和CCD探测器以及非线性拟合确定组织光学特性。结果表明:人正常胃粘膜及粘膜下层组织对六个波长的激光的有效衰减系数和光学穿透深度都是随着激光波长的变化而变化的。其有效衰减系数的最大值在640 nm,其值为1.12 mm-1,最小值在790 nm,其值为0.901 mm-1,最大差异在790 nm和890 nm之间,其值为19.9%,最小差异在690 nm和740nm之间,其值为2.83%。其光学穿透深度的最大值在790 nm,其值为1.11 mm,最小值在640 nm,其值为0.890 mm,最大差异在640 nm和790 nm之间,其值为24.7%,最小差异在690 nm和740 nm之间,其值为2.97%。

52例胃癌组织中Survivin和Bcl-2蛋白表达研究

目的探讨胃癌组织中Survivin及Bcl-2蛋白的表达及其与胃癌生物学行为的关系。方法采用免疫组化SP法检测52例胃癌组织、30例正常胃黏膜组织中Survivin及Bcl-2蛋白的表达。结果 Survivin、Bcl-2蛋白在胃癌组织中的阳性表达均高于正常胃黏膜(P<0.05);Survivin、Bcl-2蛋白表达均分别与胃癌的分化程度、淋巴结转移有关(P<0.05)。结论 Survivin、Bcl-2蛋白表达上调可能与胃癌的发生、发展有关,二者共同作用抑制凋亡。

电针足阳明经穴对家兔胃粘膜损伤防御性保护作用的研究

方法 采用电针家兔足阳明经头面“四白”穴 ,躯干“梁门”穴、下肢“足三里”穴 ,观察其对胃粘膜损伤的防御性保护作用 ,以进一步探讨足阳明经与胃的相关性。结果 电针足阳明经不同部位经穴 ,均可使家兔胃粘膜损伤指数显著降低 ,胃粘膜前列腺素E2 (PGE2 )及表皮生长因子 (EGF)的含量增加 ,其中以“足三里”穴最为明显 (P <0 0 1) ,而电针“足三里”外 2cm的对照点 ,则未见显著性差异 (P >0 0 5)。结论 电针足阳明经不同部位经穴 ,可能是通过胃粘膜组织中PGE2 与EGF发挥了对胃粘膜细胞的保护作用 ,证实了足阳明经与胃具有相关性。

土壤中重金属污染对白颈环毛蚓（Pheretime Califonica）胃肠道粘膜损伤的扫描电镜观察

本文首次报道了土壤重金属污染区的白颈环毛蚓（ｐｈｅｒｅｔｉｍｅＣａｌｉｆｏｎｉｃａ）胃肠道粘膜的扫描电镜观察，结果表明：在重污染区（Ⅰ区）蚯蚓胃粘膜出现溃疡灶，并发现有穿孔现象；在轻污染区（Ⅳ区）只发现有胃微绒毛萎缩现象。又在重污染区（Ⅰ区）发现蚯蚓肠粘膜微绒毛有明显的萎缩现象。我们首次发现蚯蚓肠粘膜上存有纤毛丛。对照区肠粘膜上纤毛整齐健壮，而在重污染区（Ⅰ区）发现肠粘膜上纤毛发生紊乱以及萎缩、纤毛顶端发生融结膨大现象。肠粘膜纤毛的病变能很灵敏地反映土壤中重金属危害排泄功能的状况。由此，我们认为：肠道纤毛的病变状况可作为土壤重金属污染监测的一项生物学指标。

冰乙酸性大鼠胃溃疡模型的建立及溃疡胃窦粘膜的光镜和透射电镜观察

目的建立冰乙酸性大鼠胃溃疡模型,并对溃疡胃窦的粘膜组织结构进行光镜和电镜观察。方法 31只Wistar大鼠随机分为冰乙酸0.01mL组、冰乙酸0.05mL组、冰乙酸0.01mL组,生理盐水0.01mL组、生理盐水0.05mL组、生理盐水0.01mL组,和正常对照组。以1mL注射器在各处理组大鼠胃窦前壁注入相应剂量的冰乙酸或生理盐水。对各组大鼠进行大体观察,对发生典型胃溃疡组大鼠和正常对照组大鼠的胃窦组织进行光镜、电镜观察。结果冰乙酸0.05mL组大鼠胃窦前壁粘膜面发生溃疡,冰乙酸0.01mL组鼠胃未见明显溃疡,冰乙酸0.01mL组大鼠胃窦前壁穿孔,生理盐水0.01mL组、生理盐水0.05mL组、生理盐水0.10mL组和正常对照组大鼠胃窦均无溃疡。光镜观察见冰乙酸0.05mL组大鼠胃窦溃疡部位粘膜腺体正常结构消失,溃疡边缘粘膜腺体间质充血水肿和结缔组织增,电镜观察见冰乙酸0.05mL组大鼠溃疡边缘胃窦粘膜粘液细胞、壁细胞、主细胞存在超微结构改变,并见坏死细胞和凋亡细胞等细胞。结论大体、光镜和电镜三水平的观察表明,以大鼠胃窦前壁注入0.05mL冰乙酸所建立的胃溃疡模型最为典型。

胃粘膜肠上皮化生与胃癌关系的病理学研究

对37例胃良性病变和42例胃癌手术标本进行了病理组织学、粘液组织化学研究，并行胃癌单克隆抗体MG7、Ras癌基因蛋白p21蛋白免疫组化染色。结果发现，胃粘膜肠上皮化生可分为单纯肠化和不典型肠化两种组织学类型，两型粘液组织化学染色均产生中性粘液、唾液酸粘液及硫酸粘液。不典型肠化胃癌单克隆抗体MG7及Ras癌基因蛋白p21多为阳性表达，单纯肠化则全部阴性，说明单纯肠化多为胃粘膜上皮的适应性改变，与胃癌发生关系不密切，不典型肠化可能与胃癌发生关系密切，并与异型增生互为因果，在此基础上易发生异型增生及癌变。