Environmental factors in Helicobacter pylori-related gastric precancerous lesions in Venezuela.

Although Helicobacter pylori (HP) infection has been acknowledged to play an etiological role in gastric carcinogenesis, its relatively weak association particularly in developing countries suggests critical roles of cofactors. Among a population with an extremely high prevalence of HP infection ( approximately 95%) in Venezuela, we examined the relationship of household characteristics, smoking, alcohol drinking, dietary consumption, and plasma nutrient levels with the prevalence of three different stages of gastric precancerous lesions, chronic atrophic gastritis (AG; n = 337), intestinal metaplasia (IM; n = 551), and dysplasia (n = 157), in comparison with those without any of these lesions (n = 1154). Length of refrigerator use was marginally inversely associated with the prevalence of the precursor lesions studied. The association was most pronounced for AG followed by dysplasia. On the other hand, smoking status was a significant predictor for IM and dysplasia. Those smoking >/=>10 cigarettes/day had 1.8-fold risk of IM and 3.6-fold risk of dysplasia compared with never smokers. There were no associations with alcohol consumption. When six food groups known to be associated with stomach cancer risk in Venezuela were tested, the prevalence of these lesions progressively increased with increasing starchy vegetable consumption and decreasing fresh fruit/fruit juice consumption. The association with fruits was more evident for dysplasia and AG and that with starchy vegetables for IM and AG. However, there were no inverse associations with plasma antioxidant vitamins. These findings offer important public health implications in preventing progression of HP-associated gastric precancerous lesions in high-risk populations.     

Neglected role of hookah and opium in gastric carcinogenesis: A cohort study on risk factors and attributable fractions

A recent study showed an association between hookah/opium use and gastric cancer but no study has investigated the relationship with gastric precancerous lesions. We examined the association between hookah/opium and gastric precancerous lesions and subsequent gastric cancer. In a population‐based cohort study, 928 randomly selected, healthy, Helicobacter pylori‐infected subjects in Ardabil Province, Iran, were followed for 10 years. The association between baseline precancerous lesions and lifestyle risk factors (including hookah/opium) was analyzed using logistic regression and presented as odds ratios (ORs) and 95% confidence intervals (CIs). We also calculated hazard ratios (HRs) and 95% CIs for the associations of lifestyle risk factors and endoscopic and histological parameters with incident gastric cancers using Cox regression models. Additionally, the proportion of cancers attributable to modifiable risk factors was calculated. During 9,096 person‐years of follow‐up, 36 new cases of gastric cancer were observed (incidence rate: 3.96/1,000 persons‐years). Opium consumption was strongly associated with baseline antral (OR: 3.2; 95% CI: 1.2–9.1) and body intestinal metaplasia (OR: 7.3; 95% CI: 2.5–21.5). Opium (HR: 3.2; 95% CI: 1.4–7.7), hookah (HR: 3.4; 95% CI: 1.7–7.1) and cigarette use (HR: 3.2; 95% CI: 1.4–7.5), as well as high salt intake, family history of gastric cancer, gastric ulcer and histological atrophic gastritis and intestinal metaplasia of body were associated with higher risk of gastric cancer. The fraction of cancers attributable jointly to high salt, low fruit intake, smoking (including hookah) and opium was 93% (95% CI: 83–98). Hookah and opium use are risk factors for gastric cancer as well as for precancerous lesions. Hookah, opium, cigarette and high salt intake are important modifiable risk factors in this high‐incidence gastric cancer area.     

Chemoprevention of gastric dysplasia: randomized trial of antioxidant supplements and anti-helicobacter pylori therapy

BACKGROUND: Previous research has identified a high risk of gastric carcinoma as well as a high prevalence of cancer precursor lesions in rural populations living in the province of Nari?o, Colombia, in the Andes Mountains. METHODS: A randomized, controlled chemoprevention trial was conducted in subjects with confirmed histologic diagnoses of multifocal nonmetaplastic atrophy and/or intestinal metaplasia, two precancerous lesions. Individuals were assigned to receive anti-Helicobacter pylori triple therapy and/or dietary supplementation with ascorbic acid, beta-carotene, or their corresponding placebos. Gastric biopsy specimens taken at baseline were compared with those taken at 72 months. Relative risks of progression, no change, and regression from multifocal nonmetaplastic atrophy and intestinal metaplasia were analyzed with multivariate polytomous logistic regression models to estimate treatment effects. All statistical tests were two-sided. RESULTS: All three basic interventions resulted in statistically significant increases in the rates of regression: Relative risks were 4.8 (95% confidence interval [CI] = 1.6-14.2) for anti-H. pylori treatment, 5. 1 (95% CI = 1.7-15.0) for beta-carotene treatment, and 5.0 (95% CI = 1.7-14.4) for ascorbic acid treatment in subjects with atrophy. Corresponding relative risks of regression in subjects with intestinal metaplasia were 3.1 (95% CI = 1.0-9.3), 3.4 (95% CI = 1.1-9.8), and 3.3 (95% CI = 1.1-9.5). Combinations of treatments did not statistically significantly increase the regression rates. Curing the H. pylori infection (which occurred in 74% of the treated subjects) produced a marked and statistically significant increase in the rate of regression of the precursor lesions (relative risks = 8.7 [95% CI = 2.7-28.2] for subjects with atrophy and 5.4 [95% CI = 1.7-17.6] for subjects with intestinal metaplasia). CONCLUSIONS: In the very high-risk population studied, effective anti-H. pylori treatment and dietary supplementation with antioxidant micronutrients may interfere with the precancerous process, mostly by increasing the rate of regression of cancer precursor lesions, and may be an effective strategy to prevent gastric carcinoma.     

宁夏海原县胃癌癌前病变危险因素分析

目的:探讨宁夏海原县胃癌癌前病变可能的危险因素,为预防胃癌提供相应依据。方法:以2018年1月至2019年1月于宁夏海原县人民医院和宁夏回族自治区人民医院宁南医院行胃镜检查的5 280例患者为筛选对象,将通过胃镜检查诊断为萎缩性胃炎,经病理诊断为肠化、异型增生的患者作为病例组。将同期行胃镜检查诊断为非萎缩性胃炎,经病理诊断无肠化、无异型增生的患者,按照1∶1配对作为对照组。用单因素、多因素非条件二元Logistic回归方法进行分析。结果:病例组与对照组单因素分析提示在体质量指数（BMI）、居住坏境、教育程度、吸烟、饮酒、饮绿茶、饮水来源、新鲜蔬菜、新鲜水果、肉蛋奶、豆类食品、腌制食品、油炸食品、烫热食品、大蒜、吃早餐、进食不规律、消化疾病史、幽门螺杆菌（Hp）感染、非甾体抗炎药服用史、睡眠时间因素方面差异均有统计学意义（P＜0.05）。通过Logistic回归分析模型分析提示吸烟、饮酒、饮用地窖水、腌制食品、油炸食品、烫热食品及Hp感染是胃癌癌前病变发生的危险因素。而较高的教育程度、饮绿茶、新鲜蔬菜、新鲜水果、吃早餐、7~8 h睡眠时间是胃癌癌前病变的保护因素。结论:影响宁夏海原县胃癌癌前病变的因素是多方面的,Hp感染、腌制、油炸和烫热食品及饮用地窖水是当地发生胃癌癌前病变最重要的危险因素。所以改变生活习惯,根除Hp是预防宁夏海原县发生胃癌癌前病变的重要措施。     

Does treatment of Helicobacter Pylori Infection Reduce Gastric Precancerous Lesions?

Background: Treatment of Helicobacter pylori (H. pylori) decreases the prevalence of gastric cancer, andmay inhibit gastric precancerous lesions progression into gastric cancer. The aim of this study was to determinethe effect of treatment on subsequent gastric precancerous lesion development. Materials and Methods: Weprospectively studied 27 patients who had low grade dysplasia at the time of enrollment, in addition to dysplasiaatrophic gastritis and intestinal metaplasia observed in all patients. All were prescribed quadruple therapy totreat H. Pylori infection for 10 days. Patients underwent endoscopy with biopsy at enrollment and then at followup two years later. Biopsy samples included five biopsies from the antrum of lesser curvature, antrum of greatercurvature, angularis, body of stomach and fundus. Results of these biopsies were compared before and aftertreatment. Results: Overall, the successful eradication rate after two years was 15/27 (55.6%). After antibiotictherapy, the number of patients with low grade dysplasia decreased significantly (p=0.03), also with reductionof the atrophic lesions (p=0.01), but not metaplasia. Conclusions: Treatment of H. pylori likely is an effectivetherapy in preventing the development of subsequent gastric premalignant lesions.     

Genetic polymorphisms of CYP2E1, GSTT1, GSTP1, GSTM1, ALDH2, and ODC and the risk of advanced precancerous gastric lesions in a Chinese population.

There have been few studies of the associations of genetic polymorphisms with precancerous gastric lesions. We conducted a cross-sectional study to compare the prevalences of several genetic polymorphisms in 302 subjects with mild chronic atrophic gastritis with prevalences in 606 subjects with deep intestinal metaplasia or dysplasia. This stratified random sample of 908 subjects was selected and analyzed for genetic polymorphisms from 2,628 individuals who had gastric biopsies with histopathology in 1989 in Linqu County, Shandong Province, China. In subjects with mild chronic atrophic gastritis, the frequencies of the variant (less common) alleles of CYP2E1 RsaI, CYP2E1 DraI, GSTP1, ALDH2, and ODC were, respectively, 0.156, 0.201, 0.189, 0.190, and 0.428. The frequencies of the null genotypes of GSTM1 and GSTT1 in the mild chronic atrophic gastritis group were 0.509 and 0.565, respectively. Comparing mild chronic atrophic gastritis with deep intestinal metaplasia or any degree of dysplasia, we found no statistically significant associations with any genotype from these loci for dominant, additive, or recessive inheritance models. There was no statistically significant evidence of multiplicative interactions between any pair of genotypes based on CYP2E1 RsaI, CYP2E1 DraI, GSTP1, GSTM1, or GSTT1; nor between Helicobacter pylori status and any of these five loci; nor between smoking status and GSTP1, GSTM1, or GSTT1; nor between alcohol consumption and ALDH2. Statistically significant interactions were noted between salt consumption and GSTP1 and between sour pancake consumption and CYP2E1 RsaI. There was, moreover, a statistically significant interaction (odds ratio, 1.78; 95% confidence interval, 1.03-3.08) between CYP2E1 DraI and smoking at least one cigarette per day. A positive but not statistically significant interaction was also seen between CYP2E1 RsaI and smoking status. These polymorphisms do not seem to govern progression from mild chronic atrophic gastritis to advanced precancerous gastric lesions, but the effects of smoking may be accentuated in individuals carrying variants of CYP2E1.     

Promoter methylation of p16 associated with Helicobacter pylori infection in precancerous gastric lesions: a population-based study

To investigate the relationship between p16 methylation and Helicobacter pylori infection in precancerous gastric lesions, a population-based study was conducted in Linqu County, a high-risk area of gastric cancer in China. Methylation status of p16 was evaluated by methylation-specific polymerase chain reaction in 920 subjects with precancerous gastric lesions. H. pylori status was determined by 13C-urea breath test and the density of H. pylori in biopsy specimens used for detecting methylation status was assessed by the modified Giemsa stain. The frequency of p16 methylation was significantly higher in subjects with H. pylori positive than those with H. pylori negative in each category of gastric lesion (p<0.001, respectively). Compared with H. pylori negative, the odds ratios (ORs) of p16 methylation were markedly elevated in subjects with H. pylori positive for superficial gastritis (OR, 9.45; 95% confidence interval [CI]: 2.94-30.41), chronic atrophic gastritis (OR, 15.92; 95%CI: 7.60-33.36), intestinal metaplasia (OR, 4.46; 95%CI: 2.44-8.13), indefinite dysplasia (OR, 3.67; 95%CI: 1.90-7.10), and dysplasia (OR, 2.48; 95%CI: 1.02-5.99). Moreover, the frequencies of p16 methylation increased steadily with the severity of H. pylori density in gastric mucosa. Compared with H. pylori negative, the OR of p16 methylation was 1.02-16.13 times higher in subjects with mild H. pylori infection, and 2.69-38.73 times higher in those with moderate/severe infection, respectively. Our findings indicate that p16 methylation was significantly associated with H. pylori infection in precancerous gastric lesions, suggesting that H. pylori infection could potently induce methylation of p16 CpG island.     

Gastric Cancer among the Japanese in Hawaii

The incidence rate of gastric cancer among men of Japanese ancestry living in Hawaii is about one-third as high as that of their counterparts living in Japan. Because of this difference, a prospective study was conducted to identify factors related to the development of gastric cancer in Hawaii. Eight thousand and six (8,006) men born from 1900-1919 were examined from 1965 to 1968 and followed for over 25 years. During this time, 250 incident cases of gastric cancer were identified. The study has found the following: 1) prior infection with Helicobacter pylori bacteria increased the risk for stomach cancer; 2) cigarette smoking was positively associated with gastric cancer with age at which smoking started being an important risk factor; 3) after taking cigarette smoking into account, alcohol intake was not related to stomach cancer risk; 4) a low pepsinogen I level identified subjects at increased risk for the intestinal histologic type of gastric cancer; 5) a low serum ferritin level was a marker for increased risk of stomach cancer; 6) there was a weak indication that the intake of vegetables and fruits was inversely related to gastric cancer; 7) there was no association of stomach cancer with levels of serum cholesterol, serum uric acid, serum micronutrients (retinol, β-carotene or α-tocopherol) or blood hematocrit; 8) there was also no association of gastric cancer with body mass index or physical activity.     

A study of precancerous gastric lesions in a high risk population

A study of precancerous gastric lesion was conducted in a randomly selected high risk population in Linqu, Shandong Province of China. 849 subjects aged from 30–64 were examined bioptically. There were 8 cases of gastric cancer, the prevalence rate was 0.9%. 169 subjects were diagnosed to be dysplasia, the prevalence rate of dysplasia was increased significantly with age. The regression equation was Y=0.47X?0.25. The prevalence of CAG was found in 36 per cent of the studied subjects and both dysplasia and CAG were more serious in the antrum than the fundus. The results showed a natural history of precancerous gastric lesions in a high risk population in a high risk area.     

Genetic polymorphism of PSCA and risk of advanced precancerous gastric lesions in a Chinese population

Objective: To evaluate the relationship between the genetic polymorphism of prostate stem cell antigen (PSCA) and the risk of advanced precancerous gastric lesions including intestinal metaplasia(IM) and dysplasia(Dys), a population-based study was conducted in Linqu County, a high-risk area of gastric cancer (GC) in China.Methods: The prevalence of gastric lesions including superficial gastritis(SG), chronic atrophic gastritis(CAG), IM and Dys was determined by histopathologic examination. The genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. The effects of PSCA genetic variant on the risks of IM and Dys were calculated by unconditional logistic regression.Results: Multivariate analysis revealed subjects carrying PSCA rs2294008 CT/TT genotype were associated with an increased risk of IM (OR=1.38, 95% CI=1.11-1.71) and Dys (OR=1.75, 95% CI=1.36-2.26), especially for subjects with H.pylori infection (IM: OR=1.34, 95% CI=1.05-1.71; Dys: OR=1.82, 95% CI=1.37-2.42). Furthermore, H. pylori infection and PSCA rs2294008 CT/TT genotype were observed to jointly elevate the risk of 1M (OR=3.32, 95% CI=2.33-4.71) and Dys (OR=4.58, 95% CI=2.99-7.04).Conclusion: This study suggested that PSCA rs2294008 might have an impact on the risk of IM or Dys among the high risk population of GC.     

Smoking Behavior and Risk of Helicobacter Pylori Infection,Gastric Atrophy and Gastric Cancer in Japanese

Although many studies have shown that smoking is an established risk factor for gastric cancer, relatively few studies have investigated on which step smoking has effects in Helicobacter pylori (H. pylori) related gastric carcinogenesis. In this study we investigated the association of smoking with risk of three steps leading to gastric cancer: H. pylori infection, gastric atrophy, and gastric cancer. Among the participants who visited Aichi Cancer Center Hospital from year 2001 to 2005, 583 cases diagnosed as gastric cancer and age-and sex-frequency-matched 1,742 cancer free controls were sampled, from whom those without serum samples or without information about smoking habit were excluded, leaving 576 cases and 1,599 controls eligible for the analyses. Anti- H. pylori IgG antibody and serum pepsinogens (PG) were measured to detect H. pylori infection and gastric atrophy. Smoking status was asked by a self-administered questionnaire. The odds ratio (OR) of H. pylori infection, as well as the OR of gastric atrophy among the H. pylori seropositive controls was not significant for smokers. The age- and sex-adjusted OR of gastric cancer was significantly elevated relative to the subjects with gastric atrophy: OR=1.62 (95% confidence interval (CI), 1.19-2.22; P=0.002) for ever smokers and 2.52 (1.75-3.64; P<0.001) for current smokers, relative to never smokers. This study revealed that smoking behavior contributed to the increased risk of gastric carcinogenesis from gastric atrophy, but had little influence on H. pylori infection or gastric atrophy development.     

p16基因甲基化与胃黏膜异型增生恶性转化的关系

目的 山东省临朐县是我国北方胃癌高发区之一,人群中胃黏膜异型增生(dysplasia,DYS)病变所占比例较高.DYS是胃黏膜癌前病变发展的高级阶段,具有显著的恶性转化潜能.本研究探讨p16基因甲基化与DYS病变恶性转化的关系,验证其作为胃癌预警标志物的应用价值.方法 以胃癌高发现场长期胃镜随访队列为基础,对101例来自山东省临朐县胃癌高发区且随访至2015-12-31的DYS病例,采用Methylight方法定量检测胃黏膜组织p16基因甲基化水平,评价其与DYS进展为胃癌风险的关系.结果 在进展为胃癌组,p16基因甲基化百分比中位数(四分位数)为1.30％(0.13％～1.87％),显著高于非进展组的0.67％(0～1.15％),P=0.047.与p16基因低甲基化者相比,高甲基化水平的DYS患者进展为胃癌的风险显著增加,OR-3.67,95％CI为1.31～10.34.进一步分析发现幽门螺杆菌(H.pylori)感染阳性者p16基因甲基化百分比中位数(0.98％)明显高于阴性者(0.01％),P＜0.001;分层分析发现,p16基因高甲基化同时H.pylori感染阳性者进展为胃癌的风险进一步增加,OR=5.14,95％CI为1.57～16.82.通过分析p16基因甲基化水平与DYS病例进展为胃癌的时间关系,发现随着胃癌诊断时间的临近,p16基因甲基化水平有缓慢升高的趋势,但差异未见统计学意义.结论 胃黏膜组织p16基因甲基化水平升高可作为DYS患者发生恶性转化的潜在预警标志物.     

河南省林州市食管鳞癌及癌前病变的影响因素研究

[目的]探讨河南省林州市食管鳞癌及癌前病变的影响因素。[方法]按照性别、年龄进行1∶1∶1匹配的原则,选取2019年5~10月在林州市食管癌医院就诊的新发食管鳞癌患者、新发中重度食管鳞状上皮异型增生患者和正常对照匹配成33个区组作为研究对象。对入组的研究对象进行问卷调查,收集其人口学、生活方式等信息,采用多元有序Logistic回归对食管鳞癌及癌前病变的影响因素进行统计学分析。[结果]单因素分析结果显示,教育程度,饮用水来源,吸烟,饮酒,饮茶,食用西兰花、大蒜、酸菜、烟熏制品,劳动强度,消化道疾病史,食管癌家族史与食管鳞癌及癌前病变发生有关(P<0.05)。多元有序Logistic回归结果显示,教育程度(小学:OR=2.128,95%CI:1.116~3.187;中学及以上:OR=1.960,95%CI:1.080~2.759),饮用浅层地下水、井水(OR=3.595,95%CI:1.051~7.130),现在吸烟(OR=2.027,95%CI:1.435~5.193),经常食用酸菜(OR=2.520,95%CI:1.030~4.498),经常食用烟熏制品(OR=1.312,95%CI:1.089~1.739),有消化道疾病史(OR=2.277,95%CI:1.038~2.828)是食管鳞癌及癌前病变的独立危险因素,而经常食用西兰花(OR=0.520,95%CI:0.031~0.855)是独立保护因素。[结论]在林州市,生活方式、饮食习惯和消化道病史均可影响食管鳞癌及癌前病变的发生,有其地域特点,应针对相关影响因素采取相应的预防措施。     

Smoking Behavior and Risk of Helicobacter Pylori Infection,Gastric Atrophy and Gastric Cancer in Japanese

Although many studies have shown that smoking is an established risk factor for gastric cancer, relativelyfew studies have investigated on which step smoking has effects in Helicobacter pylori (H. pylori) related gastriccarcinogenesis. In this study we investigated the association of smoking with risk of three steps leading to gastriccancer: H. pylori infection, gastric atrophy, and gastric cancer. Among the participants who visited Aichi CancerCenter Hospital from year 2001 to 2005, 583 cases diagnosed as gastric cancer and age-and sex-frequency-matched1,742 cancer free controls were sampled, from whom those without serum samples or without information aboutsmoking habit were excluded, leaving 576 cases and 1,599 controls eligible for the analyses. Anti- H. pylori IgGantibody and serum pepsinogens (PG) were measured to detect H. pylori infection and gastric atrophy. Smokingstatus was asked by a self-administered questionnaire. The odds ratio (OR) of H. pylori infection, as well as theOR of gastric atrophy among the H. pylori seropositive controls was not significant for smokers. The age- andsex-adjusted OR of gastric cancer was significantly elevated relative to the subjects with gastric atrophy: OR=1.62(95% confidence interval (CI), 1.19-2.22; P=0.002) for ever smokers and 2.52 (1.75-3.64; P<0.001) for currentsmokers, relative to never smokers. This study revealed that smoking behavior contributed to the increased riskof gastric carcinogenesis from gastric atrophy, and had little influence on H. pylori infection or gastric atrophydevelopment.     

食管癌高发区山东省肥城市2006年至2016年食管癌前病变转归情况分析

  目的  研究食管癌高发区中国山东省肥城市食管癌前病变自然转归情况，为食管癌前病变及食管鳞癌的防治工作提供科学依据。  方法  回顾性收集山东省肥城市2006年至2016年期间进行内镜病理诊断且未治疗并进行二次内镜随访的受检者资料进行分析，描述癌前病变病例的具体复查结果，计算进展病例的累积进展率和进展时间，分析食管癌前病变病例的转归情况。  结果  本研究共纳入1 834例食管癌前病变病例，其中1 148例（62.6%）癌前病变发生逆转，148例（8.1%）发生进展。逆转为正常状态的病例共234例（12.8%），进展为食管癌共17例（0.9%）。各级别癌前病变进展为食管癌的病例比例由高至低依次为:重度异型增生/原位癌（4.9%）、中度异型增生（1.3%）、轻度异型增生（0.2%）；其发生癌变的中位进展时间由高至低依次为:轻度异型增生（5.62年）、中度异型增生（1.76年）和重度异型增生/原位癌（1.61年）。轻度异型增生9年累积进展为重度异型增生/原位癌及以上的进展率远小于中度异型增生（1.81% vs.9.98%），重度异型增生/原位癌进展为食管癌的累积进展率始终高于中度和轻度异型增生。  结论  超过一半以上的癌前病变会逆转为较低级别病变或正常状态；食管癌前病变的累积癌变率随病变级别的增高而增大，中位进展时间随病变级别的增高而缩短。大多数癌前病变进展为食管癌的时间间隔基本与《癌症早诊早治上消化道癌筛查及早诊早治技术方案》中的随访间隔相符，可适当对轻度异型增生患者的随访间隔缩短为每2年1次。      

Outcome of Intestinal Metaplasia in Gastric Biopsy of Patients with Dyspepsia in Guilan Province,North Iran

Background: It is generally accepted that gastric carcinomas are preceded by a sequential multistage processthat includes chronic gastritis, gastric atrophy, usually with intestinal metaplasia (IM), and dysplasia. This seriesof changes in gastric carcinogenesis is often initiated by Helicobacter pylori (H pylori) infection. The aim of thepresent study was determination of gastric histopathologic changes in IM patients after at least one year in Guilanprovince, Iran. Materials and Methods: This case-series study was conducted in Guilan Gastrointestinal and LiverDisease Research Center (GLDRC) during 2010 to 2011. Gastric biopsy was performed for all 71 known cases ofIM and precanceric lesions including gastric atrophy, IM, dysplasia and H pylori infection were determined afterat least one year. Results: Of the total of 71 patients with established IM who were enrolled, 50 had complete-typeIM and 21 had incomplete-type IM. Fifty two people had H pylori infection. H pylori eradication was achievedin 39 patients (75%). Secondary pathology findings of patients with IM were complete metaplasia (39.4%),incomplete metaplasia (32.4%), dysplasia (23.9%) and other precanceric lesions (4.2%). Dysplasia (20%vs 33%)occurred in patients who had complete and incomplete IM at baseline respectively (p>0.05). Age, gender, familyhistory of gastric cancer(GC); smoking habits and NSAIDs use were not associated with gastric premalignantlesions in initial and secondary pathologies (p>0.05). The difference became statistically significant between Hpylori infection in patients with more than 3 years diagnostic intervals (p<0.05). Statistical difference betweeneradicators and non-eradicators was not significant. Conclusions: We found that incomplete IM increased therisk of subsequent dysplasia in this study.     

Evolution of precancerous lesions in a rural Chinese population at high risk of gastric cancer.

The pathogenesis of gastric cancer (GC), particularly of the intestinal type, is thought to involve a multistep and multifactorial process. Our objective was to determine the rates of transition from early to advanced gastric lesions in a population in Linqu County, China, where the GC rates are among the highest in the world. An endoscopic screening survey was launched in 1989-1990 among 3,399 residents aged 34-64 years with precancerous lesions diagnosed from biopsies taken from 7 standard locations in the stomach and from any suspicious sites. The cohort was subsequently followed, with endoscopic and histopathologic examinations conducted in 1994. Logistic regression analysis was used to estimate odds ratios (ORs) of progression to advanced lesions of various levels of severity as a function of age, sex and baseline pathology. The rates of progression were higher among older subjects, among men and among subjects with more extensive gastric lesions. 34 incident GCs were identified during the follow-up period. The ORs of GC, adjusted for age and sex, varied from 17.1, for those with baseline diagnoses of superficial intestinal metaplasia (IM), to 29.3, for those with deep IM or mild dysplasia (DYS) or IM with glandular atrophy and neck hyperplasia, to 104.2, for those with moderate or severe DYS, as compared with subjects with superficial gastritis (SG) or chronic atrophic gastritis (CAG) at baseline. Our prospective study of a high-risk population revealed sharp increases in the risk of GC and advanced precursor lesions according to the severity of lesions diagnosed at the start of follow-up. Int. J. Cancer, 83:615-619, 1999. Published 1999 Wiley-Liss, Inc.     

Association between oral health and gastric precancerous lesions

Although recent studies have suggested that tooth loss is positively related to the risk of gastric non-cardia cancer, the underlying oral health conditions potentially responsible for the association remain unknown. We investigated whether clinical and behavioral measures of oral health are associated with the risk of gastric precancerous lesions. We conducted a cross-sectional study of 131 patients undergoing upper gastrointestinal endoscopy. Cases were defined as those with gastric precancerous lesions including intestinal metaplasia or chronic atrophic gastritis on the basis of standard biopsy review. A validated structured questionnaire was administered to obtain information on oral health behaviors. A comprehensive clinical oral health examination was performed on a subset of 91 patients to evaluate for periodontal disease and dental caries experience. A total of 41 (31%) cases of gastric precancerous lesions were identified. Compared with non-cases, cases were significantly more likely to not floss their teeth [odds ratio (OR) = 2.89, 95% confidence interval (CI): 1.09-7.64], adjusting for age, sex, race, body mass index, smoking status, educational attainment and Helicobacter pylori status in serum. Among participants who completed the oral examination, cases (n = 28) were more likely to have a higher percentage of sites with gingival bleeding than non-cases [OR = 2.63, 95% CI: 1.37-5.05 for a standard deviation increase in bleeding sites (equivalent to 19.7%)], independent of potential confounders. Our findings demonstrate that specific oral health conditions and behaviors such as gingival bleeding and tooth flossing are associated with gastric precancerous lesions.     

Helicobacter pylori seropositivity and subsite-specific gastric cancer risks in Linxian, China

BACKGROUND: Helicobacter pylori carriage (i.e., persistent exposure to the organism without gastric epithelial cell invasion) is an established risk factor for noncardia gastric cancer. However, its association with the risk of cancer of the gastric cardia is controversial. Consequently, we designed this prospective, nested case-control study to further explore the subsite-specific gastric cancer risks associated with H. pylori seropositivity (a surrogate marker for persistent exposure). METHODS: A total of 99 patients with gastric cardia cancer, 82 patients with noncardia gastric cancer, and 192 cancer-free subjects were selected from among the participants (n = 29 584) of a nutrition intervention trial previously conducted in Linxian, China. H. pylori seropositivity was determined by assaying for the presence of H. pylori whole cell and CagA antibodies in baseline serum samples from all subjects. Seropositivity was defined as one or both serum assays being positive. Odds ratios (ORs) for subsite-specific gastric cancer were estimated by multivariate logistic regression analyses. All statistical comparisons were two-sided (alpha =.05). RESULTS: H. pylori seropositivity rates for subjects with gastric cardia cancer, noncardia gastric cancer, and gastric cardia and noncardia cancers combined were 70% (P =.02), 72% (P: =.01), and 71% (P =.003) compared with 56% for cancer-free control subjects. OR estimates for H. pylori seropositivity were 1.87 (95% confidence interval [CI] = 1.10 to 3.17) for gastric cardia cancer, 2.29 (95% CI = 1.26 to 4.14) for noncardia gastric cancer, and 2.04 (95% CI = 1.31 to 3.18) for gastric cardia and noncardia cancers combined. CONCLUSIONS: H. pylori seropositivity was associated with increased risks for both gastric cardia cancer and noncardia gastric cancer in this well-characterized cohort. Thus, H. pylori carriage may increase the risk of cancer throughout the stomach.