Formation of nitrite in gastric juice of patients with various gastric disorders after ingestion of a standard dose of nitrate--a possible risk factor in gastric carcinogenesis

Samples of fasting gastric juice (12-h fasting period) from patients with various upper gastrointestinal complaints and from healthy controls were collected by aspiration immediately before and 30, 90, and 240 min after ingestion of 200 mg nitrate in water. Nitrite concentration in the gastric juice of healthy controls remained essentially in a low concentration range throughout the whole sampling period (median values at various time points, 0.1-1.7 mg/L). Patients with gastric and duodenal ulcers and patients who had undergone proximal-gastral vagotomy did not show significant increases in gastric nitrite at any time when compared with healthy controls, using the Wilcoxon rank sum test. Patients with chronic atrophic gastritis and those who had undergone Billroth I or Billroth II gastric resection, however, showed significant increases in gastric nitrite, sometimes with high individual peaks: 80 mg/L in one patient with chronic atrophic gastritis, 50 mg/L in a Billroth I patient and 200 mg/L in a Billroth II patient. The results show that patients with chronic atrophic gastritis and patients who have undergone Billroth I and Billroth II gastrotomy not only have higher basal nitrite values in their gastric juice (12-h fasting) but also react with significantly higher increases in gastric nitrite to an oral dose of 200 mg nitrate, compared with healthy controls, ulcer patients and patients who have undergone proximal-gastral vagotomy. Higher nitrite levels might lead to an enhanced intragastric formation of N-nitroso compounds, and this might be relevant to the increased gastric cancer risk of these groups of patients.     

Analysis of Pathogenic Factors of Helicobacter Pylori in a High Prevalence Area of Gastric Cancer in Xinin,Qinghai Province

OBJECTIVE To analyze positive rates of the specific proteins CagA, VacA, UreA and UreB of Helicobacter pylori (Hp) in people in Xinin city Qinghai Province, a district with a high prevalence of gastric carcinoma, and to examine the relationship among the incidence, gross diagnosis and pathologic diagnosis. METHODS The gastric tissue biopsy specimens taken under endoscopy were examined by CLO,WS and Western Blot to judge the condition of the Hp infection. The positive rates of Hp CagA,VacA,UreA and UreB that had infected patients were evaluated. RESULTS The positive rate of UreA was markedly lower in chronic superficial gastritis (CSG) than in duodenal ulcer (DU) and compound ulcer, and also lower than in chronic atrophic gastritis(CAG), gastric ulcer(GU) and gastric cancinoma. However the positive rate of UreB was notably lower in duodenal ulcer and gastric ulcer than in chronic superficial gastritis and atrophic gastritis. The rates of UreB found in intestinal epithelial metaplasia, atrophic gastritis and gastric carcinoma were notably lower than in other diseases, however, it was markedly increased in chronic superficial gastritis, No differences were found among CagA and VacA of specimens with different endoscopic diagnosis or pathologic diagnosis. CONCLUSIONS The UreA in Hp may be relevant to the pathogenic mechanism of severe gastric diseases. However, UreB may have some protective effect on severe gastric diseases.     

Peptic ulcer disease and the risk of bladder cancer in a prospective study of male health professionals.

Helicobacter pylori is a risk factor for gastric and duodenal ulcers, but gastric ulcers generally occur in individuals who have low acid production and diffuse gastritis, whereas duodenal ulcers are more likely to occur with high acid output and antrum-predominant gastritis. Low acid production, gastritis, and ulcer healing each contribute to poor antioxidant absorption, oxidative stress, and elevated nitrite levels in the stomach. N-Nitrosamines are known carcinogens, and nitrate ingestion has been related to bladder cancer risk. Consequently, we hypothesized that the gastric conditions associated with gastric ulcers may contribute to elevated bladder cancer risk. We thus examined the association between self-reported history of peptic ulcer disease and the risk of bladder cancer (414 cases) over 14 years of follow-up in the Health Professional Follow-Up Study. Cox proportional hazards models were performed to adjust for known risk factors of bladder cancer. Men who reported a gastric ulcer before 1986 had a significantly higher risk of bladder cancer compared with those with no history of gastric ulcer (relative risk = 1.55, 95% confidence interval = 1.03-2.33, controlling for smoking and other potential confounders). No association was observed for duodenal ulcers (multivariate relative risk = 0.97, 95% confidence interval = 0.68-1.38). The ulcers in this study were based solely on self-report and not medical records; consequently, misclassification of ulcers may have occurred. Although intriguing, these findings need to be replicated.     

幽门螺杆菌感染与胃部疾病的相关性

[目的]探讨幽门螺杆菌（Hp）感染在胃癌发生发展中的作用。[方法]选择2009年1月至2012年12月经胃镜检查病理确诊胃部疾病439例患者,其中慢性浅表性胃炎163例、慢性萎缩性胃炎64例、胃食管反流病47例、胃溃疡79例、十二指肠溃疡54例、胃不典型增生12例和胃癌20例。采用C14呼气实验和快速尿素酶法,二项任意一项阳性均被诊断胃Hp阳性。[结果]胃部疾病439例患者中Hp阳性219例,阳性率为49．89％。胃癌患者的Hp阳性率比慢性胃炎患者Hp阳性率高（65．00％VS43．17％,χ^2=3．850,P=0．043）,也比胃食管反流病患者Hp阳性率高（65．00％vs34．04％,χ^2=5．477,19=0．019）,但与胃、十二指肠溃疡患者比较Hp阳性率无统计学差异（65．00％V863．91％,χ^2=0．009,／9=0．925）。60岁以下者,随年龄增长Hp感染率逐渐升高。[结论]胃幽门螺杆菌感染与胃溃疡、不典型增生和胃癌的发生有着密切的关系,幽门螺杆菌感染是胃癌的危险因素。根除Hp感染治疗可能有助于降低胃癌发生的风险。     

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

The coexistence of gastric cancer with duodenal ulcer has been found empirically to be rare, but why it is rare is difficult to explain satisfactorily. To elucidate this question, we carried out a literature review of the subject. The frequency with which the two diseases coexist is 0.1–1.7%, and the main factor associated with both gastric cancer and duodenal ulcer is Helicobacter pylori infection. However, there are marked differences between the disorders of hyperchlorhydria in duodenal ulcer, and hypochlorhydria in gastric cancer. The most acceptable view of the reason for the difference may be that the acquisition of H. pylori infection occurs mainly in childhood, so that the time of acquisition of atrophic gastritis may be the most important, and if atrophic gastritis is not acquired early, high levels of gastric acid may occur, and consequently acute antral gastritis and duodenal ulcer may occur in youth, whereas, in elderly individuals, persistent H. pylori infections and the early appearance of atrophic gastritis may be the causes of low gastric acid, and consequently gastric cancer may occur. In patients with duodenal ulcer, factors such as nonsteroidal anti-inflammatory drugs (NSAIDs) and dupA-H. pylori strains may contribute to preventing the early acquisition of atrophic gastritis, while acid-suppressive therapy and vascular endothelial growth factor and other entities may inhibit atrophic gastritis. In contrast, in gastric cancer, factors such as excessive salt intake, acid-suppressive therapy, polymorphisms of inflammatory cytokines, and the homB-H. pylori strain may contribute to the early acquisition of atrophic gastritis, while factors such as NSAIDs; fruits and vegetables; vitamins A, C, and E; and good nutrition may inhibit it.     

The ambulatory care of patients with precancerous diseases of the stomach

Two hundred and ninety-four patients with precancerous lesions of the stomach were followed and treated. The group included cases of gastric ulcer (101), polyps (78), atrophic-hyperplastic gastritis (81) and 34 patients who had undergone gastric resection for duodenal ulcer. Pathologic foci were surrounded by areas of epithelial dysplasia of varying degree in almost all patients. In the course of follow-up and treatment, dysplasia regressed in several cases and progressed to early cancer of the stomach in three. Recommendations for periodicity of check-ups of patients with chronic cancer of the stomach depending on degree of mucosal epithelium dysplasia were developed.     

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.     

Vagotomy--a prospective, randomized study.

This is a report of a prospective randomized study of 3 operations for duodenal ulcer; parietal-cell vagotomy alone (without drainage), selective vagotomy with antrectomy, and truncal vagotomy with antrectomy. All patients in the study have been followed for a minimum of 1 yr and despite the small number of patients (total 23 in this report), there has been a statistically significant return of gastric secretory activity to preoperative levels in the parietal cell vagotomy group, while both other groups maintained decreased acid secretion at the 1-yr period. To date there has been one recurrent ulcer and one other suspected ulcer in the parietal cell vagotomy group, while both other groups have no ulcer recurrence even though morbidity has been higher (bile reflux gastritis, and so forth). This preliminary evaluation suggests strongly that extreme caution be used in applying parietal-cell vagotomy alone as a definite operation for duodenal ulcer, but because of the small number of patients involved no conclusions can be drawn at this time.     

The risk of pancreatic cancer in patients with gastric or duodenal ulcer disease

Although Helicobacter pylori (H. pylori) seropositivity is linked to an excess risk of pancreatic cancer, the biologic mechanism is unknown. Gastric ulcer is primarily associated with corpus colonization of H. pylori, atrophic gastritis and formation of N-nitrosamines. Duodenal ulcer is a marker of antral colonization, hyperacidity and uninhibited secretin release. We estimated relative risks for pancreatic cancer among patients with gastric or duodenal ulcer, based on a register-based retrospective cohort study with 88,338 patients hospitalized for gastric ulcer and 70,516 patients for duodenal ulcer recorded in the Swedish Inpatient Register between 1965 and 2003. Following operation, the 14,887 patients who underwent gastric resection and 8,205 with vagotomy were analyzed separately. Multiple record-linkages allowed complete follow-up and identification of all incident cases of pancreatic cancer until December 31, 2003. Standardized incidence ratios (SIRs) estimated relative risks. During years 3-38 of follow-up, we observed a 20% excess risk (95% confidence interval [CI] 10-40%) for pancreatic cancer among unoperated gastric ulcer patients. The excess increased to 50% (95% CI 10-110%) 15 years after first hospitalization (p for trend = 0.03). SIR was 2.1 (95% CI 1.4-3.1) 20 years after gastric resection. Unoperated duodenal ulcer was not associated with pancreatic cancer risk, nor was vagotomy. Our results lend indirect support to the nitrosamine hypothesis, but not to the hyperacidity hypothesis in the etiology of pancreatic cancer.     

慢性胃病伴肠上皮化生、胃癌与幽门螺旋杆菌感染的关系

目的探讨慢性胃病伴肠上皮化生、胃癌与幽门螺旋杆菌（helicobacter pylore,HP）感染的关系。方法采用warthin—strarry银染色方法,对380例慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡组织及胃癌的癌旁组织进行HP检测．应用（alcianblue—PH2．5-periodic—schiff,AB—PAS）、（high-iron—diamine-alcianblue—PH2．5,HID-AB）黏液组织化学方法,区别慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡组织及胃癌的癌旁组织伴有肠上皮化生的类型。结果总例数380例。HP阳性率为69．74％。慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡组织及胃癌的癌旁组织伴肠上皮化生的HP感染率分别为77．78％、85．71％、100．00％、80．95％。慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡及胃癌的癌旁组织伴肠上皮化生AB—PAS染色阳性率分别为86．84％、91．43％、93．33％、100．00％;HID—AB染色阳性率分别为34．21％、42．86％、53．33％、85．71％。癌旁组织的肠上皮化生中,78．57％为不完全大肠型,慢性浅表性胃炎、慢性萎缩性胃炎、胃溃疡伴肠上皮化生中,不完全小肠型比例分别为52．63％、54．28％、53．33％;不完全大肠型比例分别为28．95％、31．43％、20．00％。结论HP感染与慢性胃病伴肠上皮化生及胃癌的发生密切相关。癌旁组织的不完全大肠型肠上皮化生与胃癌的发生密切相关;慢性胃病组织当中的小灶状不完全大肠型上皮化生具有潜在发生癌变的可能性。     

Effect of human gastric juice on dimethylamine nitrosation by sodium nitrite

The study was concerned with evaluation of the effect of human gastric juice (samples obtained from 157 subjects) on in vitro dimethylnitrosamine nitrosation by sodium nitrite versus gastric mucosa pathology (gastritis, polyps, ulcer, cancer), gastric juice pH and nitrate ion level. Also, the influence of gastric juice glycosaminoglycans and glycoproteins levels as well as N-acetylneuraminic acid isolated from porcine blood was assessed. An increased nitrosating activity of gastric juice was observed in cases of gastritis and ulcer and in those with low nitrate ion activity. Glycosaminoglycans and glycoproteins were found to inhibit nitrosation. N-acetylneuraminic acid in the concentrations used exerted no effect on dimethylnitrosamine nitrosation by sodium nitrite.     

An investigation of possible risk factors associated with gastric cancer after benign ulcer operations

The risk of developing gastric cancer has been investigated in a case-control study and in a prospective investigation. In the case-control study, 1495 cases of gastric cancer were identified in five city hospitals and matched with autopsy controls from the same hospitals. The frequency of operations for benign ulcer [partial gastrectomy (PG) and gastroenterostomy] was similar in the two groups. Thus, there was no increased risk for late gastric cancer after an ulcer operation. A total of 140 operated ulcer subjects [80 truncal vagotomy and drainage (TVD), 60 PG and 78 nonoperated cases attending with dyspepsia (C)] were examined by endoscopy, multiple gastric biopsy and analysis of gastric juice for nitrite. Biopsies were graded for gastritis and a gastritis index was derived (normal, 1; superficial gastritis, 2; chronic atrophic gastritis: mild, 3; moderate, 4; severe, 5). More atrophic gastritis was found in operated subjects than in controls: TVD, 2.3 +/- 0.08 (mean +/- SE); PG, 2.6 +/- 0.1 versus C, 1.8 +/- 0.08, p less than 0.01. The severity of atrophic gastritis increased after an operation interval of 20 years in PG subjects (p less than 0.05). Intestinal metaplasia was a common change, but unequivocal epithelial dysplasia was not observed. Two cases of operated stomach cancer were found. High levels of nitrite were positively correlated with pH and a high gastritis index. This evidence does not suggest that ulcer surgery leads to either an increased risk of cancer or a precancerous condition.     

Low frequency of intestinal metaplasia in gastric biopsies from Mexican patients: a comparison with Japanese and Swedish patients.

A systematic analysis of the cellular and structural components of intestinal metaplasia (IM) was carried out in 691 consecutive endoscopic gastric biopsies from Mexicans patients. Two-thirds of the patients (461 or 66.7%) had chronic gastritis, 27.6% (or 191 patients) had gastric ulcers and 5.6% (39 patients) gastric carcinomas. IM was found in 17.4% of the gastric biopsies. While IM was present in 27.7% of patients with gastric peptic ulcer, patients with gastric malignancy had only 18.7%, and the lowest rate (13.4%) was found in 461 biopsies from patients with chronic gastritis. IM was influenced by the age but not by the sex of the patients. Only one of 120 biopsies with IM (0.8%) had incomplete IM (a lesion claimed to be a precursor of gastric carcinoma). In a previous study it was found that 32.3% of 359 Swedish patients and 59.2% of 625 Japanese patients with chronic gastritis had IM, the proportion of incomplete IM being 23.3% and 25.1%, respectively. The low frequency of IM among Mexicans (a population with a low incidence of gastric carcinoma), contrasts with the moderate frequency of IM among Swedes (who have a moderate gastric cancer incidence) and with the high frequency of IM among Japanese (with a high incidence of gastric carcinoma). These findings recorded in disparate geographical regions strongly support the view that IM is a lesion evoked by environmental factors and associated with gastric carcinogenesis.     

Low Frequency of Intestinal Metaplasia in Gastric Biopsies from Mexican Patients: A Comparison with Japanese and Swedish Patients

A systematic analysis of the cellular and structural components of intestinal metaplasia (IM) was carried out in 691 consecutive endoscopic gastric biopsies from Mexicans patients. Two-thirds of the patients (461 or 66.7%) had chronic gastritis, 27.6% (or 191 patients) had gastric ulcers and 5.6% (39 patients) gastric carcinomas. IM was found in 17.4% of the gastric biopsies. While IM was present in 27.7% of patients with gastric peptic ulcer, patients with gastric malignancy had only 18.7%, and the lowest rate (13.4%) was found in 461 biopsies from patients with chronic gastritis. IM was influenced by the age but not by the sex of the patients. Only one of 120 biopsies with IM (0.8%) had incomplete IM (a lesion claimed to be a precursor of gastric carcinoma). In a previous study it was found that 32.3% of 359 Swedish patients and 59.2% of 625 Japanese patients with chronic gastritis had IM, the proportion of incomplete IM being 23.3% and 25.1%, respectively. The low frequency of IM among Mexicans (a population with a low incidence of gastric carcinoma), contrasts with the moderate frequency of IM among Swedes (who have a moderate gastric cancer incidence) and with the high frequency of IM among Japanese (with a high incidence of gastric carcinoma). These findings recorded in disparate geographical regions strongly support the view that IM is a lesion evoked by environmental factors and associated with gastric carcinogenesis.     

Age and severity of mucosal lesions influence the performance of serologic markers in Helicobacter pylori-associated gastroduodenal pathologies

OBJECTIVE: The course of Helicobacter pylori infection and antibody response to CagA in patients with preneoplastic lesions and gastric cancer has not been thoroughly studied. We aimed to study H. pylori infection and antibody response to CagA in patients with non-atrophic gastritis, preneoplastic lesions, and gastric cancer. METHODS: We studied patients attending one Oncology Hospital and one General Hospital in Mexico City. Diagnosis was based on endoscopy and histopathology in biopsies from six stomach regions. H. pylori infection was assessed by histology and serology, and antibodies against CagA were measured with immunoassay. RESULTS: We included 618 patients, 368 with non-atrophic gastritis, 126 with precancerous lesions, and 65 with gastric cancer; in addition, 59 patients with duodenal ulcer were studied. Detection of infection and IgG against CagA had a significant increase from non-atrophic gastritis to mild and up to advanced stages of metaplasia (P < 0.05), followed by decreased infection and IgG to CagA in patients with gastric cancer (P < 0.05). However, infection and CagA antibodies were associated with young gastric cancer cases. Duodenal ulcer showed a significant association with infection detected by histology and serology, particularly among women, and a trend to associate with IgG to CagA. CONCLUSIONS: This study shows that H. pylori infection and CagA are risk markers for intestinal metaplasia. The prevalence of these risk markers decreases in gastric cancer, probably reflecting that infection decreases after advanced atrophy and metaplasia in the gastric mucosa. State of the disease, age, and sex influence the association of H. pylori infection and IgG response to CagA with gastroduodenal diseases.     

Helicobacter pylori infection and gastric diseases--pathogenesis and effects of eradication

H. pylori infection is associated with major gastroduodenal diseases, i.e. peptic ulcer, cancer and MALT lymphoma in the stomach. The pathogenesis of H. pylori in these diseases has been elucidated. Non-atrophic diffuse antral gastritis is correlated with duodenal ulcer and multifocal atrophic gastritis is correlated with both gastric ulcer and cancer. It is well known that Japanese tend to have multifocal atrophic gastritis. H. pylori eradication therapy dramatically reduces the recurrence rates of gastroduodenal ulcers in humans and bacterial eradication for peptic ulcer patients has been recommended in many countries. Mongolian gerbils have provided an excellent model of gastric carcinogenesis and H. pylori enhanced (promoted) chemical carcinogen-induced carcinogenesis in the stomach using this model. H. pylori eradication reduced the incidence of gastric cancer in the Mongolian gerbil model. It was a recently discovered that a transforming clone carrying the translocation t (11;18) (q21;q21) forms a MALT lymphoma, the growth of which is independent of H. pylori and will not respond to bacterial eradication. In the early stage, the tumor can be successfully treated by eradication, but at a later stage additional genetic abnormality in the lymphoma may show no response to H. pylori eradication therapy.     

电子胃镜联合miR-21检测对胃癌诊断的意义

目的 探讨电子胃镜检查联合组织miR-21表达水平检测对胃癌诊断的意义.方法 纳入2011年6月至2012年12月进行胃镜检查的患者96例,胃镜检查同时胃镜下钳取患者胃内病变组织,通过对比胃镜诊断与病理诊断结果计算胃镜确诊率及漏诊率;应用实时荧光定量PCR对组织进行miR-21表达水平检测,对比胃镜下不同表现的各种疾病的miR-21表达水平.结果 胃癌、胃溃疡、慢性浅表性胃炎、胃食管反流性胃炎、慢性萎缩性胃炎检出率分别为28.12％（27/96）、30.21％（29/96）、18.75％（18/96）、10.42％（10/96）、12.50 ％（12/96）,胃镜检查胃癌确诊率为100.00％,漏诊率6.90％（2/29）;胃癌组miR-21相对表达量为54.41±6.66,明显高于胃溃疡组及其他疾病组（P＜0.01）.结论 电子胃镜检查能较好地对胃癌患者进行筛查,胃镜下钳取组织行miR-21表达水平检测能提高胃镜对胃癌筛查的准确率,两者联合对胃癌诊断具重要价值.     

HP感染的消化性溃疡伴胃癌前病变与自噬因子的相关性研究

目的：探讨幽门螺杆菌（helicobacterpylori,HP）感染伴胃黏膜癌前病变与自噬因子LC3B表达水平之间的相关性。方法收集经胃镜及黏膜下活检确诊为消化性溃疡的患者263例,采用半定量RT-PCR方法检测所有患者的自噬因子LC3B表达水平,同时行碳14呼气试验进行HP检测,分别比较患者的HP阳性检出率与自噬因子LC3B表达水平之间的相关性;以及HP感染的消化性溃疡伴胃癌前病变与自噬因子LC3 B表达水平之间的相关度。结果自噬因子LC3B mRNA高表达与HP检出率呈正相关;自噬因子LC3B mRNA高表达与慢性胃炎伴不典型增生组的发病率呈正相关。结论自噬因子LC3B mRNA高表达与HP感染及消化性溃疡伴胃黏膜不典型增生具有相关性。     

Polymorphisms in TNF and HSP‐70 show a significant association with gastric cancer and duodenal ulcer

Tumour Necrosis Factor (TNF) and Heat Shock Protein 70 (HSP70) are important molecules in inflammatory, infectious and tumoral processes. The genes codifying these molecules are polymorphic and certain alleles have been associated with susceptibility to disease. Gastric cancer is associated with an Helicobacter pylori‐induced chronic inflammatory response. The aim of this work was to analyze whether polymorphisms in inflammation‐related genes are associated with the development of gastric cancer. We studied 447 Mexican adult patients including 228 with non‐atrophic gastritis, 98 with intestinal metaplasia, 63 with gastric cancer and 58 with duodenal ulcer, and 132 asymptomatic individuals as well. DNA from peripheral white blood cells was typed for the Single Nucleotide Polymorphisms (SNPs) ?308 of TNF‐α, +252 of TNF‐β, +190 of HSP70‐1, +1267 of HSP70‐2 and +2437 of HSP70‐HOM. Compared with the asymptomatic group, we found a significant association of TNF‐β*A and HSP70‐1*C alleles with gastric cancer (OR 5.69 and 3.76, respectively) and HSP70‐1*C with duodenal ulcer (OR 3.08). Genotype TNF‐β G/G showed a significant gene‐dose effect with gastric cancer (OR 0.09); whereas HSP70‐1 C/G showed significant association with both, gastric cancer (OR 13.31) and duodenal ulcer (OR 16.19). Polymorphisms in TNF and HSP70 showed a significant severity‐dose‐response as risk markers from preneoplastic lesions to gastric cancer in Mexican population, probably because of their association with an intense and sustained inflammatory response.     

Cytotoxin Genes of Helicobacter pylori in Chronic Gastritis, Gastroduodenal Ulcer and Gastric Cancer: An Age and Gender Matched Case-Control Study

Helicobacter pylori (H. pylori) infection is involved in many gastrointestinal diseases, such as chronic gastritis (CAG), peptic ulcer and gastric cancer (GCA). Both host factors and H. pylori strain differences may contribute to differences in the diseases. Thus, we conducted an age and gender matched case-control study of 35 patients each with CAG, gastric ulcer (GUL), duodenal ulcer (DUL) and gastric cancer (GCA) to examine the role of strain differences of the H, pylori cytotoxin genes cagA and vacA in these diseases. We employed polymerase chain reaction to examine the gastric juice for H. pylori DNA. The test was positive for 26 (74.3%) CAG, 29 (82.9%) GUL, 28 (80.0%) DUL and 27 (77.1%) GCA patients, showing no statistically significant difference among the diseases (P= 0.84). cagA and vacA genes (picked up by using a vacA l+ vacA 2 primer pair which detected nonvariable regions of the vacA gene) were detected by PCR in the H. pylori DNA-positive cases as follows: CAG, 92.3% and 76.9%; GUL, 100% and 86.2%; DUL, 89.3% and 89.3%; GCA, 92.6% and 85.2%, respectively. No statistically significant differences were found in the frequencies of these cytotoxin genes in H. pylori -positive cases among the various gastric diseases ( P =0.39 for cagA and P=0.64 for vacA ).