消化病患者胃肠引流液中幽门螺杆菌检出率和患者Vit C水平

目的探讨胃肠引流液中幽门螺杆菌(Helicobacterpylori,H.pylori)的检出率及患者VitC水平。方法用PCR技术、细菌培养、快速尿素酶试验检测胃肠引流液中的H.pylori,用反相液相色谱法检测患者胃肠引流液及血浆中VitC含量。结果282例患者胃肠引流液中H.pylori检出率为41.1%(116/282),PCR、细菌培养及快速尿素酶试验阳性率分别为42.9%(121/282)、11.3%(32/282)、41.1%(116/282)。胃溃疡、十二指肠溃疡、复合溃疡、胃癌、急性肠梗阻、急性胆囊炎及门静脉高压合并食管胃底静脉曲张患者H.pylori检出率分别为54.6%(30/55)、52.2%(24/46)、58.3%(7/12)、48.2%(27/56)、22.2%(8/36)、27.6%(16/58)、21.1%(4/19),差异具显著性(P<0.01)。胃溃疡、十二指肠溃疡、复合溃疡、胃癌H.pylori阳性患者与H.pylori阴性患者血浆及胃肠引流液VitC浓度相比,差异均具有显著性(P<0.01)。结论胃肠引流液中可检出H.pylori,且能分离培养出活菌;PCR技术是一种敏感、有效的检测胃引流液中H.pylori的方法。H.pylori感染人体后引起胃肠引流液及血浆中VitC含量的减少,可能与胃十二指肠疾病的发生有关。     

N-nitrosamines in gastric juice of patients with gastric ulcer before and during treatment with histamine H2-receptor antagonists

The clinical implications of N-nitrosamines (NAs) were studied by analyzing their concentration in the gastric juice of 72 healthy subjects and 279 patients with gastric ulcer before and during treatment with histamine H2-receptor antagonists. NAs were measured by combined gas chromatography and thermal energy analyzer. The detection ratios of N-nitrosodimethylamine (NDMA) and N-nitrosodiethylamine (NDEA) in the patients were 35.3% and 34.6%, respectively, which were significantly higher than the corresponding values in healthy subjects (19.4% and 16.7%, P less than 0.01). Analysis among the patients showed that this trend was mainly due to higher values in patients who were given histamine H2-receptor antagonists, as their detection ratios increased to 40.2% (NDMA) and 39.9% (NDEA). Patients without histamine H2-receptor antagonists showed moderate increases of detection ratios (NDMA; 24.2% NDEA; 22.6%) compared with healthy controls. The differences in these values between those receiving and not receiving histamine H2-receptor antagonists were statistically significant (P less than 0.01). The maximum concentrations of NDMA and NDEA were 7.9 and 9.8 ng/ml in patients, and 1.2 and 1.3 ng/ml in healthy subjects (the difference between the 2 groups P less than 0.02). These results indicated that patients with gastric ulcer had higher detection ratios and concentrations of NDMA and NDEA in gastric juice and that, while significant increases occurred during treatment with histamine H2-receptor antagonists, the extent of increase was below toxic or experimental carcinogenic levels.     

Link betweenHelicobacter pylori-associated gastritis and duodenal ulcer

We examined the interrelationships among the degree of fundic mucosal atrophy, the prevalence ofHelicobacter pylori in the gastric antrum, the gastric juice, and the duodenum with and without gastric metaplasia, in 20 duodenal ulcer patients and 20 non-duodenal ulcer patients. The detection rates ofH. pylori in the antrum, the gastric juice, and the duodenum were significantly higher in duodenal ulcer patients (80%, 65%, and 60%) than in non-duodenal ulcer subjects (50%, 20%, and 5%). The frequency ofH. pylori was significantly lower in the gastric juice (30%) and the duodenum (10%) in non-duodenal ulcer patients with antralH. pylori, compared with those in duodenal ulcer patients with antralH. pylori. All of seven patients with both gastric metaplasia andH. pylori infection in the duodenum had duodenal ulcer, whereas only 1 of 14 patients without either gastric metaplasia orH. pylori infection in the duodenum had duodenal ulcer. There was normal or mild atrophic mucosa in the fundus of duodenal ulcer patients withH. pylori in the antrum, whereas moderate or severe atrophic mucosa in non-duodenal ulcer patients withH. pylori gastritis. These results suggest that the preserved fundic mucosa, gastric metaplasia in the duodenum, and a greater load ofH. pylori to the duodenum through the gastric juice may be prerequisites for the formation of duodenal ulcers.     

A population based study of Helicobacter pylori infection in a European country: the San Marino Study. Relations with gastrointestinal diseases.

Helicobacter pylori is present worldwide but few large population studies exist on the epidemiology of the infection. A random cross sectional study was performed of H pylori infection in the adult population of San Marino, a European country with high gastric cancer rate, to assess its prevalence and to evaluate its relations with gastrointestinal disease. In 2237 subjects (77% of the initial sample) H pylori IgG antibodies were detected with enzyme linked immunosorbent assay (ELISA) and immunoblotting. A questionnaire including questions about occupation, place of birth, and smoking was given to all subjects. Dyspepsia, peptic ulcer, and gastric cancer in the subjects, relatives, and partners as well as use of drug, dental treatment/prostheses, and gastrointestinal endoscopies, were evaluated by multivariate analysis. H pylori prevalence was of 51%, increased with age from 23% (20-29 years) to 68% (> or = 70 years), and was higher among manual workers. H pylori was independently associated with ulcer (OR = 1.63, 95% confidence intervals (CI) = 1.16 to 2.27), H2 antagonists (OR = 1.94, 95% CI = 1.21 to 3.10), and benzodiazepines (OR = 1.57, 95% CI = 1.02 to 2.42), dental prostheses (OR = 1.25, 95% CI = 1.05 to 1.49), gastroscopy in the past five years (OR = 1.50, 95% CI = 1.05 to 2.14), peptic ulcer in siblings (OR = 1.52, 95% CI = 1.09 to 2.12), gastric cancer in father (OR = 1.61, 95% CI = 1.02 to 2.52). The association of seropositivity with history of ulcer, gastric cancer in family, gastroscopy, and H2 antagonists suggests that H pylori is an epidemiological key factor in the pathogenesis of gastroduodenal diseases in this area.     

DNA甲基化和胃液固有荧光光谱联合检测在胃癌诊断中的意义

目的探索在胃癌患者胃液、外周血清中检测基因甲基化的可行性，并结合胃液稀释固有荧光光谱评价二者在胃癌诊断中的作用。方法采用甲基化特异性PCR方法，检测50例胃癌患者的原发肿瘤组织、外周血清和胃液脱落细胞的死亡相关蛋白（DAP）激酶、p16基因启动子区域甲基化状态，并以胃良性溃疡和慢性浅表性胃炎各20例、慢性萎缩性胃炎30例作为对照，同时检测胃癌患者和对照者的胃液稀释固有荧光光谱。结果50例胃癌患者的肿瘤组织、外周血清和胃液脱落细胞中p16和DAP激酶基因甲基化阳性率分别为74．4％和68．1％、52．0％和58．0％、58．6％和76．0％，20例慢性浅表性胃炎患者中均未检测到基因异常甲基化；20例胃溃疡患者溃疡周边组织、胃液脱落细胞中p16和DAP激酶甲基化阳性率为10．0％和20．0％、5．0％和15．0％，在外周血清中未检测到异常甲基化；30例慢性萎缩性胃炎患者胃黏膜组织、外周血清、胃液脱落细胞p16和DAP激酶基因甲基化阳性率分别为10．0％和23．3％、3．3％和3．3％、3．3％和20．0％。胃癌患者胃液固有荧光光谱强度较对照者明显增强（P〈0．05）；以P1FI≥111．8为分界点分析胃液固有荧光光谱诊断胃癌的敏感性和特异性分别为76．1％和78．6％。p16和DAP激酶基因甲基化和胃液固有荧光光谱结合后诊断胃癌的敏感性提高到95．6％和97．8％。结论胃癌患者外周血清及胃液脱落细胞中可检测到与原发肿瘤组织一致的基因异常甲基化，胃液固有荧光光谱和DNA甲基化联合对检测胃癌有良好的临床应用价值。     

N-Nitrosamines in gastric juice of patients with gastric ulcer before and during treatment with histamine H2-receptor antagonists

The clinical implications of N-nitrosamines (NAs) were studied by analyzing their concentration in the gastric juice of 72 healthy subjects and 279 patients with gastric ulcer before and during treatment with histamine H₂-receptor antagonists. NAs were measured by combined gas chromatography and thermal energy analyzer. The detection ratios of N-nitrosodimethylamine (NDMA) and N-nitrosodiethylamine (NDEA) in the patients were 35.3% and 34.6%, respectively, which were significantly higher than the corresponding values in healthy subjects (19.4% and 16.7%, P<0.01). Analysis among the patients showed that this trend was mainly due to higher values in patients who were given histamine H₂-receptor antagonists, as their detection ratios increased to 40.2% (NDMA) and 39.9% (NDEA). Patients without histamine H₂receptor antagonists showed moderate increases of detection ratios (NDMA; 24.2% NDEA; 22.6%) compared with healthy controls. The differences in these values between those receiving and not receiving histamine H₂-receptor antagonists were statistically significant (P<0.01). The maximum concentrations of NDMA and NDEA were 7.9 and 9.8 ng/ml in patients, and 1.2 and 1.3 ng/ml in healthy subjects (the difference between the 2 groups P<0.02). These results indicated that patients with gastric ulcer had higher detection ratios and concentrations of NDMA and NDEA in gastric juice and that, while significant increases occurred during treatment with histamine H₂-receptor antagonists, the extent of increase was below toxic or experimental carcinogenic levels.     

Complications associated with ulcer recurrence following gastric surgery for ulcer disease.

The present study is an attempt to assess the risks of the complications associated with recurrent ulcers in patients who have undergone gastric surgery and to determine whether these risks differ from those observed in patients receiving long term maintenance treatment with H2-receptor antagonists for ulcer disease. One hundred and thirty studies reported in the literature during the past three decades have been analysed to determine both the approximate rate of ulcer recurrence and the proportion of patients with recurrent ulcers who have presented with either haemorrhage or perforation following the various types of gastric surgery for ulcer disease. From these data, estimates of the risks of haemorrhage and of perforation during the years following gastric surgery have been calculated. Vagotomy and antrectomy is associated with a low risk of ulcer recurrence (less than 1%) and the risk of complications in later years is accordingly very small (less than 0.5%). Partial gastrectomy, although associated with low recurrence rates, has a higher risk of complications (1.3% for haemorrhage, 0.3% for perforation) because the proportion of recurrent ulcers that present with haemorrhage or perforation is high (33% and 8%, respectively). Truncal vagotomy plus drainage (TV + D) and highly selective vagotomy (HSV) are associated with recurrence rates of 9% and 12%, respectively, but ulcer recurrences following these operations are less frequently accompanied by complications then recurrences after gastric resection and, as a result, the risks of haemorrhage (1.7% for TV + D; 1.3% for HSV) are similar to the risks after gastric resection. During long term (five years or more) maintenance treatment with H2-receptor antagonists, the risks of haemorrhage and perforation are less than 2% and less than 0.5%, respectively. It appears, therefore, that the likelihood of developing haemorrhage or perforation following gastric surgery is of the same order as that during maintenance treatment with H2-receptor antagonists, at least during the first decade of follow-up.     

Distribution and prevalence of Campylobacter pylori in the stomach

We investigated the distribution and prevalence of Campylobacter pylori in the stomach and duodenum. In this study, 500 biopsy specimens were obtained from 245 patients. In each case, biopsy specimens were taken from more than 2 sites. C. pylori was detected by culture, urease test and acridine-orange stain. C. pylori was not detected on the intestinal metaplasia, gastric cancer tissue and duodenal mucosa without gastric metaplasia. In 21% of cases, C. pylori was detected in only one site. Because of the patchy distribution of C. pylori, more than 2 biopsy specimens from different sites were needed to avoid sampling error. Detection rate of C. pylori was almost equal in antrum, angle and body as well as in male and female. H2 receptor antagonists did not affect the detection rate of C. pylori. According to the endoscopic diagnosis of the biopsied site, C. pylori was detected in 87% of gastric ulcer, 60% of duodenal ulcer (duodenal mucosa with gastric metaplasia), 73% of chronic gastritis and 62% of endoscopically normal gastric mucosa.     

Hydroxyl radical formation in human gastric juice

The hydroxyl radical is the most potent free radical derived from oxygen, and has been implicated in damage caused to the gastroduodenal mucosa. The ability of human gastric juice to generate hydroxyl radicals has been investigated in 54 adults with endoscopically normal gastroduodenal mucosa and in 39 patients with chronic duodenal ulcer. Hydroxyl radical production was measured by the formation of formaldehyde from dimethylsulfoxide. Unlike other body fluids, this reaction could proceed without the extraneous addition of catalysts such as hydrogen peroxide (H2O2), ascorbate and iron. Measurement of H2O2, iron and ascorbate showed that these catalysts are already present in the gastric juice. There was no significant difference in the concentration of these components in gastric juice between normal subjects and patients with duodenal ulcer, except that H2O2 levels were slightly higher in duodenal ulcer patients. Although generation of free radicals has been investigated in other body fluids, this is the first reported case regarding the production of these active species in normal human gastric juice. Since hydroxyl production is not significantly enhanced in duodenal ulcer, we suggest that attention may be turned to mucosal antioxidant defences in this disease.     

The electrophoresis of human gastric juice: Part II In patients with gastric ulcer

The electrophoretic patterns of the proteins of the gastric juice of a series of patients with gastric ulcer, a control group, and a group of patients with miscellaneous gastric and systemic diseases were studied, autodigestion being prevented by maintaining the pH of the gastric contents above 7.

A slow moving anodal band (band 2) was present in 50% of the observations on gastric ulcer patients, whereas this band was present in only 10% of the patients who did not have a gastric ulcer.

     

Influence of gastric colonization with Candida albicans on ulcer healing in rats: effect of ranitidine, aspirin and probiotic therapy

OBJECTIVE: Candida albicans frequently inhabits the gastrointestinal tract of humans leading to gastrointestinal candidiasis, especially following suppression of gastric acidity, but studies on the relation between this fungal infection and gastric pathology are limited due to lack of convenient animal models resembling Candida infection in humans. MATERIAL AND METHODS. We compared the effects of C. albicans and vehicle inoculation on gastric secretion and healing of gastric ulcers induced by acetic acid in rats treated with 1) ranitidine (30 mg kg(-1) day(-1) s.c.) and 2) aspirin (ASA) (60 mg kg(-1) day(-1) i.g.) with or without probiotic bacteria Lactobacillus acidophillus. At day 0 and at 4, 15 and 25 days after ulcer induction, the ulcer area, the gastric blood flow (GBF), the quantitative gastric cultures of Candida and the expression of mRNAs for pro-inflammatory cytokines IL-1beta and TNF-alpha and growth factors EGF and TGFalpha were assessed in the gastric mucosa. RESULTS: Gastric acid output was reduced by over 40% soon after Candida inoculation and this effect persisted during all time intervals tested. The area of ulcers in control rats significantly decreased at day 15 and the ulcers disappeared almost completely after 25 days of their induction. In contrast, the ulcers were present until day 25 in Candida-inoculated rats followed by a fall in GBF and a rise in plasma gastrin levels, these effects being significantly attenuated by the co-treatment with Lactobacillus. Candidiasis was accompanied by up-regulation of mRNA for IL-1beta, TNF-alpha, EGF and TGFalpha and a significant increment in plasma IL-1beta and TNF-alpha levels. CONCLUSIONS: 1) Persistent colonization with Candida could be achieved in rats treated with antisecretory agents or non-steroidal anti-inflammatory drugs (NSAIDs) such as ASA; 2) candidiasis reduces gastric acid secretion, while delaying ulcer healing possibly due to the impairment in GBF in the ulcer area and enhanced expression and release of IL-1beta and TNFalpha and 3) probiotic therapy could be useful in the treatment against the deleterious action of fungal infection on the healing of pre-existing gastric ulcers.     

Complications associated with ulcer recurrence following gastric surgery for ulcer disease

The present study is an attempt to assess the risks of the complications associated with recurrent ulcers in patients who have undergone gastric surgery and to determine whether these risks differ from those observed in patients receiving long term maintenance treatment with H2-receptor antagonists for ulcer disease. One hundred and thirty studies reported in the literature during the past three decades have been analysed to determine both the approximate rate of ulcer recurrence and the proportion of patients with recurrent ulcers who have presented with either haemorrhage or perforation following the various types of gastric surgery for ulcer disease. From these data, estimates of the risks of haemorrhage and of perforation during the years following gastric surgery have been calculated. Vagotomy and antrectomy is associated with a low risk of ulcer recurrence (< 1%) and the risk of complications in later years is accordingly very small (< 0.5°/o). Partial gastrectomy, although associated with low recurrence rates, has a higher risk of complications (1.3% for haemorrhage, 0.3% for perforation) because the proportion of recurrent ulcers that present with haemorrhage or perforation is high (33% and 8%, respectively). Truncal vagotomy plus drainage (TV+D) and highly selective vagotomy (HSV) are associated with recurrence rates of 9% and 12%, respectively, but ulcer recurrences following these operations are less frequently accompanied by complications then recurrences after gastric resection and, as a result, the risks of haemorrhage (1.7% for TV+D; 1.3% for HSV) are similar to the risks after gastric resection. During long term (five years or more) maintenance treatment with H2-receptor antagonists, the risks of haemorrhage and perforation are < 2% and < 0.5%, respectively. It appears, therefore, that the likelihood of developing haemorhage or perforation following gastric surgery is of the same order as that during maintenance treatment with H2-receptor antagonists, at least during the first decade of follow-up.     

Detection ofHelicobacter pylori DNA in gastric juice by the polymerase chain reaction: Comparison with findings in bacterial culture and the detection of tissue IgA and serum IgG antibodies againstHelicobacter pylori

The detection ofHelicobacter pylori in gastric juice by the polymerase chain reaction (PCR) was undertaken in 124 patients with peptic ulcer or chronic gastritis. PCR products were evaluated by agarose gel electrophoresis and Southern hybridization ofH. pylori-specific DNA sequences. Positive and negative results of the PCR analysis in 72 examinations were compared with those from bacterial culture, and with the detection of tissue IgA antibody againstH. pylori by enzyme-linked immunosorbent assay ELISA; Serion, Wuerzburg, Germany, and detection of serum IgG antibody againstH. pylori by ELISA; Radim Pomezia, Italy. Thirty-four PCR-positive samples evaluated by electrophoresis and hybridization coincided with positive samples in 56% of bacterial cultures, 59% of tissue IgA antibody identifications, and 94% of serum IgG antibody evaluations; 26 PCR-negative samples coincided with negative samples in 96% of bacterial cultures, 81% of tissue IgA antibody evaluations, and 38% of serum IgG assessments. We compared the detection achieved with theH. pylori PCR assay in gastric juice with that in biopsies taken from the antrum and upper corpus in 90 examinations, and found them to be both positive in 34 (38%) and 36 (40%) of specimens, both negative in 37 (41%) and 30 (33%) specimens, gastric juice-positive but biopsynegative in 10 (11%) and 12 (13%) specimens, and vice versa in 9 (10%) and 12 (13%) specimens, when detected by electrophoresis and hybridization, respectively, showing equivalent detection rates. In relation to the type of disease, the positive PCR assay results with gastric juice, evaluated by electrophoresis and hybridization, respectively, were: gastric ulcer 34/53 (64%) and 39/53 (74%), duodenal ulcer 23/38 (61%) and 25/38 (66%), and chronic gastritis 20/33 (61%) and 23/33 (70%), showing no significant difference in positive rates between peptic ulcer and chronic gastritis. Of the samples of 16 patients withH. pylori-positive gastric juice by the PCR assay, 7 were negative by PCR assay analyzed by electrophoresis and hybridization after the completion of treatmentH. pylori. However, after treatment, 3 were negative on electrophoresis but still had positive results with hybridization, indicating that a minimal number of bacilli may have still remained. Detection ofH. pylori in gastric juice has potential advantages for examiningH. pylori infection in the entire stomach and for follow up after treatment for the eradication ofH. pylori. This study was supported by Grants-in-Aid for Cancer Research from the Ministry of Health and Welfare, Japan.     

Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations.

Ascorbic acid, the reduced form of vitamin C, may protect against gastric cancer and is secreted by the normal stomach. Secretion is impaired in Helicobacter pylori (H pylori) associated chronic gastritis. This study examined if eradication of H pylori improves gastric juice ascorbate values. Fasting gastric juice and plasma samples were collected at endoscopy from patients participating in trials of H pylori eradication for duodenal ulcer disease and intestinal metaplasia before and up to 15 months after attempted eradication. Ascorbic acid and total vitamin C concentrations were determined by high performance liquid chromatography. In 12 patients in whom H pylori was successfully eradicated gastric juice ascorbate and total vitamin C concentrations and the ratio of juice to plasma vitamin C rose after treatment. Analysis after treatment suggested that the rise was greatest in patients with high final plasma vitamin C concentrations, even though these did not change with treatment. By contrast, in 22 patients in whom H pylori eradication was unsuccessful there were no significant changes in juice or plasma concentrations after treatment. It is concluded that successful eradication of H pylori improves secretion of vitamin C into gastric juice. It is speculated that this increases protection against gastric cancer.     

Mutagenicity in gastric juice.

Mutagenicity has been measured in the gastric juice of 228 patients using the Ames bacteriological test system; while mutagenicity in control and duodenal ulcer patients did not differ from saline controls, mutagenicity was significantly increased compared with controls in patients suffering gastric ulcer (p less than 0.002), carcinoma (p less than 0.002), and in patients after gastric resection (p less than 0.01). A transient rise in mutagenicity was seen following H2 antagonist ingestion (p less than 0.002). Increased levels of mutagenicity were found to correlate closely with gastric juice pH and bacterial count. Histidine concentrations in gastric juice did not explain the mutagenicity results.     

The interaction of H. pylori infection and NSAIDs in cyclooxygenase-2 mRNA expression in gastric antral, corpus mucosa, and gastric ulcer

BACKGROUND: Although Helicobacter pylori infection and use of nonsteroidal anti-inflammatory drugs (NSAIDs) are the two major causes of gastric ulcer, their interaction remains controversial. We constructed a prospective cohort study to evaluate how these two factors influence the expression of COX-2 mRNA in gastric antral, corpus mucosa, and gastric ulcer. METHODS: Tissues were obtained by endoscopic biopsy of gastric antral, corpus mucosa, and gastric ulcer. The presence of H. pylori was determined by culture or histology using Giemsa stain. NSAID use was assessed by structured questionnaire and medical record review. The expression of COX-2 mRNA was detected by the TaqMan quantitative RT-PCR system. RESULTS: H. pylori infection was associated with increased COX-2 expression only in antral mucosa (0.77 +/- 0.13 vs. 0.31 +/- 0.07, P < 0.01). NSAID use was significantly associated with decreased COX-2 expression in ulcer (4.49 +/- 1.50 vs. 9.82 +/- 2.48, P < 0.05) but not in antral or corpus mucosa. Regarding the interaction between H. pylori and NSAID, we found that H. pylori infection was associated with increased COX-2 expression in antral mucosa for both NSAID users and nonusers. In NSAID users, H. pylori infection was not associated with increased COX-2 expression in ulcer edge. CONCLUSION: H. pylori infection was associated with increased COX-2 expression in gastric antral mucosa for both NSAID users and nonusers, but not in gastric ulcer, where the effect of NSAID inhibition plays a major role. With these observations, we can interpret indirectly that H. pylori eradication does not interfere with gastric ulcer healing in NSAID users.     

Benign gastric ulcer associated with Candida infection in a healthy adult

A case of benign gastric ulcer associated with Candida infection in a healthy adult is reported. The patient was a 46-year-old man complaining of epigastralgia. Endoscopic examination of the upper digestive tract revealed an elevated lesion with ulceration having an unclear border and thick exudates. The clinical diagnosis based on endoscopic findings was a benign gastric ulcer; however, biopsy was performed to distinguish it from malignant lymphoma. Histological examination of biopsy samples obtained from the base and the edge of the ulcer revealed numerous Candida. Therefore, the patient was diagnosed with Candida-infected gastric ulcer. The ulcer resolved after the administration of antiulcer drugs for 2 months. Predisposing factors for fungal infection were excluded. These observations suggest that Candida-infected gastric ulcer should be suspected in patients with a gastric submucosal tumor-like lesion with a thick, yellowish-white coated ulcer of unclear border on its summit, and this lesion should be distinguished from malignant diseases. Received: November 6, 1998 / Accepted: April 16, 1999     

Gastric juice nitrite and vitamin C in patients with gastric cancer and atrophic gastritis: is low acidity solely responsible for cancer risk?

BACKGROUND: N-nitroso compounds are carcinogens formed from nitrite, a process that is inhibited by vitamin C in gastric juice. Helicobacter pylori infection has been reported to increase nitrite and decrease vitamin C in gastric juice. Therefore, susceptibility to gastric cancer in H. pylori-infected patients may be derived from increased N-nitroso compounds in gastric juice. However, most H. pylori-infected patients do not develop gastric cancer. OBJECTIVE: To investigate additional factors that may affect susceptibility to gastric cancer, we compared nitrite and vitamin C levels in gastric juice from H. pylori-infected patients with and without gastric cancer. METHODS: Serum and gastric juice were obtained from 95 patients undergoing diagnostic endoscopy, including those with normal findings, duodenal ulcer, gastric ulcer, atrophic gastritis and gastric cancer. Serum was analysed for H. pylori antibody, nitrate and nitrite, gastrin and pepsinogens; gastric juice was analysed for pH, nitrite and vitamin C. RESULTS: pH and nitrite levels were increased and vitamin C levels decreased in the gastric juice of patients with atrophic gastritis and gastric cancer compared with other patients. However, in patients with a similar gastric acidity (pH 5-8), nitrite concentrations in the gastric juice were significantly higher and vitamin C levels significantly lower in patients with gastric cancer than in those with atrophic gastritis. CONCLUSION: Although hypochlorhydria increases intraluminal nitrite and decreases intraluminal vitamin C, which increases the intraluminal formation of N-nitroso compounds, our results indicate that patients with gastric cancer may have additional factors that emphasize these changes.     

多巴胺、肾上腺素及胆碱能神经在实验性溃疡病中的相互作用

本文通过多巴胺能，α及β肾上腺素能和乙酰胆碱能拮抗剂及激动剂，检测了实验动物MPTP溃疡时上述三种神经可能的相互作用，发现溴隐亭能减轻，面吗丁啉能加重MPTP溃疡；心得安对MPTP溃疡无明显影响，但它能显著减少胃液的分泌；哌唑嗪和育亨平能明显保护十二指肠溃疡，对胃溃疡影响不大；阿托品亦仅能保护十二指肠溃疡。提示MPTP溃疡发生过程中尤其十二指肠溃疡发生过程中多巴胺起了先导作用，肾上腺素能和乙酰胆碱能神经亦参与了作用。     

Evidence for the role of gastric mucosa at the secretion of soluble triggering receptor expressed on myeloid cells （strem-1） in peptic ulcer disease

AIM: To investigate the role of gastric mucosa at the secretion of sTREM-1 in peptic ulcer. METHODS: Seventy two patients were enrolled; 35 with duodenal, 21 with gastric ulcer and 16 with chronic gastritis. Patients were endoscoped and gastric juice was aspirated. Patients with duodenal and gastric ulcer underwent a second endoscopy post-treatment. Biopsies were incubated in the absence/presence of endotoxins or gastric juice. Supernatants were collected and sTREM-1 and TNFα were measured by enzyme immunoabsorbent assays. Scoring of gastritis was performed before and after treatment according to updated Sydney score. RESULTS: Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis. sTREM-1 was higher in supernatants of tissue samples of H pylori-positive than of H pylori-negative patients with gastric ulcer. Median (± SE) sTREM-1 was found increased in supernatants of patients with gastric ulcer before treatment (203.21 ± 88.91 pg/1000 cells) compared to supernatants either from the same patients post-treatment (8.23 ± 5.79 pg/1000 cells) or from patients with chronic gastritis (6.21 ± 0.71 pg/1000 cells) (P < 0.001 and < 0.001, respectively). Similar differences for sTREM-1 were recorded among LPS-stimulated tissue samples of patients (P = 0.001). Similar differences were not found for TNFα. Positive correlations were found between sTREM-1 of supernatants from patients withboth duodenal and gastric ulcer before treatment and the degree of infiltration of neutrophils and monocytes. CONCLUSION: sTREM-1 secreted by the gastric mucosa is an independent mechanism connected to the pathogenesis of peptic ulcer. sTREM-1 was released at the presence of H pylori from the inflamed gastric mucosa in the field of gastric ulcer.