2.63 消化性溃疡患者合并幽门螺杆菌感染时胃肠动力及胃肠激素的改变

目的为探讨幽门螺杆菌(Hp)感染对消化性溃疡患者胃肠动力及胃肠激素的影响.方法对85例消化性溃疡患者进行了胃肠测压和血浆胃动素(MTL)的测定.结果消化性溃疡患者与正常对照组相比消化间期胃肠动力明显减低,主要表现为消化间期移行性复合运动(MMC) Ⅲ期缺失和收缩波幅减低;而血中MTL水平,Hp阳性组明显高于Hp阴性组,也高于正常对照组.结论本研究表明消化性溃疡患者存在胃肠动力障碍和胃肠激素的异常改变 .Hp感染对胃肠动力无明显影响,但可促进MTL的分泌或释放.     

2.64 幽门螺杆菌感染对消化性溃疡患者胃肠动力及胃肠激素的影响

目的幽门螺杆菌(Hp)感染与消化性溃疡的发生有密切关系.本工作通过对消化性溃疡患者胃肠测压和血浆胃动素(MTL)及血浆生长抑素(SS)的变化的研究,探讨Hp对胃肠动力和胃肠激素的影响.方法对选自1998～1999年经胃镜确认的消化性溃疡(Pu)85例进行胃十二指肠压力检测,并测定血浆胃动素(MTL)和生长抑素(SS).结果消化性溃疡患者无论是否存在Hp感染,其消化间期胃肠运动均比正常对照组明显减弱,主要表现为MMC Ⅲ期缺失和收缩波幅减低.消化性溃疡患者SS水平失去正常周期性变化,在MMC Ⅰ期明显低于正常对照组;而在Hp阳性和Hp阴性两组之间无显著差异 .血浆MTL水平在Hp阳性溃疡病组呈现明显增高趋势,而Hp阴性溃疡病组呈减低趋势.结论消化性溃疡患者存在胃肠动力低下及激素分泌异常.     

十二指肠溃疡患者上胃肠道运动及胃肠激素的研究

对30例十二指肠溃疡（Du）患者和15例正常对照者进行了消化间期移行性复合运动波（MMC）的检测及血浆胃动素（MTL）、生长抑素（SS）的放免测定．结果显示：Du患者MMC正常者仅为16．7％,明显低于对照组（60％,P＜0.001）且胃窦MMCⅢ期持续时间缩短（P＜0．05）;胃窦、十二指肠近端MMCⅡ期的收缩频率、收缩波幅均较对照组减少（P＜0.05,P＜0．001）。Du患者MMCⅡ、Ⅲ期的MTL明显低于对照组（P＜0．05）,而SS则高于对照组（P＜0．05,P＜0．55）．结果提示：胃肠道运动异常和胃肠激素的释放与Du有着密切关系。     

消化性溃疡患者合并幽门螺杆菌感染时胃肠动力及胃肠激素的改变

消化性溃疡患者合并幽门螺杆菌感染时胃肠动力及胃肠激素的改变     

幽门螺杆菌相关性十二指肠溃疡与胃肠激素的关系

目的探讨幽门螺杆菌(Hp)相关性十二指肠溃疡(DU)患者Hp根除前后胃粘膜及血中促胃液素(Gas)和生长抑素(SS)含量变化的意义。方法采用放射免疫分析法测定Hp相关性DU患者42例Hp根除前后及正常对照者20例胃粘膜及血中Gas和SS含量。结果Hp相关性DU的患者胃粘膜及血中Gas的含量明显高于Hp阴性患者(粘膜:ng/g,226±65vs380±98;血清:ng/L,107±33vs50±8),而Hp根除后Gas含量则明显下降,Hp阳性者SS的含量低于Hp阴性患者(粘膜:ng/L,11±2 vs 42±8;血浆:ng/L,5.6±1.2vs10.2±2.3),Hp根除后SS含量显著升高,Hp感染时胃粘膜炎细胞浸润程度对Gas和SS的含量亦有一定影响。结论Gas和SS与Hp相关性DU密切相关,是参与DU发病的重要因素之一。     

健康小儿胃肠内分泌功能的研究

目的探讨健康小儿胃肠内分泌功能。方法采用放射免疫分析法测定空腹和摄入液体实验餐后60m in时外周血胃泌素(Gas)、胃动素(MTL)、生长抑素(SS)水平。结果健康小儿餐后与餐前比较,Gas及MTL无明显差异(P>0.05),SS水平则明显升高(P<0.01)。结论Gas、MTL和SS水平的变化反应了健康小儿胃肠激素餐后分泌前整个过程。     

胃十二指肠疾病时胃液表皮生长因子及CagA幽门螺杆菌感染的关系

为探讨胃液表皮生长因子（EGF）含量变化及幽门螺杆菌（Hp）感染与胃十二指肠疾病的相关性。以幽门螺杆菌感染阳性的78例消化性溃疡和61例慢性胃炎患者为研究对象,健康人20例作对照,观察胃液EGF含量变化与胃十二指肠疾病的相关性。结果发现,消化性溃疡和慢性胃炎患者胃液EGF含量分别为175．1±103．5ng／L和240．9±182．1ng／L,明显低于正常人,511.9±54．1ng／L,（均P＜0.01）。消化性溃疡患者EGF含量明显低于慢性胃炎患者,P＜0．01。具有CagA基因的Hp感染的消化性溃疡患者EGF含量明显低于慢性胃炎组,P＜0．05。表明胃液EGF含量与Hp感染有关,尤其是具有CagA基因的幽门螺杆菌感染。     

吸烟饮酒对胃部疾病幽门螺旋杆菌感染的影响

幽门螺旋杆菌（helicobacter pylori,Hp）是慢性胃炎、消化性溃疡、胃癌的主要致病因子之一。Hp阳性患者胃窦炎症活动性显著重于Hp阴性者,多数国家超过90%的十二指肠溃疡患者和将近70%的胃溃疡患者伴有Hp感染[1]。     

西沙必利对糖尿病胃肠运动功能障碍的影响

观察西沙必利对糖尿病患者胃肠运动功能障碍的影响。通过胃肠测压与胃电图同步检测的方法观察糖尿病患者服用西沙必利前后消化间期胃肠动力及胃电图的变化。结果服药前30例糖尿病患者中有21例缺乏MMC3期。服药2周后，21例中有11例恢复正常MMC3期。MMC3期和2期收缩液振幅较治疗前明显升高。胃电图治疗后表现为主频比（PDF）的增加。结论：西沙必利可促进消化间期胃肠动力，有利于糖尿病胃轻瘫的治疗。     

血清胃蛋白酶原和胃泌素水平与幽门螺杆菌相关性消化性溃疡的相关性评价

目的:研究血清胃蛋白酶原(Pepsinogen,PG)和胃泌素(Gastrin,G)水平与幽门螺杆菌相关消化性溃疡之间的关系.方法:分别选择我院2019年12月至2021年4月收治的105例幽门螺杆菌阳性消化性溃疡患者(阳性组),106例幽门螺杆菌阴性消化溃疡患者(阴性组)以及112例健康体检者(健康体检组),对三组受试者的血清胃蛋白酶原和胃泌素水平进行检测,分析检测结果的差异.结果:三组受试者比较,阳性组患者血清PGⅠ、PGⅡ、G-17水平明显高于阴性组与健康体检组(P<0.05).幽门螺杆菌消化性溃疡患者比较,阳性组中胃溃疡患者的血清PGⅠ、PGⅡ、G-17水平均高于阴性组中胃溃疡患者(P<0.05);阳性组中十二指肠溃疡患者的血清PGⅠ、PGⅡ、G-17水平均高于阴性组中十二指肠溃疡患者(P<0.05).Logistic多因素回归分析显示,血清PGⅠ、PGⅡ、G-17水平与幽门螺杆菌相关性消化性溃疡之间正相关(OR>1,P<0.05).结论:血清胃蛋白酶原、胃泌素水平与幽门螺杆菌相关性消化性溃疡之间存在相关性,可作为诊断幽门螺杆菌相关性消化性溃疡的重要危险因素.     

Peptic ulceration may be a hormonal deficiency disease

Evidence is reviewed that Helicobacter pylori infection may cause a deficiency of the hormone secretin that allows peptic ulcer disease to develop by impairing the body's defenses to gastric acid. Secretin is released into the circulation from the S-cells of the duodenal crypts in response to gastric acid entering the duodenum. Once in the circulation, secretin has five well-documented effects that protect the upper intestine from gastric acid: it stimulates secretion of bicarbonate rich exocrine pancreatic juice; it stimulates secretion of alkaline bile; it stimulates secretion of alkaline mucus from the duodenal submucosal glands of Brunner; it inhibits the humoral phase of gastric secretion; and it inhibits gastric motility, thereby delaying gastric emptying. Impaired secretin release and reduced duodenal S-cells have been documented in peptic ulcer patients compared with control patients. Clinical evidence that patients with H. pylori infection and peptic ulceration have increased gastric secretion and motility and decreased duodenal bicarbonate response to gastric acid, all of which normalize after eradication of the infection, could be explained by reversible impairment of the secretin mechanism. Gastric metaplasia in the duodenum with H. pylori infection is known to reduce the S-cell population. The fact that not all patients with H. pylori infection develop peptic ulceration suggests that degree of secretin deficiency determined by extent of the infection must reach a critical level for peptic ulceration to occur. Peptic ulceration may be a hormonal deficiency disease, a result of secretin deficiency caused by H. pylori infection. It may be the first example of a specific hormonal deficiency disease caused by a specific bacterial infection.     

Enzyme-linked immunosorbent assay for Helicobacter pylori needs adjustment for the population investigated

Helicobacter pylori infection and peptic ulcer disease are common in developing countries, e.g., Vietnam. An enzyme-linked immunosorbent assay (ELISA) for screening of patients and for seroepidemiology is a useful tool but needs to be validated in the population studied. We used in-house ELISA with sonicated Swedish and Vietnamese strains as antigens to measure immunoglobulin G antibodies after absorption with sonicated Campylobacter jejuni in sera from 270 H. pylori culture-confirmed peptic ulcer patients, 128 Swedish urea-breath test and immunoblot-positive healthy controls, and 432 Vietnamese immunoblot-positive population controls. Sonicated whole-cell antigen based on the local strains showed a significantly better performance. Immunoblot-positive peptic ulcer patients had significantly higher antibody concentrations than immunoblot-positive population controls, necessitating a lower cutoff level if serology is used for screening or epidemiological purposes. The study shows that the parameters of ELISA for H. pylori need to be adjusted for the population being investigated.     

The polymorphic IL-1B and IL-1RN genes in the aetiopathogenesis of peptic ulcer

Besides environmental factors, the genetic background of an individual may contribute to the development and final outcome of peptic ulcer disease. Interleukin-1beta (IL-1beta) and the interleukin-1 receptor antagonist (IL-1ra) are cytokines that play a key role in modulating the inflammatory response in the gastrointestinal mucosa. This study aimed to investigate whether polymorphisms in the IL-1B and IL-RN genes are involved in the susceptibility to and final outcome of peptic ulcer disease. DNA from 179 unrelated Spanish Caucasian patients with peptic ulcer diseases and 99 ethnically matched healthy controls was typed for the TaqI polymorphism at position + 3954 in the IL-1B gene and the variable number of tandem repeats polymorphism in intron 2 of the IL-1RN gene. The determination of Helicobacter pylori status and non-steroidal anti-inflammatory drug (NSAIDs) use was studied in all patients and in controls. H. pylori infection and NSAID use were more frequent in ulcer patients than in controls. There were no significant differences in carriage rate, genotype and allele frequencies of the IL-1RN and the IL-1B(+3954) gene polymorphisms between peptic ulcer patients and controls. However, a strong allelic association between IL-1B and IL-1RN genes was found in duodenal ulcer patients (P < 0.0006). Logistic regression identified H. pylori infection and NSAIDs use as independent risk factors for peptic ulcer diseases whereas the simultaneous carriage of IL-1B(+3954) allele 2 and IL-1RN allele 2 was associated with reduced risk for duodenal ulcer disease (OR: 0.37, 95% CI = 0.14-0.9). Our data suggest that IL-1B and IL-1RN genes in addition to bacterial and environmental factors play a key role in determining the final outcome of peptic ulcer disease.     

Association of Helicobacter pylori with gastritis and peptic ulcer diseases

The occurrence of Helicobacter pylori(H.pylori) and its relationship with gastric mucosa were studied by light and electron microscopy and culture of biopsy specimens from gastric mucosa of 160 patients with upper gastrointestinal symptoms. H. pylori were present in 96.6% of patients with active chronic gastritis, 100% of patients with duodenal ulcer and 76.9% of patients with gastric ulcer, while present in only 6.3% of individuals with histologically normal gastric mucosa. The bacteria colonized the antral mucosa more frequently than the body or than the duodenal cap mucosa. The bacteria were rarely seen in the intestinalized epithelium per se, but there was no significant difference in prevalence of H. pylori between gastritis with intestinal metaplasia and gastritis without intestinal metaplasia. H. pylori could be seen in close association with the surface of gastric epithelial cells below the mucus layer without evidence of intracellular parasitism, All of the strains tested were susceptible to penicillin, erythromycin, and most of them susceptible to tinidazole and bismuth salts. It is concluded that H. pylori are highly associated with gastritis and peptic ulcer diseases and its prevalence rates in patients with those diseases is higher than in developed countries. This strong association of H. pylori infection with gastritis and peptic ulcer diseases suggest a possible etiologic role for the bacterium in those diseases.     

Eradication of Helicobacter pylori in clinical situations

Helicobacter pylori is prevalent worldwide, especially in developing countries, and is associated with several upper gastrointestinal diseases. Since it is present in over 90% of duodenal ulcer patients, empirical eradication in these patients is often recommended. In gastric ulcer patients, eradication is indicated only after the infection is confirmed. Testing for H. pylori infection should be carried out in patients with peptic ulcer hemorrhage, because eradication has been shown to reduce recurrent bleeding. Both H. pylori and NSAIDs are risk factors for peptic ulceration, and it is reasonable to screen for and eradicate H. pylori infection in peptic ulcer patients taking NSAIDs. H. pylori is a group I carcinogen for gastric adenocarcinoma, and should be eradicated for the primary prevention of this cancer. Eradication of this organism has been reported to result in regression of early low-grade mucosa-associated lymphoid tissue lymphoma. The role of H. pylori infection in the causation of gastroesophageal reflux and non-ulcer dyspepsia is not clearly established. Several tests are available for the diagnosis of H. pylori infection. These include invasive tests, such as histology, culture and urease test, and non-invasive tests, such as serology, urea breath test and stool antigen test. The choice of test is determined by clinical indication, pretest probability of infection, as well as the availability, cost, sensitivity and specificity of the test. H. pylori eradication therapy using proton pump inhibitor with clarithromycin and amoxycillin for 7 days has a success rate of 85-90%. Improved living standard and sanitation are vital in the control of H. pylori transmission and infection. Future development may include the use of vaccines against H. pylori, and therapies specifically targeting cagA strains of the bacteria.     

Helicobacter pylori non-cytotoxic genotype enhances mucosal gastrin and mast cell tryptase.

AIMS: To determine the association, if any, between H pylori genotype and the gastric mucosal variations in the levels of gastrin, somatostatin, tryptase, and histamine. METHODS: 49 patients affected by duodenal ulcer and 48 by non-ulcer dyspepsia were studied. To identify the H pylori genotype, the presence of the cagA gene and vacA alleles m1, m2, s1, and s2 were analysed by polymerase chain reaction. Gastrin, somatostatin, tryptase, and histamine were measured in antral mucosal biopsies. RESULTS: 57 patients were infected with H pylori (30 with duodenal ulcer and 27 with non-ulcer dyspepsia). Gastrin and tryptase were increased in patients with H pylori infection, although the variations were statistically significant only for gastrin; somatostatin and histamine were not influenced by H pylori infection. In patients with non-ulcer dyspepsia the absence of the cagA gene and the presence of vacA alleles s2 and m2 were associated with higher values of tryptase and to a lesser extent of gastrin. These associations were not found in patients with duodenal ulcer. CONCLUSIONS: The cagA negative s2m2 strain of H pylori may be less dangerous for the gastric mucosa than other H pylori strains since it enhances tryptase production by gastric mucosal mast cells; this enzyme is thought to stimulate tissue turnover and favour wound healing.     

Helicobacter pylori infection in sickle cell disease

Abdominal pain is a common presenting symptom in adults with sickle cell disease (SCD). One case of Helicobacter pylori gastritis has been reported in a child with sickle cell anemia. H. pylori-induced peptic ulcer disease (PUD) has not previously been reported in adults with SCD. We report eight cases of H. pylori infection in adult sickle cell patients presenting with acute or recurrent abdominal pain and/or gastrointestinal bleeding. In all cases, H. pylori serology (IgG) was positive, and three patients had gastric or duodenal ulcer by endoscopic examination. All patients responded to H. pylori treatment with complete resolution of symptoms by 4 weeks. The prevalence of H. pylori infection in SCD is unknown, but patients may be at increased risk for H. pylori-induced PUD and complications due to pre-existing anemia, increased nonsteroidal anti-inflammatory drug use, and alloimmunization which may delay necessary transfusion. It is important that the differential diagnosis of abdominal pain in adults with SCD include nonsickle cell-related disorders such as PUD. When confirmed, a definitive etiology of PUD must be determined so that appropriate treatment strategies can be initiated promptly and excess morbidity avoided.     

Cytotoxin production by Helicobacter pylori from patients with upper gastrointestinal tract diseases.

A cytotoxin produced by some Helicobacter pylori strains has recently been identified. The cytotoxin induces intracellular vacuolization of cultured cells. The aim of the present study was to examine the frequency of occurrence of cytotoxin-producing strains of H. pylori from subjects with upper gastrointestinal disease including nonulcer dyspepsia, gastric and duodenal ulcer disease, gastroesophageal reflux disease, and gastric cancer. Broth culture filtrates of clinical isolates of H. pylori recovered from 175 patients were used to inoculate Vero and HeLa cell monolayers for the detection of vacuolating cytotoxin activity. The results obtained demonstrated that the highest percentage of strains producing cytotoxin were found in subjects with peptic ulcer disease (gastric ulcer, 65%; duodenal ulcer, 66%; P < 0.01 compared with nonulcer dyspepsia, 38%). Of the 11 patients with gastroesophageal reflux disease, 4 of 5 patients in this group who had esophageal ulcers, were found to be infected with strains that produced cytotoxin. Three of the four patients with carcinoma of the stomach were also found to be infected with cytotoxic strains of H. pylori. With increasing severity of mucosal damage in subjects with a normal upper gastrointestinal tract, macroscopic gastritis, duodenitis, and peptic ulceration, there were corresponding increase in the proportion of strains producing cytotoxin; these increases were 32, 46, 50, and 66%, respectively. H. pylori strains from subjects with ulcer disease commonly produced vacuolating cytotoxin, suggesting that it may be a virulence factor in the pathogenesis of peptic ulcer disease.     

胃十二指肠溃疡患者血中生长抑素和胃泌素水平及其在不同状态下的变化

本文对55例胃十二指肠溃疡患者空腹血浆中SS、Gas水平作了测定,并就其在溃疡出血、幽门螺旋菌感染、H_2RA治疗后等多种状态下的进一步改变作了观察。结果表明溃疡病患者SS水平显著高于正常,并发出血、幽门螺旋菌感染、H_2RA治疗后,血中SS和Gas水平未受显著影响。     

Helicobacter pylori infection affects eosinophilic cationic protein in the gastric juice of patients with idiopathic chronic urticaria

BACKGROUND: Helicobacter pylori, the main cause of gastritis and peptic ulcer, has been associated with idiopathic chronic urticaria (ICU), an immunological skin disorder of unknown origin. Eosinophilic cationic protein (ECP) is a cytotoxic molecule secreted by the activated eosinophils involved in the pathogenesis of ICU. We assessed serum/gastric juice ECP levels and gastric mucosal eosinophil infiltration in ICU patients infected or not with H. pylori and evaluated the modification after bacterium eradication. METHODS: 33 patients with ICU and 25 dyspeptic controls underwent upper gastrointestinal endoscopy for histological evaluation and assessment of H. pylori infection. One-week triple therapy was given to H. pylori-positive patients. Serum and gastric juice ECP levels, eosinophil infiltration from gastric mucosal sections and urticaria symptoms were evaluated in all patients at enrollment and 8 weeks after eradication. RESULTS: 19 of 33 (57%) ICU patients and 16 of 25 (64%) controls were found to be infected with H. pylori. Serum ECP was significantly higher in ICU patients compared to controls, regardless of infectious status. Gastric juice ECP and gastric eosinophil infiltration were significantly higher in infected ICU patients when compared both to uninfected ICU patients and controls. H. pylori eradication determined a significant decrease in gastric juice ECP and gastric eosinophil infiltration only in ICU patients. Moreover, a total or partial remission of urticaria symptoms was observed only in ICU patients in whom the bacterium was eradicated. CONCLUSIONS: Although H. pylori infection affects gastric juice ECP and eosinophil infiltration of ICU patients, the role of the bacterium in the pathogenesis of this skin disorder still remains uncertain.