Helicobacter pylori infection and perforated peptic ulcer prevalence of the infection and role of antimicrobial treatment

Although the role of Helicobacter pylori infection on noncomplicated peptic ulcer disease has been definitively established, the precise relationship between the organism and complicated ulcer has hardly been studied. The mean prevalence of H. pylori infection in patients with perforated peptic ulcer is of only about 65-70%, which contrasts with the almost 90-100% figure reported in noncomplicated ulcer disease. However, H. pylori infection rates in various studies range markedly from 0% to 100%, suggesting that differences in variables as number and type of diagnostic methods used to diagnose H. pylori infection, or frequency of nonsteroidal anti-inflammatory drug intake, may be responsible for the low prevalence reported in some studies. Recurrent ulcer disease after peptic ulcer perforation mainly occurs in patients with H. pylori infection, which suggests that the microorganism plays an important role in this complication. All patients with perforated peptic ulcer should be treated by simple closure of the perforation and with therapy aimed at healing of the ulcer and eradicating the H. pylori infection, as disappearance of the organism prevents, or at least decreases, ulcer recurrence and ulcer perforation in patients with H. pylori-associated perforated ulcers after simple closure. Therefore, H. pylori eradicating treatment should be started during the immediate postoperative period. The patients with intractable recurrent symptoms of peptic ulcer despite adequate medical treatment, but without H. pylori infection (e.g. a patient using nonsteroidal anti-inflammatory drugs), is probably the only remaining indication for elective definitive surgical treatment of peptic ulcer disease.     

Radiation Processed Amniotic Membranes in the Treatment of Non-Healing Ulcers of Different Etiologies

The amniotic membranes were collected from the placentae of selected and screened donors. Processing was done by washing the fresh amniotic membrane successively in sterile saline, 0.05% sodium hypochlorite solution and sterile distilled water until it was completely cleared of blood particles. The membranes were sterilized by gamma irradiation at 25 kGy. The processed amniotic membranes were applied to 50 open wounds comprising of 42 full thickness defects and eight partial thickness defects. These included leprotic, diabetic, traumatic, gravitational ulcers and superficial burn in the form of scald and corrosive burn. The radiation processed amniotic membranes favoured healing of unresponsive and non-healing ulcers of different etiologies. Ulcers with duration of minimum 3 weeks to maximum 12 months were found to heal in 2-6 weeks by the application of amniotic membranes.     

The N-terminal tridecapeptide fragment of gastrin-17 inhibits gastric acid secretion

After a meal the serum concentrations of the N-terminal tridecapeptide-like fragment of gastrin-17, (1-13)G-17, increased markedly in patients with active duodenal ulcer, but less so in healthy subjects. Consequently the synthetic (1-13)G-17 was infused intravenously in doses that resulted in concentrations similar to those measured in duodenal ulcer patients in order to examine whether the N-terminal fragment influences gastric acid secretion. Doses of 125 and 400 pmol (1-13)G-17/kg per h inhibited the meal-stimulated acid secretion by 36% (P less than 0.05) and 66% (P less than 0.05) respectively. The release of endogenous C-terminal gastrin immunoreactivity was not influenced. The infusion of (1-13)G-17 also inhibited the acid response to exogenous gastrin-34, gastrin-17 and Peptavlon, but not to gastrin-4. The results suggest that the N-terminal gastrin-17 fragment--although devoid of the hitherto considered only active site of gastrin--plays a significant role in the regulation of the gastric acid secretion in patients with active duodenal ulcer.     

Normalization of phospholipids concentration of the gastric mucosa was observed in patients with peptic ulcer after eradication of Helicobacter pylori

Background. Phospholipids concentration in the gastric mucosa decreased in patients with Helicobacter pylori infection. The aim of this study is to examine the effects of eradication of H. pylori on decreasing the phospholipids concentration in the gastric mucosa in patients with gastric or duodenal ulcer. Materials and Methods. Phospholipids (phosphatidylcholine, phosphatidylethanolamine, and sphingonomyeline) were measured in biopsy specimens from the antrum and corpus using thin‐layer chromatography. In H. pylori positive patients with gastric ulcer (n = 26) and duodenal ulcer (n = 13), and H. pylori negative controls (n = 20), the biopsy specimens were obtained before and 3 months after eradication. Eradication was performed using lansoprazole, amoxycillin, and clarithromycin. Results. Compared with the H. pylori negative control group, the concentrations of phosphatidylcholine and phosphatidylethanolamine decreased significantly in the gastric ulcer group in both antrum and corpus mucosa, and in the duodenal ulcer group in antrum mucosa. This decrease returned to the control level after eradication. Conclusions. This study demonstrates that the eradication of H. pylori in patients with peptic ulcer normalized the decrease of phosphatidylcholine and phosphatidylethanolamine in the gastric mucosa.     

Prevalence of duodenal ulcer-promoting gene (dupA) of Helicobacter pylori in patients with duodenal ulcer in North Indian population

BACKGROUND: The duodenal ulcer (DU)-promoting gene (dupA) of Helicobacter pylori has been identified as a novel virulent marker associated with an increased risk for DU. The presence or absence of dupA gene of H. pylori present in patients with DU and functional dyspepsia in North Indian population was studied by polymerase chain reaction (PCR) and hybridization analysis. MATERIALS AND METHODS: One hundred and sixty-six patients (96 DU and 70 functional dyspepsia) were included in this study. In addition, sequence diversity of dupA gene of H. pylori found in these patients was analyzed by sequencing the PCR products jhp0917 and jhp0918 on both strands with appropriate primers. RESULTS: PCR and hybridization analyses indicated that dupA gene was present in 37.5% (36/96) of H. pylori strains isolated from DU patients and 22.86% (16/70) of functional dyspepsia patients (p < or = .05). Of these, 35 patients with DU (97.2%) and 14 patients with functional dyspepsia (81.25%) were infected by H. pylori positive for cagA genotype. Furthermore, the presence of dupA was significantly associated with the cagA-positive genotype (p < or = .02). CONCLUSION: Results of our study have shown that significant association of dupA gene with DU in this population. The dupA gene can be considered as a novel virulent marker for DU in this population.     

Acute and sub acute toxicity study on Sangu parpam

Peptic ulcer is described in the siddha system of medicinal classification of 4448 diseases. Information on the use of Sangu Parpam in treating peptic ulcer is known. Therefore, it is of interest to document the acute and sub acute toxicity analysis on Sangu parpam in this regard.     

脉冲染料激光治疗婴幼儿体表溃烂型血管瘤疗效研究

目的:观察波长为585 nm脉冲染料激光治疗婴幼儿体表溃烂型血管瘤的临床疗效。方法:采用波长为585 nm的脉冲染料激光,对76例(男26例,女50例)体表溃烂型血管瘤(平均瘤体表面积22.1 cm2)患者进行照射治疗,激光能量为5.8 J/cm2~8 J/cm2(平均6.6 J/cm2),间隔4周治疗一次,治疗二次后瘤体无消退者予口服类固醇辅助治疗,类固醇辅助治疗4周无效者再联合干扰素治疗,直至创面愈合和瘤体消失。结果:68例患儿在治疗二次后创面完全愈合,瘤体明显缩小,经一至八次(平均四次)激光治疗后瘤体完全消退,8例患儿辅以类固醇治疗,6例治愈,2例无效后予干扰素联合治疗后瘤体消退,总治愈率100%;经过平均12个月随访,所有患儿无溃疡复发和血管瘤再发。结论:脉冲染料激光治疗婴幼儿体表溃烂型血管瘤,具有良好疗效,是一种行之有效的治疗方法。     

Critical effect of Helicobacter pylori infection on the effectiveness of omeprazole for prevention of gastric or duodenal ulcers among chronic NSAID users

Background. The recently reported OMNIUM and ASTRONAUT NSAID ulcer prevention trials using omeprazole to prevent endoscopic ulcer recurrence among chronic NSAID users suggested superiority over misoprostol or ranitidine. Aim. To test the hypothesis the results from the OMNIUM and ASTRONAUT studies would not be generalizible as ulcer healing and ulcer recurrence would differ in relation to Helicobacter pylori status. Methods. The data regarding H. pylori status were made available by AstraZenca allowing separate analysis of the outcome of those with NASID ulcers (i.e. without H. pylori infection) and those NSAID use was complicated with the presence of an active H. pylori infection. Results. Reanalysis confirmed that omeprazole was superior to placebo for the prevention of ulcer recurrence in chronic NSAID users. However, overall omeprazole was not significantly better than the subtherapeutic dose (400 µg/day) of misoprostol (14.5% vs. 19.6%, respectively, p = .93); 400 µg of misoprostol was actually superior to omeprazole for the prevention of gastric ulcers among those NSAID ulcers (8.2% vs. 16.6% for misoprostol and omeprazole, respectively; p < .05). Omeprazole was also not statistically different from misoprostol for gastric ulcer prevention in those whose NSAID use was complicated by an active H. pylori infection. Omeprazole was not significantly different from 300 mg of ranitidine for the prevention of NSAID gastric ulcers (14.6% vs. 11.6%, respectively, p = .56). Duodenal ulcers were over represented among H. pylori infected NSAID users and duodenal ulcer prevention was more sensitive to acid suppression than gastric ulcer. Conclusion. The OMNIUM and ASTRONAUT trials may have provided an unrealistic sense of security regarding the effectiveness of omeprazole for protection against ulcer recurrence in chronic NSAID users.     

Eradication of Helicobacter pylori does not reduce the incidence of gastroduodenal ulcers in patients on long-term NSAID treatment: double-blind, randomized, placebo-controlled trial

BACKGROUND: Helicobacter pylori and nonsteroidal antiinflammatory drugs (NSAIDs) are the major causes of gastroduodenal ulcers. Studies on the benefit of eradication of H. pylori in NSAID users yielded conflicting results. OBJECTIVE: To investigate whether H. pylori eradication in patients on long-term NSAIDs reduces the incidence of gastroduodenal ulcers. METHODS: Patients on long-term NSAID treatment and who are H. pylori positive on serologic testing, were randomly assigned to either H. pylori eradication (omeprazole, amoxicillin, and clarithromycin) or placebo. Primary endpoint was the presence of endoscopic gastric or duodenal ulcers 3 months after randomization. RESULTS: One hundred sixty-five (48%) of a total of 347 patients were on gastroprotective medication. At endoscopy, gastroduodenal ulcers were diagnosed in 6 (4%) and 8 (5%) patients in the eradication and placebo group, respectively (p = .65). During follow-up of 12 months, no symptomatic ulcers or ulcer complications developed. No significant differences were found in the development of gastroduodenal erosions, dyspepsia, or in quality of life. CONCLUSION: H. pylori eradication therapy in patients on long-term NSAID treatment had no beneficial effect on the occurrence of ulcers, erosions, or dyspepsia. Ulcer rates in both study arms are remarkably low, in both patients with and without gastroprotective therapy.     

Purification and Properties of Catalasc from a Methanol-utilizing Yeast,Candida sp. N-16

Defatted soybean extract was fractionated into protein fractions and low molecular weight fractions with gel filtration. NAD-dependent aldehyde dehydrogenase from bovine liver mitochondria and from yeast was found to oxidize aldehyde in both fractions. These enzymes, therefore, were used to determine the quantity of aldehyde. When the protein fraction obtained by gel filtration was subjected to gel filtration again, aldehyde was recovered in the protein fractions. The level of aldehyde in the protein fractions was unchanged before and after digestion of the protein with pepsin. When the soybean extract was incubated beforehand with aldehyde dehydrogenase and NAD⁺ and the subjected to gel filtration, no aldehyde was detected in the protein fractions. These results indicate that aldehyde dehydrogenase acts on the soybean protein-bound aldehyde. Alcohol dehydrogenase from horse liver in the presence of NADH did not convert the bound aldehyde to alcohol.

A large portion of the aldehyde in the extract was separated from the protein by acid precipitation of the protein. Aldehyde dehydrogenase acts on the aldehyde remaining in the protein after acid precipitation. Thus acid precipitation helps to save NAD⁺ required for complete removal of aldehyde from the soybean protein by aldehyde dehydrogenase.     

三叶肽：从结构到功能

三叶结构域是一段由38－39个氨基酸组成的多肽序列,其中包含6个高度保守的半胱氨酸残基,这6个半胱氨酸残基以1－5,2－4,3－6的交联方式形成三对二硫,窝囊鑫肽链折叠成特征性的三叶结构。已发现的哺乳动物三叶肽有三种：pS1、SP及ITF。三叶肽通常位于消化道腔面的粘膜层,具有保护和修复功能,在维持粘膜的完整性中发挥着重要作用。     

北方军人消化性溃疡流行病学调查

目的：了解消化性溃疡（PU）在我军区部队中的发病情况以及相关危险因素,为进一步预防和治疗研究提供基础。方法：通过整群抽样的方法,运用统一的自填问卷,调查研究对象PU的发病情况和暴露因素以及其它影响因素。结果：军人PU相关症状发生率（Sc≥5）为8.41%（618/7345,95%CI=7.77%~9.03%）。多因素分析发现,兵龄、消化性溃疡的家族史、NSAID用药史、精神紧张、脾气易怒与PU症状积分（Sc≥5）发生率显著相关,其他因素（年龄、BMI、文化程度、出生地、吸烟、饮酒、刺激食物、饮食规律）与PU症状的发生率未见明显关系。结论：北方部队PU症状的发生率低于南方部队,兵龄、消化性溃疡的家族史、NSAID用药史、精神紧张、脾气易怒可能是军人消化性溃疡的危险因素。     

胃复春片联合西药治疗胃溃疡的临床疗效

目的：探讨胃复春片联合西药治疗胃溃疡的临床疗效。方法：选取本院收治的胃溃疡患者80 例,随机分为观察组和对照组, 每组40 例。对照组给予奥美拉唑和阿莫西林治疗,观察组在对照组基础上加用胃复春治疗。观察并比较两组治疗前后血清TNF- 琢及IL-8 水平变化、临床疗效、幽门螺杆菌根除率、不良反应发生率,并采用采用视觉模拟评分法（Visual Analogue Scale/Score,V AS）评定治疗前后的腹部疼痛程度。结果：观察组治疗总有效率为92.50 %,对照组治疗总有效率为80.00 %,两组差异有统计学意 义（P＜0.05）;两组治疗后的VAS评分较治疗前均有明显下降（P＜0.05）,但观察组优于对照组（P＜0.05）;观察组幽门螺旋杆菌清 除率为97.50 %,显著高于对照组的77.50 %（P＜0.05）;观察组不良反应发生率为12.50 %,明显低于对照组的30.00 %（P＜0.05）。 两组治疗后的TNF-alpha、IL-8 浓度均有所下降,且观察组下降程度明显高于对照组,差异具有统计学意义（P＜0.05）。结论：对于胃溃 疡患者,在西药治疗的基础上加以胃复春片治疗,可以显著提高治疗效果,缓解临床症状,且不良反应少。     

Protective and therapeutic effects of resveratrol on acetic acid-induced gastric ulcer

Sprague Dawley rats of both sexes were injected with either saline or RVT (10 mg/kg) either before or after acetic acid ulcer induction and decapitated 3, 5 or 10 days after ulcer. In the saline-treated ulcer groups, macroscopically evident ulcers were observed, while RVT-pretreated or RVT-treated groups had lower macroscopic ulcer scores. Likewise, the microscopic damage scores were lower for the RVT-administered groups. Gastric myeloperoxidase activity, malondialdehyde, collagen and tumour necrosis factor-alpha levels, as well as luminol- and lucigenin-enhanced chemiluminescence levels that were elevated in the saline-administered ulcer groups, were depressed with both RVT-pretreatment and RVT-treatment. Moreover, depleted glutathione levels in the ulcer groups were increased back to control levels by both pre- and post-treatments of RVT. Results demonstrate that resveratrol has both protective and therapeutic effects on oxidative gastric damage by suppressing pro-inflammatory cascades, including the activation of pro-inflammatory cytokines, accumulation of neutrophils and release of oxygen-derived free radicals.     

原发性皮肤隐球菌病合并热带念珠菌感染1例

报告1例原发性皮肤隐球菌病.患者因“面部溃疡半年”来我科就诊.皮肤科检查：右侧额头见约5 cm×5 cm不规则地图状溃疡,病理检查示：溃疡组织中大量炎细胞浸润,PAS染色、六氨银染色均见带荚膜的圆形孢子.真菌培养为热带念珠菌.综合考虑,诊断为原发性皮肤隐球菌病合并热带念珠菌感染.经伊曲康唑治疗迅速好转.     

对氯苯丙氨酸对迷走神经刺激诱发溃疡的抑制作用

本研究采用免疫组化结合细胞显微分光扫描测定及图象分析的方法,定位定量观察了对氯苯丙氨酸对大鼠胃粘膜内源性５－羟色胺含量的影响,并进一步探讨了对氯苯丙氨酸抑制迷走神经刺激诱发溃疡的作用。研究结果表明,对氯苯丙氨酸腹腔注射（１００ｍｇ·ｋｇ－１·ｄ－１）后３ｄ,胃粘膜５－羟色胺含量明显下降,细胞显微分光扫描测定及图象分析结果显示给药组５－羟色胺的减少与对照组相差显著。同剂量对氯苯丙氨酸可以减轻迷走神经刺激诱发的溃疡。结果提示,对氯苯丙氨酸可能通过抑制胃内源性５－羟色胺的合成而抑制迷走神经刺激引起的溃疡。