(1) Only a minority of patients infected with H pylori will eventually develop a duodenal ulcer.

(2) Thus H pylori infection combined with active ulceration may cause the increased basal acid secretion seen in duodenal ulcer disease.

(3) It is now generally acknowledged that Helicobacter pylori infection is the major cause of antral gastritis.

(4) Results Eighty three patients with H pylori positive gastric ulcers entered the study.

(5) The Pyloriset detects IgG antibodies by agglutination, using Latex particles coated with acid extracted antigen of H pylori.

(6) It has also been proposed that H pylori ammonia production will lead to mucosal damage by denaturing the protective mucus layer.

(7) After eradication of H pylori, duodenal ulcers do not usually recur and the associated chronic gastritis gradually disappears.

(8) H pylori was identified by culture and histology as previously described.

(9) The studies were designed to evaluate the H pylori eradication potency of the various regimens and the post-therapeutic course of ulcer disease.

(10) Most investigators have observed that H pylori infection causes a greater percentage increase in the postprandial gastrin than fasting gastrin.

(11) The present study indicates that H pylori infection is not the unknown factor.

(12) H pylori was not examined because its importance in duodenal ulcer disease was not widely recognised when this study was being planned.

(13) The high rate of H pylori ammonia production in uraemic patients should accentuate any ammonia induced effects.

(14) In conclusion, we investigated the influence of Helicobacter pylori colonisation on gastric mucosal eicosanoid synthesis in patients taking NSAIDs.

(15) Bismuth has also become popular in recent years as a treatment in peptic ulcer to eradicate Helicobacter pylori.

(16) Future studies evaluating mechanisms of gastrin release have to take into account the H pylori state.

(17) The role of the increased serum gastrin concentration induced by H pylori in the pathogenesis of duodenal ulcer disease is also unknown.

(18) In theory the increased prostaglandin synthesis seen with Helicobacter pylori might explain such a reduction in minor mucosal injury.

(19) There have been conflicting reports concerning the form of gastrin that is increased in H pylori infection.

(20) There are few data concerning the role of anti- H pylori treatment in gastric ulcer disease.

(21) Meretek, a Nashville firm that manufactures the test, claims it is 95 percent accurate in detecting H. pylori.

(22) Increased basal serum gastrin is related to both atrophy and H pylori infection but not to ageing perse.

(23) One month after completion of this treatment their C-urea breath test was repeated to assess the H pylori state.

(24) Therefore, additional evidence clearly pointing to a causal relation between H pylori infection and gastric ulcer disease has to be provided.

(25) This would show that acid secretion is of superior importance compated with H pylori.

(26) The fall in basal acid secretion found may not necessarily be due to the eradication of H pylori.

(27) We have shown that the serum pepsinogen-I: -II ratio is significantly lower in H pylori positive subjects than in uninfected persons.

(28) It therefore seems justified to recommend amoxicillin/omeprazole as the treatment of choice to eradicate H pylori in H pylori related gastroduodenal diseases.

(29) On logistic regression, the presence and extent of gastric metaplasia was not significantly associated with H pylori infection.

(30) The results of gastric juice against plasma concentrations according to H pylori status are shown in Figure 3.

(31) Twelve of these children received previous antibiotic therapy for various reasons, with possible inadvertent effects on the diagnosis of H pylori.

(32) However, acid secretion in old subjects without atrophy was not different to that in young subjects, irrespective of H pylori status.

(33) These differences persisted when subgroups of patients were analysed according to Helicobacter pylori colonisation or degree of mucosal injury.

(34) Endoscopy in the nine H pylori positive non-uraemic patients showed oesophagitis in one patient and active duodenal ulcer in another.

(35) In healthy men without atrophy, gastric acid secretion is preserved with ageing and is independent of H pylori status.

(36) Further studies are needed to clarify the presence of H pylori in saliva or plaque, and also in faeces.

(37) It has previously been reported that H pylori infection raises serum pepsinogen I in non-uraemic patients but only by about 25%.

(38) Similarly our study found a strong association between dyspepsia and colonisation by Helicobacter pylori in patients taking NSAIDs.

(39) In the present study we also analysed the relation between active H pylori infection and serum pepsinogen-I and pepsinogen-II concentrations.

(40) We conclude from this study that H pylori eradication enhances gastric juice ascorbate secretion, and thus increases intragastric anti-oxidant protection.

(41) Activated pepsinogen was significantly reduced in the stomach of H pylori positive patients only.

(42) Decreased concentrations of activated pepsinogen were found in H pylori positive patients only. Duodenal biopsies were tested in 76 patients.

(43) H pylori has variable effects on serum gastrin concentrations and gastric acid secretion.

(44) Patients classified as having H pylori infection received an eradication regimen; 107 were reassessed 4 weeks after therapy.

(45) Helicobacter pylori increases plasma gastrin concentrations by 50% to 100% and values fall to normal after the organism has been eradicated.

(46) The mechanism by which H pylori infection stimulates the release of G17 is not known.

(47) The strong association between antral tumours and chronic active gastritis suggests the possibility that H pylori infection may have a pathogenic role.

(48) Demanding oral triple therapy eradicates H pylori in up to 96% of patients treated but does have considerable side effects.

(49) This led us to ask if there was intrafamilial spread of H pylori.

(50) Can gastric juice ascorbic acid secretion be restored by eradication of H pylori?

(51) H pylori positive gastritis, and the combination of active duodenitis and gastric metaplasia were independent predictors of duodenal ulceration.

(52) The finding of enhanced fasting gastrin concentrations in H pylori positive subjects and in duodenal ulcer disease can not easily be explained.

(53) These tests have been shown to be reliable in detecting H pylori infection in patients with and without renal failure.

(54) Decreased concentrations of activated pepsinogen were found in H pylori positive patients only./pylori.html

(55) Helicobacter pylori also tended to increase thromboxane B 2 synthesis although this was not statistically significant.

(56) In the nine H pylori negative non-uraemic patients, one had erosive duodenitis and another a deformed duodenum.

(57) Although H pylori does not invade the mucosa, bacterial proteins may activate monocytes with a local T-cell mediated immune response.

(58) In healthy volunteers, H pylori state was determined by the C urea breath test.

(59) In addition, H pylori eradication speeds up ulcer healing and is associated with healing of previously refractory ulcers.

(60) Thus, in addition to duodenal ulcer disease, H pylori eradication may also cure gastric ulcer disease.

(61) Helicobacter pylori is recognised as a significant cause of chronic antral gastritis and important in the aetiology of peptic ulceration.

(62) There are no studies in the literature to date linking miners with an increased risk of developing gastric H pylori infection.

(63) One of the H pylori negative patients was on maintenance haemodialysis and eight were on continuous ambulatory peritoneal dialysis.

(64) H pylori infection was proved by positive cultures or histological identification, or both in antral specimens from 113 patients.

(65) In conclusion, our findings suggest that H pylori infection may have been predominantly acquired at a young age in the past.

(66) Seven of the parents were positive for H pylori on urease testing, histology, and on culture.

(67) The association between gastric histopathology and Helicobacter pylori was also investigated.

(68) The H pylori negative and positive healthy volunteers were similar for both basal and peak acid output.

(69) Patients were divided into three groups according to the presence of histological gastritis and evidence of H pylori infection by at least one criterion.

(70) Atrophy, which is closely related to H pylori infection, is associated with a decline in acid secretion.

(71) Taylor suggests that in more than 50% of cases of acute H pylori infection, hypochlorhydria lasts for several weeks.

(72) Of the nine H pylori negative uraemic patients, two had oesophagitis and one had scattered petechiae in stomach and duodenum.

(73) This finding provides support for the belief that adequate treatment of H pylori infection will give longterm protection from duodenal ulcer recurrence.

(74) These findings support the hypothesis that H pylori colonisation is directly involved in the hypergastrinaemia.

(75) The high pepsinogen C concentrations in patients with duodenal ulcer are probably related to H pylori related chronic active gastritis.

(76) The primary aim of the second trial was to see if eradication of H pylori led to resolution of intestinal metaplasia.

(77) Omeprazole monotherapy merely suppressed bacterial colonisation, especially in the antral region, and eradicated H pylori in individual cases only.

(78) Discussion Our current results confirm that treatment which both heals duodenal ulcers and eradicates H pylori significantly decreases basal plasma gastrin concentrations.

(79) H pylori infection has been shown in prospective epidemiological studies to be a risk factor for gastric cancer.

(80) It is concluded that successful eradication of H pylori improves secretion of vitamin C into gastric juice.

(81) The dynamics and importance of H pylori reduced altered mucosal peptic activity is far from being clarified.

(82) It may be secondary to the recent findings of reduced somatostatin concentrations in the presence of H pylori infection.

(83) This study aimed to analyse H pylori infection within family groups.

(84) The mechanism of hypergastrinaemia associated with H pylori infection is not known but the accompanying antral gastritis might be involved.

(85) One explanation for this finding would be that H pylori infection is acquired by people throughout their lives.

(86) After eradication of H pylori in the duodenal ulcer patients both their basal acid output and basal gastrin fell by 50%.

(87) The one parent who was H pylori negative has histological evidence of mild inflammation.

(88) To evaluate our first impressions we examined transmission electron microscopy findings in 40 H pylori positive cases out of 94 randomised cases.

(89) Cyclical changes in H pylori infection may cause the variations in basal acid secretion that are seen in duodenal ulcer disease.

(90) H pylori infection was a strong predictor of ulcer recurrences.

(91) Helicobacter pylori organisms were identified in all but two patients with type B gastritis and in two patients with type C gastritis.

(92) Martin etal found that among Helicobacter pylori positive patients ingestion of NSAIDs significantly increased the risk of gastric ulceration.

(93) Values were too low to judge whether there was any effect associated with Helicobacter pylori colonisation in controls.

(94) H pylori like organisms were detected in two patients and persisted despite metronidazole.

(95) H pylori infection was eradicated in 32 patients and persisted in 18 patients.

(96) Increased basal serum gastrin is related to atrophy and to infection with H pylori.

(97) The vacuolating cytotoxin is a unique proteinous cytotoxin produced by H. pylori that showed no striking primary sequence homology with other known bacterial toxins.

(98) Aim To reveal the virulence variation related to vacuolating cytotoxicity of coccoid Helicobacter pylori .

(99) "Stomach ulcers are caused by stress" — accepted medical diagnosis, until Dr. Marshall proved that H. pylori caused gastric inflammation by deliberately infecting himself with the bacterium.

(100) Malodour can be caused by rotting teeth, unhealthy gums, poor digestion, the ulcer bacteria Helicobacter pylori or any number of other illnesses.

(101) Objective To explore the research progress of coccoid H. pylori.

(102) The strongest association with Helicobacter pylori is with peptic ulceration -- over 85 % of duodenal ulcers.

(103) Conclusion Eradicating helicobacter pylori infection is valuable for confining the occurrence of arterial sclerosis.

(104) Objective To investigate the association of recurrent aphthous ulcer (RAU) with Helicobacter pylori (Hp) infection and digestive diseases.

(105) Among garlic's targets are H. pylori, the bacteria associated with some ulcers and stomach cancer.

(106) Method:It pass through this antibacterial extrasomatic test for helicobacter pylori provided reliable and effective drug for clinical medicine.

(107) Objective To investigate the carcinogenetic and tumor promoting effect of concentrated Helicobacter pylori culture supernatant ( CHCS ).

(108) Analysis of causes in eradication of Helicobacter pylori and control measures.

(109) BACKGROUND: Antimicrobial resistance has decreased eradication rates for Helicobacter pylori infection worldwide.

(110) Pylori positive rate in seamen mouth may be one of the causes for the high incidence of dry socket in seamen. Oral prophylaxis before extraction can prevent dry socket effectively.

(111) AIM: To observe the eradicative effect of dioctahedral smectite (DS) combined with omeprazole on Helicobacter pylori (HP) and its efficacy in treatment of peptic ulcer.

(112) Objectives To study the effect of Helicobacter pylori( HP) on gastric epithelial apoptosis, and the relationship between apoptosis and nitric oxide(NO)levels in gastric mucosas .

(113) Spread of H. pylori between siblings of infected children who are vomiting is also common.

(114) Helicobacter pylori is associated with as chronic gastritis, peptic ulcer , gastric lymphoma and gastric cancer.

(114) try its best to gather and create good sentences.

(115) Objective : To detect the infection of Helicobacter pylori in gaster and oral cavity.

(116) These data presented herein, a certain state of higher molecular weight whey protein can be implicated in the activity of inhibiting adhesion of H. pylori.

(117) In Europe, two other strategies to eliminate persistent H. pylori infection have been popular.

(118) Studies are ongoing to examine the type and extent of damage to normal stomach tissue in patients who have had H. pylori that has been eradicated.

(119) Next, the researchers pitted the dragon's blood compounds in test tubes against two foes: ulcer-causing H. pylori bacteria and thrombin, a blood-clotting agent.

(120) Objective To find a cost - effect method to pylori ( HP ) infection.

(121) It pass through this antibacterial extrasomatic test for helicobacter pylori provided reliable and effective drug for clinical medicine .

(122) Objective:To study the relationship between helicobacter pylori(HP) infection and perioral dermatitis.

(123) A hundred years ago, nearly everyone was infected with H. pylori. But the use of antibiotics has beaten back the bug.

(124) We are still learning a lot about the connection between H. pylori infection and gastric cancer.

(125) Because H. pylori is more common in developing countries, eradication might make more sense in those areas, although Greenberg and his colleagues take no position on whether it should be done.

(126) Results:Older patients enteron symptom was not apparent, and drug-related helicobacter pylori infection rates high, 57.95%.

(127) Objective To study Helicobacter pylon (H. pylori ) in dental plaque and its relevance to chronic gastritis.

(128) An area of active research is looking at the effect of H. pylori eradication on people at high risk for ulcers over time.

(129) Helicobacter pylori eradication in infected patients decrease the risk of NSAIDs-associated lesions but is less effective than concomitant antisecretory treatment.

(130) Helicobacter pylori infection will affect the level of circular and endogastric growth hormone -releasing peptide.

(131) Helicobacter pylori is a spiral Gram's negative bacterium, living in microaerophilic environment.

(132) My father, who is 89 and in generally excellent health, recently spent a few days in the hospital because of an ulcer caused by H. pylori.

(133) Method To compare to chronic gastritis group and treatment group, dental plaque and gastric biopsy samples were respectively collected for detection of H. pylori by in vitro culture.

(134) Aim To testify the pathogenicity of coccoid Helicobacter pylori in vivo.

(135) H. pylori may also be a cause or co-factor for gastric cancer, as its presence increases the risk of developing stomach tumours.

(136) But the carcinogenesis mechanism of H. pylori is not clear now.

(137) Objective To evaluate clinical significance of co-determination of serum CEA, CA19-9 and H. pylori antibody in gastric carcinoma.

(138) Methods and Results To review the literatures, and summarize the contents from the overview, pathogenicity, virulent genes and possible mechanisms of coccoid conversion in H. pylori .

(139) One size does not fit all – time to regionalize Helicobacter pylori eradication?

(140) The standard treatment is antibiotics but, worryingly, in many patients H . pylori has now become resistant to antibiotics.

(141) Aim To reval the virulence variation related to vacuolating cytotoxicity of coccoid Helicobacter pylori.

(142) Cell density cultivation and high level expression of recombinant urease A fusion protein in Helicobacter pylori.

(143) But then further studies discovered that infection with H. pylori was protective against esophageal reflux and cancer of the esophagus(), and may also reduce the incidence of asthma.

(144) In 1982, when two Australian physicians first said H. pylori caused ulcers, the international medical community scoffed.

(145) Objective: To clarify the relationship between blood group ABO and duodenal ulcer ( DU ) in patients with H. pylori ( Hp ) infection.

(146) The improved broth medium could revive Helicobacter pylori from its transformed coccal form.

(146) try its best to collect and create good sentences.

(147) This paper reviews the research development of natural product against Helicobacter pylori.

(148) Objective:To understand the effect of coccoid Helicobacter pylori on proliferation of gastric carcinoma epithelial line SGC-7901 cultured in vitro.

(149) Objective: To study the dry socket occurrence rate of patients with gastric diseases, and to investigate the relationship between dry socket and helicobacter pylori (HP).