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PubMed1999

[Effects of antibiotic therapy on endoscopic examination of the upper gastrointestinal tract in children with Helicobacter pylori infections].

The aim of the study was defining the antibiotic influence for endoscopic picture of the upper segment of gastrointestinal tract in Helicobacter pylori infection. We remained retrospectively analysis of 790 endoscopies. In 62 of the analysed patients we found Helicobacter pylori infection. We divided these children into two groups. The first group, contained 15 children, who received antibiotics for the previous year, for any reasons. The second, comparative group was made up of 47 children, who didn't receive antibiotics. We compared 18 characteristics of endoscopic picture in the oesophagus, stomach and duodenum mucosa. As a result of this study we conclude, that: 1) the most frequently the endoscopic changes were found in the stomach, as an erythema, an oedema and a nodularity of mucosa; 2) the inflammatory changes were in oesophagus and duodenum, as well; 3) we didn't observe the clear influence of antibiotics on the development of endoscopic changes in Helicobacter pylori infection; 4) in children, who didn't receive antibiotics, we observed polypus in the oesophagus, erosions in the stomach and ulcer in the duodenum. This may suggest the preventive role of antibiotics on intensity of gastrointestinal changes in Helicobacter pylori infected children.

Anti-Bacterial Agents↗
PubMedDate not supplied

Helicobacter pylori infection.

Helicobacter pylori colonizes the stomach of man, especially during childhood. However, H. pylori strains are not created equal, with major differences in virulence factors such as the vacuolating cytotoxin A and the cytotoxic-associated gene A, probably accounting for different clinical symptoms. The majority of infected subjects remain asymptomatic. Symptoms are aspecific. Helicobacter pylori infection is correlated with socioeconomic conditions and hygienic circumstances, resulting in an extremely high prevalence in children in developing countries. The golden standard technique to diagnose Helicobacter infection is culture of gastric biopsies; specificity and sensitivity of serology are low during childhood. Carbon-13 urea breath tests are a useful in the diagnosis but especially during follow-up. Recommended treatment consists of proton pump inhibitors in combination with two antibiotics out of amoxycillin, clarithromycin and metronidazole. The importance or clinical relevance of Helicobacter infection in asymptomatic individuals remains to be determined.

Child↗
PubMedDate not supplied

Helicobacter pylori-induced hyperproliferation: relevance for gastric cancer development in connection with mutagenic factors.

AIMS: Current data on Helicobacter pylori induced regenerative hyperproliferation of the antral gastric mucosa and significance in cancer development are still under discussion and investigation. An improved method for evaluation of the regeneratory process in antral mucosa is introduced and compared with the conventional method used for determination of proliferating cells in perpendicular sections of the gastric mucosa. METHODS: Using a combination of immunohistochemistry and PAS-staining the expression of Ki-67 (MiB1)-proliferation associated antigen was analyzed in 50 Helicobacter pylori (Hp) positive and 35 negative biopsies of the gastric antrum. PAS-staining was performed to identify the proliferative zone of the antral gastric glands. The degree of inflammation was evaluated by grades on routinely H & E-stained slides. RESULTS: Proliferative activity is significantly increased in Hp-positive cases (p = 0.00095) compared to negative ones. By using the conventionally applied proliferation index, every nucleus has to be counted and the proliferation zone is identified by at least one positive stained nucleus. The method presented here seems to be easier because the proliferative zone is clearly identified by PAS staining of neutral glycoproteins characteristic for the proliferation zone of antral glands. The density of labeled nuclei is determined and is expressed as a proliferation factor. This factor gives more distinct values, is easier to evaluate and shows a better correlation with the helicobacter status and the degree of inflammation. These results are discussed in relation to the data from the literature and with a view to other relevant factors in the course of carcinogenesis, such as growth factors, mainly EGF, p53 mutation and role of apoptosis, genetic instability and local production of oxidants. CONCLUSION: Helicobacter pylori induces an increase of regenerative proliferation activity. Under these conditions the chance of mutation is increased and time for DNA repair reduced. This could be at least a part of multiple step carcinogenesis. The newly introduced combination of staining procedures (PAS/MiBI) allows a more differentiated evaluation of the proliferation zone and its widening. This method can be more easily handled in follow-up studies than the method using perpendicular sections because in this method heavy irregularities of gland pattern induced by accompanying inflammatory processes considerably hinder evaluation.

Cell Division↗
PubMed2000

[Regression of gastric MALT lymphoma after eradication of Helicobacter pylori infection followed by endoscopic ultrasound].

The authors report a case of a 42 year-old female patient, who was admitted with epigastric pain and weight loss to our department. Upper gastrointestinal endoscopy two ulcerated lesions revealed in the stomach at the corpus-antrum border. Histologically the lesion proved to be a low grade, malignant B cell MALT lymphoma. Coexistent Helicobacter pylori infection was detected with modified Giemsa staining. Endoscopic ultrasonography was performed to determine the depth of tumorous infiltration of the gastric wall: the tumor was confined to the mucosa and submucosa. No regional lymph node was observed. As a result of successful Helicobacter pylori eradication the regression of MALT lymphoma occurred. The follow-up examinations showed the regression of the tumour and the patient became asymptomatic. A control ultrasonographic examinations demonstrated the normal five layers structure of the gastric wall without any alteration. In our patient Helicobacter pylori eradication was an effective therapy for gastric MALT lymphoma as well. Our results similar as are published in the literature. Endoscopic ultrasonography is very useful in the assessment of the tumours involvement of the gastric wall. In the proper follow-up examinations of the patient endoscopy, histology and endoscopic ultrasound together are the methods to apply including Helicobacter pylori control.

Adult↗
PubMed1999

[The presence and significance of Helicobacter pylori in patients with enterogastric reflux].

The aim of the study is assessment of the relationship between enterogastric reflux and the presence of Helicobacter pylori infection as a factors that cause gastritis, peptic ulcer and adenocarcinoma ventriculi. The study was performed in 52 patients with different digestive disorders, using gamma camera, during 90 minutes (1 frame/min) after intravenous injection of 185 MBq 99mTc-dietil IDA in cubital vein. According to time activity curves from the region of hepatobiliary system and gaster, index of enterogastric reflux was assessed (EGR). There is no correlation between the presence of Helicobacter pylori and EGR (r = 0.181, DF = 52, P < 0.05). However, Helicobacter is present more frequently in the patients with positive EGR (p 0.01). However, there is no significant difference (p < 0.05) in reflux value in patients with both positive and negative finding of Helicobacter.

Duodenogastric Reflux↗
PubMed2000

[Helicobacter pylori and chronic gastritis: relationship between infection and inflammatory activity in a high risk population for gastric cancer].

BACKGROUND: Helicobacter pylori has been involved in gastric epithelial cell damage and gastric gland loss or atrophy. AIMS: To evaluate role of Helicobacter pylori infection in acute and chronic changes of chronic gastritis in a high gastric cancer-risk population. MATERIAL AND METHODS: 200 patients with chronic gastritis were selected from pathological files of Temuco Hospital. A complete histopathological protocol was fulfilled considering the presence of infection by Helicobacter pylori-like-organism (HLO), acute and chronic inflammatory infiltrate, epithelial cell damage and epithelial cell regeneration. RESULTS: 82% of patients showed infection by HLO. Moreover, this infection reached a frequency of 92.7% in gastric ulcer patients and 94.4% in duodenal ulcer patients. A statistically significant positive correlation was found between HLO infection and polymorphonuclear infiltrate, lymphocytic infiltrate, mucus depletion and epithelial regenerative activity. There was not a statistical correlation between HLO infection and atrophy. Finally, 90% of patients with multifocal atrophic gastritis and 100% of patients with diffuse antral gastritis had HLO infection. CONCLUSIONS: HLO gastric infection frequently caused acute inflammatory changes in gastric mucosa with chronic gastritis. Sometimes these changes were severe, with marked polymorphonuclear migration throughout epithelium and severe epithelial cell damage. Recovery of these changes could be considered as a goal in Helicobacter pylori eradication therapy decision.

Chronic Disease↗
PubMed2000

Helicobacter hepaticus infection triggers inflammatory bowel disease in T cell receptor alphabeta mutant mice.

The T cell receptor alpha chain-deficient (TCR alpha-/-) and TCR beta chain-deficient (TCR beta-/-) mice develop chronic intestinal inflammation that resembles inflammatory bowel disease by 3 to 4 months of age. The objective of the study reported here was to determine the role of infection with the bacterial pathogen Helicobacter hepaticus in the pathogenesis of disease in TCR alphabeta mutant mice. The H. hepaticus-infected TCR alphabeta mutant mice were rederived by use of embryo transfer to produce Helicobacter-free animals. Helicobacter-free TCR alpha-/-, TCR beta-/-, and TCR alpha-/- beta-/- mice were inoculated with H. hepaticus. Experimentally infected mice and uninfected control mice were examined for intestinal lesions at 3, 6, and 9 months after inoculation. The TCR alphabeta mutant mice inoculated with H. hepaticus developed intestinal epithelial cell hyperplasia and mucosal inflammation. By 6 months after inoculation, infected animals had moderate cecal and colonic lesions. Helicobacter-free TCR alpha-/- mice, but not TCR beta-/- or TCR alpha-/- x beta-/- mice, also developed H. hepaticus-independent colitis by 9 months after inoculation. Infection with H. hepaticus is sufficient to cause chronic proliferative intestinal inflammation in TCR alphabeta mutant mice. However, H. hepaticus infection is not necessary for intestinal disease in TCR alpha-/- mice.

Animals↗
PubMed2000

Topics in Helicobacter pylori infection: focus on a 'search-and-treat' strategy for ulcer disease.

Several new and interesting issues regarding Helicobacter infection are discussed. Test-and-treat strategies in young dyspeptics will do little to reduce the burden of ulcer disease. The prevalence of Helicobacter infection in young people is low and still declining; the incidence of ulcer disease is therefore low. Ulcer disease has a high prevalence and most cases occur in older people. There is a large pool of people who have suffered from a documented peptic ulcer in the past and most are still intermittently symptomatic. If we are to decrease the prevalence of ulcer disease we ought to promote case finding. Only 'search-and-treat' strategies will help to eliminate ulcer disease. These can focus on patients with an ulcer history or on populations that regularly use acid suppressants. Such strategies, of which several examples are discussed, are cost-effective and lead to improved health in the target population. We also discuss the use of serology as a follow-up instrument after anti-Helicobacter therapy and discuss issues regarding Helicobacter therapy in relation to antimicrobial resistance in The Netherlands.

Antacids↗
PubMed2000

[Diagnosis of Helicobacter pylori with the 13C-labeled urea breath test: study methodology].

Helicobacter pylori is one of the most common causes of chronic bacterial infection in humans, and it is associated with many diseases of the upper gastrointestinal tract. The 13C urea breath test (13C-UBT) is a simple, non-invasive and global test for Helicobacter pylori detection. The test reflects the hydrolysis of 13C-labelled urea by Helicobacter pylori urease. The 13C-UBT is the gold standard test for Helicobacter pylori infection. Since the original description (in 1987) several modifications of 13C-UBT have been published to simplify and optimise the test. However, neither Standardised European Protocol nor Standard US Protocol were accepted. This paper gives the methodology of the 13C-UBT based on eur own study and on the review of the literature.

Breath Tests↗
PubMed2001

Decreasing prevalence of helicobacter antibodies in Finland, with reference to the decreasing incidence of gastric cancer.

Time trends and geographical variation of Helicobacter pylori antibodies in Finland were investigated by enzyme immunoassay in 20- to 34-year-old randomly selected females from six localities during 1969-73 (n = 375), and 15- to 45-year-old females representing nine communities and four geographical areas in 1983 (n = 882) and 1995 (n = 842). In the six communities investigated at three different time points, the overall prevalence declined from 38 to 12%, with an emphasis on the latter 12 years. The regionally varying rate of decrease in helicobacter prevalence changed the pre-existing geographical variation, leaving northern Finland with the highest rate. A 10%-units higher local helicobacter prevalence seemed to predict a 23% (95% CI 3-44%) higher gastric cancer incidence 20 years later. The overall decline in helicobacter seropositivity is consistent with earlier reports from Finland and other developed countries, and supports the cohort theory as an explanation for the age-related increase in H. pylori seroprevalence.

Adolescent↗
PubMed2001

[Endoscopic aspect of ulcerated tumor-like gastritis associated with Helicobacter heilmannii].

We report on 5 cases with an endoscopic aspect exceptionally described of ulcerated tumor-like gastritis associated with Helicobacter heilmannii. This rare but ubiquitary bacteria, belonging to the same family as Helicobacter pylori, is epidemiologically and structuraly different. When these endoscopic lesions are detected, Helicobacter heilmannii has to be looked for carefully. The treatment, which is the same than for Helicobacter pylori, must lead to complete repair of endoscopic and histologic lesions.

Aged↗
PubMed2001

[Healing peptic ulcer disease with therapy of Helicobacter pylori infection--an overview].

Over the last 15 years several new aspects in the pathogenesis and basic changes in therapeutic strategies for healing of peptic ulcers have been introduced. The discovery of Helicobacter pylori, the possibility of treatment of the infection and consecutive healing of peptic ulcer disease have changed the understanding of the pathophysiology of the peptic ulcer disease. Most gastric or duodenal ulcers are based on Helicobacter pylori infection. Newer therapeutic strategies to cure Helicobacter pylori infection consist of proton pump inhibitor (PPI) based triple therapy, containing in addition two antibiotics chosen from clarithromycin, amoxicillin and metronidazole, administered over 7 days. The other main cause of gastroduodenal ulcers are non-steroidal antirheumatic drugs or aspirin intake. PPI are therapeutic strategies of choice for treatment of such lesions. Main topics of this overview are the principles and the therapeutic proceeding in the management of Helicobacter pylori-associated peptic ulcer disease. The differences between duodenal and gastric ulcer are especially dealt with.

Anti-Bacterial Agents↗
PubMed2000

Immunological aspects of Helicobacter pylori infection.

Host defence against Helicobacter pylori infection is a complex system of both specific and non-specific reactions. Among the non-specific defense mechanisms acting on bacteria before they reach the mucus layer in the stomach are digestive enzymes, lyzozyme, lactoferrin and other components with antimicrobal activity. The mucus layer is the final non-specific barrier against the bacteria reaching the gastric mucosa cells. On reaching the gastric mucosa Helicobacter pylori adheres to epithelial cells and bacterial antigens, chemotaxins and other components are liberated. Helicobacter pylori antigens are presented to immunate B lymphocytes, which interact with T-helper lymphocytes to become mature IgA-, IgD-, IgE-, IgG and Ig-M producing plasma cells. IgA dimers of secretory IgA are secreted through the gastric epithelium. IgE antibodies bind to basophils, which mature to histamine-producing mast cells. Histamine activates the acid production in the stomach and contributes to the chronic inflammation and tissue destruction. In addition, T lymphocytes are possible activated by Helicobacter pylori and contribute to the chronic inflammation.

Duodenitis↗
PubMed2001

[The prevalence and mechanism of Helicobacter pylori resistance to clarithromycin in Beijing].

OBJECTIVE: (1) To determine the prevalence of Helicobacter pylori strains resistant to clarithromycin in Peking. (2) To determine the genetic mutation in relation to clarithromycin resistance. METHODS: Helicobacter pylori were cultured from gastric biopsies obtained from 89 patients during upper endoscopy. Minimal inhibitory concentrations of clarithromycin were determined by Etest method. Genomic DNA was prepared by the hexadecyltrimethylammonium bromide (CTAB)-phenol extraction method. Mutations in clarithromycin-resistant strains were identified by polymerase chain reaction and restrictions analysis. RESULTS: (1) The prevalence of Helicobacter pylori strains resistant to clarithromycin was 13.5% in Beijing. (2) All twelve clarithromycin-resistant strains had the new BsaI site which is characteristic of the A2143G point mutation in 23S rRNA gene, none of the tested twenty-four susceptible strains had the A2142G or A2143G mutation. CONCLUSION: The prevalence of clarithromycin-resistant strains was not rare in Beijing. Mutations in 23S rRNA are associated with clarithromycin resistance in Helicobacter pylori.

Anti-Bacterial Agents↗
PubMed1999

[Determination of serum calicotonin gene-related peptide in patients with duodenal ulcer infected with Helicobacter pylori].

OBJECTIVE: To investigate the effect of calicotonin gene-related peptide(CGRP) on duodenal ulcer caused by Helicobacter pylori infection. METHOD: The serum levels of CGRP were determined by radioimmunoassay in 30 patients with duodenal ulcer associated with Helicobacter pylori infection and 20 healthy volunteers. RESULTS: The mean CGRP serum level was higher in duodenal ulcer associated with Helicobacter pylori group than that in the healthy group. CONCLUSION: The CGRP level might be one of the important factors in which Helicobacter pylori infections induce duodenal ulcer.

Adult↗
PubMedDate not supplied

Association of polymorphisms of interleukin-1 beta gene and Helicobacter pylori infection with the risk of gastric ulcer.

BACKGROUND/AIMS: Interleukin-1 beta (IL-1 beta) plays an important role in gastric inflammation and physiology. Functional polymorphisms of IL-1 beta gene have been related to different risks of gastric cancer and duodenal ulcer but their role in gastric ulcer remains unknown. In this study, we investigate a plausible association between gastric ulcer and the polymorphisms in the IL-1 beta and IL-1 receptor antagonist (IL-1RN) genes. The relationships among the cytokine genotyping, other environmental risks such as Helicobacter pylori infection and smoking, and clinical characteristics of gastric ulcer were also determined. METHODOLOGY: Peripheral blood DNAs from 120 unrelated Taiwan Chinese patients with gastric ulcer and 238 ethnically matched healthy controls were genotyped for the promoter (position -31 and -511) and Taq I polymorphism (position +3954) in the IL-1 beta gene and the variable number of tandem repeats polymorphisms in intron 2 of the IL-1RN gene. The status of Helicobacter pylori infection was determined by serology. RESULTS: The seropositive rate of Helicobacter pylori (95/120 vs. 134/238, OR: 2.95, 95%CI 1.77-4.91), habitual smoking (67/120 vs. 82/238, OR: 2.40, 95%CI 1.54-3.77) and blood group O (63/120 vs. 98/238, OR: 1.55, 95%CI 1.0-2.41) were significantly higher in patients with gastric ulcer than controls. The distributions of allele frequencies of IL-1 beta (-31 C/T or -511 C/T or +3954) and IL-1RN were similar between patients with gastric ulcer and controls. No significant differences were observed, including those analyzed after stratification of the infected population and by the ulcer subgroup. CONCLUSIONS: Our data suggested that Helicobacter pylori infection, cigarette smoking, and blood group O are risk factors of gastric ulcer and IL-1 beta or IL-1RN polymorphisms do not influence susceptibility to gastric ulcer in a Taiwanese population.

Aged↗
PubMed2002

[Epidemiology of Helicobacter pylori infection].

About 50% of adults in the developed and 80-90% in the developing countries are estimated to be infected by Helicobacter pylori. Being 68% nationally, this rate is higher in the northern continental parts of Croatia, which also have higher gastric cancer rates. Low socio-economic status, poor living conditions in childhood (the age when Helicobacter pylori is typically acquired), and exposure to the stomach content of an infected person are risk factors for Helicobacter pylori. Most of the infected are symptomless, with 10 to 20% subsequently developing the disease, and this mainly from peptic ulcer, asymptomatic chronic gastritis and chronic dyspepsia. Less than 5/10,000 become affected with adenocarcinoma, MALT lymphoma or primary non-Hodgkin's gastric lymphoma. Helicobacter pylori is under intensive study for possible association with other diseases. As transmission route of the infection is still unclear, any mechanism allowing the bacteria entry into a non-infected individual's stomach is probably a possibility. In addition to improved socio-economic status, eradication or vaccination may be contributors to the reduction in the number of the infected.

Adolescent↗
PubMed2002

[Gastric ulcer and Helicobacter pylori infection].

Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAID) are considered to be the two major risk factors implicated in the development of gastric ulcer. Helicobacter pylori infection related chronic gastritis is known to be the underlying condition which may lead to gastric ulcer. Development of gastric ulcer as the consequence of underlying chronic gastritis is caused by many factors. Treating Helicobacter pylori infection entails the healing of gastric ulcer, it concomitantly prevents recurrences and complications of gastric ulcer, primarily bleeding, and changes the natural course of gastric ulcer disease. Continuation of antisecretory maintenance treatment beyond ulcus healing and eradication of Helicobacter pylori infection is only indicated in risk groups. Patients with gastric ulcer caused by NSAID use are managed with antisecretory therapy.

Female↗