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[Campylobacter (Helicobacter) pylori in chronic erosive gastritis, duodenitis and gastroduodenitis].

The presence and degree of manifestation of Campylobacter (Helicobacter) pylori in gastroduodenal mucosa were studied in 100 patients (56 men, mean age 51.4 years, and 44 women, mean age 46.5 years) with endoscopically proved chronic erosive gastritis (52 patients), erosive duodenitis (36 patients) and erosive gastroduodenitis (12 patients). The examinations revealed the presence of Campylobacter (Helicobacter) pylori in mean 77% of the patients with erosive gastritis, duodenitis and gastroduodenitis. Campylobacter (Helicobacter) pylori was found most often in patients with chronic erosive duodenitis--83.3%, whereas in the patients with erosive gastritis it was found in 73.07%. In 83.33% of the patients with chronic erosive gastritis, duodenitis and gastroduodenitis the campylobacter infection was well manifested--(++) according to Le Bodie et al (1987). The results allow the conclusion that one of the important pathogenetic factors of erosive gastritis, duodenitis and gastroduodenitis is the Campylobacter (Helicobacter) pylori infection of gastroduodenal mucosa.

Chronic Disease↗

[Helicobacter pylori and ulcer disease: significance for diagnosis and therapy].

Helicobacter pylori can cause acute gastritis. It is also associated with chronic gastritis and peptic ulcers. The clinical significance of chronic gastritis is not clear, there are apparently no connections between chronic gastritis and dyspeptic complaints. There is hitherto no reason to treat Helicobacter pylori infestation in patients with gastritis or non ulcerating dyspeptic disease. In patients with ulcers several studies have suggested that the rate of recurrence of ulcers is diminished after eradication of Helicobacter. Unfortunately most of these studies have methodologic deficiencies. Treatment with the goal to eradicate helicobacter is tedious, carries a substantial risk of side effects and has a limited chance for success. These treatments are of an experimental nature and should essentially be reserved for controlled studies. These will have to compete with the established and safe treatment by H2-antagonists.

Gastritis↗

[Chronic inflammation of the gastric mucosa and some immunologic aspects of Helicobacter pylori infection].

UNLABELLED: The aim of the study was to determine what is the correlation between immunological phenomena and pathological changes in chronic gastritis and how it refers to the histology and endoscopy. PATIENTS AND METHODS: 42 patients with dyspepsia underwent following procedure: 1) gastroscopy and antral biopsy of 3 specimens; 2) histology; 3) immunofluorescence of the specimens in purpose to detect bound immunoglobulins using antibodies anti-human IgA + IgG + IgM labelled with rhodamine; 4) serologic test for anti-H.pylori antibodies. The research included 17 females and 25 males (ages 30-86, median 53.4 +/- 15.47). The obtained data were compared referring to mutual correlations and presented according to the kind of pathological changes depending on:--presence or absence of Helicobacter pylori infection;--presence or absence of anti-Helicobacter pylori antibodies;--presence or absence of lymphocytic infiltration;--presence or absence of bound immunoglobulins in gastric mucosa. RESULTS: --We have not observed ulcerations in anti-Helicobacter pylori seronegative group;--intestinal metaplasia and gastric ulcer were more frequent in bound immunoglobulins positive group;--biliary reflux was observed less frequently in lymphocyte infiltration negative group then in the positive one. CONCLUSION: pathological changes in chronic gastritis may depend not only on the presence of Helicobacter pylori infection, but also on the presence and quality of immunological response on its antigens.

Adult↗

[Helicobacter pylori infections: familial clustering and transmission].

BACKGROUND: The importance of Helicobacter pylori for the development of gastritis and gastro-duodenal ulceration is generally accepted. The objective of the presented work was to find out whether its transmission is involved in families of children examined on account of upper dyspeptic syndrome. Aggregation and transmission of Helicobacter pylori infection were not described so far in the Czech Republic. METHODS AND RESULTS: The authors examined IgG antibodies (ELISA) against Helicobacter pylori in 411 subjects incl. 102 children with non-ulcerative or ulcerative dyspepsia and in 115 children of similar age but without gastrointestinal complaints and in 194 family members of children with dyspepsia. The specificity of the ELISA test is 97.1% and the sensitivity 92.1% (discrimination analysis). Children with dyspepsia had more frequently a positive finding of IgG antibodies against H. pylori (p = 0.0001), as compared with the control group of children of the same age but without dyspepsia. A statistically significant source of infection with H. pylori for dyspeptic children was the mother (p = 0.0006) and both parents (p = 0.0069), who were also a source of infection for other family members (p = 0.0003 and 0.0084). The most frequent positive IgG finding was in fathers (76.7%), but the father was not a statistically significant source of infection for the examined children (p = 0.6120) nor for other members of the family (p = 0.2330). IgG positive mothers had 85.2% positive husbands, IgG negative mothers had 68.4% positive husbands (p = 0.1601). The frequency of IgG antibodies in the mother and father (in couples) was thus statistically independent. However, there was a significant correlation (p = 0.01) of (P/N) IgG antibodies in couples--i.e. father and mother of the examined children. Siblings of IgG positive children had a significantly higher mean value of antibodies (p = 0.05) and were older. CONCLUSIONS: The presented facts provide evidence that in the investigated group the Helicobacter pylori infection is more frequent in children with the upper dyspeptic syndrome than in children of similar age without gastrointestinal complaints. In families of children with dyspepsia the infection aggregates and is transmitted. The mother and both parents are involved in the transmission to children. Nevertheless it is probable that there is also mutual transmission in children and from adults to children outside the family and in another environment.

Adolescent↗

[Epidemiology of Helicobacter pylori infection in Hungary (comparative sero-epidemiologic study)].

In the last decade pathogenetical role of Helicobacter pylori infection has been proved in development of gastroduodenal alterations. DNA-RNA hybridisation and protein profile studies proved that Helicobacter pylori is an organism distinct from other bacteria. Therefore serology became a useful method to study the epidemiology of Helicobacter pylori infection in various populations. In Hungary sera were collected from adults aged 20-60 in blood banks (Military Hospital, Tolna County Hospital) in 1993. The samples were classified in 5 year increment groups and questionnaires were filled out. Anti-H. pylori IgG were tested using Cobas Core kit (Roche Diagnostic). The overall rate of seropositivity was 63.3%. The prevalence according to age was the following: 20-24 yrs = 44%, 25-29 yrs = 40%, 30-34 yrs = 52%, 35-39 yrs = 64%, 40-44 yrs = 75%, 45-49 yrs = 73%, 50-54 yrs = 77%, 55-59 yrs = 83%. There were no statistical difference between gender, living in urban or rural areas at the time of collection or in childhood, between the level of education, type of labour or social status. However we found statistical correlation between anti-H. pylori seropositivity and epigastric symptoms. The same characteristics of Helicobacter pylori infection were found in Hungary as well as in other countries. In groups between 20 and 30 years has been proved lower prevalence in Hungary than in Poland, Bulgaria.

Adult↗

Helicobacter pylori positivity in Belgium.

Epidemiological data about the prevalence of Helicobacter pylori positivity are presented in a large population of symptom-free paediatric and adult patients in Belgium (n: 1180, age range: 1 to 40 years). The investigated patients belonged to different ethnic backgrounds and are representative for the general population of Brussels. The overall prevalence of Helicobacter pylori positivity was 18.0%. We observed a significant increase in the number of positive patients with advancing age, ranging from 6.4% in the youngest age group (1 to 5 years) to 36.4% in the age group from 36 to 40. Furthermore, a significantly higher prevalence was observed in non-Caucasian patients when compared to caucasian subjects, even if both groups were born in Belgium and have been living in the same area ever since (p < 0.001). We conclude that the overall prevalence of Helicobacter pylori positivity in asymptomatic subjects in Belgium should not be underestimated. Their number increases with age and there are significant ethnic differences. The meaning of these "asymptomatic carriers" still needs to be elucidated, but their prevalence should be considered in future studies about the role of Helicobacter pylori in upper gastro-intestinal pathology.

Adolescent↗

A nested case-control study on the association between Helicobacter pylori infection and gastric cancer risk in a cohort of 9775 men in Taiwan.

A nested case-control study was carried out to investigate the association between Helicobacter pylori infection and gastric cancer risk in Taiwan. A total of 29 patients newly affected with gastric cancer and 220 healthy controls matched with cases on age, sex and residence were selected from a cohort of 9,775 men recruited from 1984 through 1986. Frozen serum samples collected at recruitment examination were tested for IgG antibodies against Helicobacter pylori by an enzyme-linked immunosorbent assay. The average interval between serum collection and cancer diagnosis was 3.1 years. Gastric cancer cases had a higher seropositive prevalence (69%) than matched controls (59%) giving an odds ratio of 1.6 (95%) confidence interval = 0.7-2.6). Compared with previous nested case-control studies, Helicobacter pylori infection in early childhood may be a risk factor for gastric cancer. However, a long induction period seems required for gastro-carcinogenesis associated with Helicobacter pylori infection.

Adult↗

Chronic active hepatitis in mice caused by Helicobacter hepaticus.

Helicobacter infections cause chronic gastroenteritis in humans and several animal species. We recently discovered a new Helicobacter (H. hepaticus) that is the etiological agent of a unique chronic active hepatitis in mice. Natural infection appeared to be acquired early in life in enzootically infected colonies. Liver lesions arose as focal necrosis and focal nonsuppurative inflammation by 1 to 4 months of age in susceptible mouse strains. By 6 to 8 months, extensive liver involvement included hepatocytomegaly, bile ductular (oval cell) hyperplasia, and cholangitis. There was an age-related increase in proliferating cell nuclear antigen hepatocyte nuclear labeling index. The bacteria were usually found within bile canaliculi as determined by ultrastructural evaluation of liver lesions, the Steiner modification of the Warthin-Starry stain and immunohistochemistry with a rabbit antibody to Helicobacter pylori. Naturally infected mice showed an age-related increase in serum IgG antibodies to Helicobacter hepaticus proteins. The disease was experimentally reproduced by intraperitoneal injection of liver suspensions from affected livers or bacteria cultivated in vitro. The earliest lesions of the experimental disease appeared 4 weeks after injection. The course of spontaneous and experimental infection was slow and insidious and resulted in high titers of antibodies to bacterial proteins. This chronic bacterial infection represents a new model of chronic liver disease.

Animals↗

[Occurrence of Helicobacter pylori in mucous membrane of stomach in patients with duodenal ulcer and inflammation of stomach mucous membrane].

In 1990-1991 microbiological studies were performed aimed at determination of frequency of occurrence of Helicobacter pylori in patients treated because of peptic ulcer in Department of Gastroenterology in Katowice. Studies were performed in 112 patients. Out of these, in 73 duodenal ulcer was detected endoscopically (group I), in 26--inflammation of stomach mucous membrane with erosion (group II), and in 13--both duodenal ulcer and erosion of stomach membrane (group III). Samples from mucous membrane of pylorus and of stomach taken endoscopically were tested microscopically and in culture. Helicobacter pylori was found in 74 patients (66.1%). Frequency of isolation was different in individual groups. Helicobacter pylori was found in 51 patients (70%) of group I, 15 (58%) of group II and in 8 (61%) of group III. Helicobacter pylori was most frequently isolated from patients with duodenal and stomach ulcer (81.3%).

Adult↗

Role of Helicobacter pylori infection and duodenogastric reflux in the pathogenesis of alkaline reflux gastritis after gastric operations.

In patients undergoing gastric operations, we studied the relationship between data suggesting alkaline reflux gastritis (symptoms, endoscopic alterations and histologic lesions) and two factors that produce chronic gastritis (helicobacter pylori and duodenogastric reflux). Of 225 patients who underwent operations for gastroduodenal gastric ulcer at our General Surgery Unit between 1980 and 1982, 63 agreed to undergo endoscopy and biopsies. Of these 63 patients, 38 agreed to a test to quantify duodenogastric reflux (24 hour gastric pH monitoring associated with the determination of bile acids in gastric juice). According to the clinical questionnaire, patients were classified as symptomatic and asymptomatic. Endoscopy was considered either normal with mucosal lesions or mucosal lesions plus bile. In the histologic study, we considered normal mucosa, superficial chronic gastritis and atrophic chronic gastritis. Furthermore, the presence of atrophy, metaplasia, foveolar hyperplasia and helicobacter pylori was studied. Symptoms, endoscopic alterations and histologic lesions were not significantly related to helicobacter pylori, but were significantly related to the quantity of duodenogastric reflux. The symptomatic patients presented with a greater quantity of reflux than the asymptomatic patients (p < 0.05). The patients with mucosal lesions plus bile who had endoscopy showed a greater quantity of reflux than those with normal endoscopy (p < 0.001) and those with mucosal lesions without bile (p < 0.02 for pH values and p < 0.001 for bile acids). The patients with atrophic chronic gastritis presented with a greater quantity of reflux than those with normal mucosa and superficial chronic gastritis (p < 0.05, respectively), and the patients with atrophy and metaplasia and foveolar hyperplasia had more reflux than those without (p < 0.001, respectively). The patients who were helicobacter positive and negative presented with similar quantities of reflux.

Biopsy↗

[Oral triple therapy for eradication of Helicobacter pylori in duodenal ulcer disease].

25 patients with Helicobacter pylori-associated active duodenal ulcer disease (bleeding: n = 5, penetrating: n = 1, stenosis of the bulb: n = 4, frequent ulcer relapse: n = 18) were treated with 3 x 600 mg bismuth subsalicylate (BSS), 3 x 400 mg metronidazole and 3 x 500 mg tetracycline in addition to 300 mg ranitidine. 23 out of 25 patients (92%) proved to be Helicobacter pylori-negative four weeks after cessation of study medication as judged from negative urease test, specific culture and histology after modified Giemsa staining. 24/25 ulcers (96%) had healed after six weeks. In one patient on NSAIDs a small duodenal ulcer was detected on the final endoscopic examination despite successful Helicobacter pylori eradication. Twelve out of 25 (48%) patients complained side effects that did not lead to discontinuation of therapy. In conclusion, oral triple therapy with BSS, metronidazole and tetracycline is highly effective in Helicobacter pylori eradication, but there was a rather high rate of more or less serious side effects, diminishing the attractiveness of this therapeutic regimen.

Administration, Oral↗

[A study on the relationship between Helicobacter pylori and chronic gastritis and peptic ulcer by the case-control method and sequential analysis].

The association between Helicobacter pylori and the chronic gastritis and peptic ulcer was investigated by the case-control method, 1:1 matched study and sequential analysis. The results of three methods showed that the degree of association between Helicobacter pylori and the chronic gastritis and peptic ulcer was significant (chi 2 = 22.70, P < 0.001, OR = 15.63, 95% CI of OR was 5.05, 48.43), especially that between Helicobacter pylori and active chronic gastritis (OR = 20.92). The results indicate that Helicobacter pylori might be an etiological factor for patients with chronic gastritis and peptic ulcer.

Case-Control Studies↗

[Peptic ulcer and Helicobacter pylori. Comments on the authors' cases].

The presence of Helicobacter was tested on a group with antral or duodenal ulcer with or without gastritis, versus a group without gastric or duodenal pathology. Furthermore an open trial was performed between omeprazole and colloidal bismuth subcitrate (CBS) on patients similarly affected by peptic disease. Although CBS did eliminate Helicobacter in more than a half of patients, what was not obtained by omeprazole, this result did not mean a better control of peptic disease: in fact the omeprazole was remarkably more active in our series on clinical and endoscopic ground, whether the Helicobacter was present or not, and further studies are required to assess the real significance of Helicobacter pylori in the above conditions.

Adult↗

Diagnostic tests for Helicobacter pylori--can they help select patients for endoscopy?

AIM: Dyspepsia is a common symptom and some selection process for endoscopy is required. This study seeks to determine if noninvasive tests for Helicobacter pylori could be useful as a screening test to help select patients for endoscopy. METHODS: Consecutive patients attending for upper gastrointestinal endoscopy were interviewed prior to endoscopy and the endoscopic diagnoses was recorded. The presence of Helicobacter pylori infection was assessed by serology. Some patients also had a 13C urea breath test or rapid urease test (CLO test). RESULTS: 436 consecutive patients were evaluated. The endoscopy findings were normal in 44%, 29% had reflux oesophagitis, 18% had duodenal ulcer, duodenitis or gastric ulcer and 9% had other diagnoses. 54.8% of patients were positive for Helicobacter serology. Using either the CLO test or 13C urea breath test as the confirmatory test for the diagnosis of Helicobacter pylori, the sensitivity of the serology test was 96% and 91% respectively and the specificity was 66.6 and 82%. Patients with negative serology and no history of recent NSAID or aspirin use comprised 34% of the total with dyspepsia or reflux symptoms. There were no gastric or duodenal ulcers in this group. CONCLUSION: The serology test may have some potential or the initial evaluation of dyspepsia. These tests need to be prospectively evaluated in general practice.

Adolescent↗

[MALT-type low-grade B-cell lymphomas of the stomach and Helicobacter pylori].

From January 1 1994 to March 1 1995 we observed 6 patients with gastric low-grade B-cell lymphoma of MALT type in association with Helicobacter pylori infection. Endoscopically only 3 of the 6 patients presented with pathological findings. All but one patient with metastatic carcinoma received antibiotic therapy for Helicobacter pylori. Follow-up was not possible in one patient who died unexpectedly. In all 4 patients followed-up, eradication of Helicobacter pylori resulted in regression of the malignant lymphoma. During the median follow-up time of 7 months (2-13 months) no relapse of lymphoma was observed. Our results confirm that gastric low-grade B-cell lymphoma of MALT type can regress after eradication of Helicobacter pylori.

Adult↗

Comparison of diagnostic methods for detection of Helicobacter pylori.

Of two hundred Ethiopian patients with dyspepsia, multiple biopsies were taken from the antrum of the stomach. Helicobacter pylori was cultured from 85% of duodenal ulcer and in 75% of chronic antral gastritis patients. The overall Helicobacter pylori positivity was 70%. The sensitivity, specificity, positive and negative predictive values of the tests as compared to culture were as follows, respectively: direct urease test 100%/87%/95%/100%, direct gram stain 60%/98%/99%/51%, histological gram stain 66%/97%/98%/56%, Giemsa stain 100%/97%/99%/100% and Gimenez stain 100%/87%/95%/100%. It is concluded that gram staining of direct tissue smear or histology is an insensitive method in the diagnosis of Helicobacter pylori. All the other tests, are shown to be valid. Urease test is an excellent test for provision of presumptive diagnosis of Helicobacter pylori while awaiting confirmation either by culture of histology.

Adolescent↗

[Infection with Helicobacter pylori and its serologic detection].

Pathogenicity of Helicobacter pylori is based partially on the production of toxic substances. On the other hand the gastric mucosal injury may be caused by the Helicobacter pylori-induced host inflammatory response. Considerable antibody response during Helicobacter pylori infection provides a ground for indirect non-invasive serological detection. Appropriate clinical applications of serological tests are based on a good understanding of the antibody response characteristics during Helicobacter pylori infection.

Antibodies, Bacterial↗

Development of duodenal ulcer concomitant with successful Helicobacter pylori eradication.

The discovery of an association of the bacterium Helicobacter pylori and gastroduodenal ulcer disease has changed our thinking about the pathogenesis of peptic ulcers. The focus of treatment has been directed away from acid suppression as the only therapeutical component to the additional use of antibiotics for eradication of this microorganism. We present the case of a woman with chronic peptic ulcer disease in whom the development of a duodenal ulcer was documented concomitant with Helicobacter pylori eradication therapy utilizing omeprazole and amoxycillin. This regimen had been successful in both healing another peptic lesion in the duodenal bulb and eradicating Helicobacter pylori, yet it proved unable to prevent the early rise of a new ulcer. In conclusion, this finding suggests that Helicobacter pylori and hypersecretory states are not the only causes of relapsing duodenal ulceration.

Adult↗