Role of metronidazole resistance in therapy of Helicobacter pylori infections.

Susceptibility to metronidazole was determined by disk diffusion tests for 559 strains of Helicobacter pylori isolated from patients. The overall metronidazole resistance was 26%. In males metronidazole-resistant strains made 18% of all H. pylori strains, and in females the corresponding figure was 40% (P less than 0.001). MICs of metronidazole were determined for H. pylori strains from 86 patients undertaking triple therapy, i.e., treatment with colloidal bismuth subcitrate, amoxicillin, and metronidazole. Of the nonresponders who remained culture positive despite the therapy, 69% had strains with metronidazole MICs of greater than or equal to 32 micrograms/ml before the therapy, and all nonresponders had metronidazole-resistant strains after the therapy. Metronidazole resistance was, however, also found in 27% of responders before therapy. To find whether the MICs of metronidazole for H. pylori strains remained constant for longer periods, consecutive isolates sampled several years apart from the same patients were tested in parallel and no changes in the MICs were found. H. pylori was successfully eradicated by the triple therapy from 91% of patients with metronidazole-susceptible pretreatment strains and from 63% of patients with metronidazole-resistant strains before the therapy (P less than 0.01). Although resistance to metronidazole has a significant role in treatment failures in H. pylori infections, high eradication rates can be achieved with the use of the present triple therapy even in populations with a high overall metronidazole resistance rate.     

Diagnosis of Helicobacter pylori infection in patients with atrophic gastritis: comparison of histology, 13C-urea breath test, and serology

BACKGROUND: Atrophic gastritis, a risk factor for gastric cancer, is a late consequence of Helicobacter pylori infection in approximately one-third of the infected patients. It has been suggested that gastric cancer would develop less frequently if H. pylori were eradicated. However, the prevalence of H. pylori infection may be underestimated in patients with atrophic gastritis and intestinal metaplasia if only biopsy-based diagnostic methods are used. METHODS: We compared histology, 13C-urea breath test (13C-UBT), and serology in H. pylori diagnostics in 50 male patients with atrophic corpus gastritis. RESULTS: H. pylori was detected in 15 (30%) patients by histology and in 14 (28%) by 13C-UBT, whereas increased serum antibody levels indicating H. pylori infection were found in 41 (82%) patients (P < 0.0001 between serology and both histology and 13C-UBT). H. pylori infection was associated with atrophic corpus gastritis in 84% of the present patients (in one patient with normal antibody titres H. pylori was defined histologically). CONCLUSIONS: H. pylori infection would have been missed in most patients with atrophic gastritis without the analysis of H. pylori antibodies. Therefore, in patients with atrophic gastritis, the use of serology is encouraged in diagnosing H. pylori infection.     

Normal serum pepsinogen I levels in adults: a population-based study with special reference to Helicobacter pylori infection and parietal cell antibodies

OBJECTIVE: Low serum pepsinogen I (PG I) values are common in subjects with advanced corpus atrophy with or without parietal cell antibodies (PCA). Elevated values are usual during Helicobacter pylori infection. MATERIAL AND METHODS: PG I levels were determined in two randomly selected cross-sectional adult population samples using the Gastroset PGI test kits. The sera (408 in 1973 and 504 in 1994), tested earlier for H. pylori infection and now for PCA, represented subjects living in Vammala, Finland. RESULTS: In the PCA-negative population, the mean (+/-SD) PG I level was significantly higher in men than in women among both H. pylori-negative (88.13+/-34.16 microg/l versus 72.43+/-29.31 microg/l; p<0.0001) and H. pylori-positive (110.50+/-50.59 microg/l, versus 97.74+/-44.82 microg/l, p<0.0001) subjects; the difference between all H. pylori-positive and -negative subjects was also significant (p<0.001). In the 10-year age groups, age had no impact on the mean PG I levels in H. pylori-negative subjects (p=0.860). In the PCA-positive population, the 10 H. pylori-positive subjects had higher mean PG I levels (112.96+/-53.62 microg/l) than the 13 H. pylori-negative subjects (32.57+/-27.59 microg/l; p=0.002); the latter mean was also significantly lower than that of the PCA- and H. pylori-negative subjects (80.08+/-32.69 microg/l; p<0.0001). CONCLUSIONS: Men had higher normal PG I values than women, but there was no significant variation by age. H. pylori infection was associated with elevated PG I levels and a small decrease with increasing age. Non-infected PCA-positive subjects showed the lowest mean PG I level.     

Detection of Helicobacter species in chronic liver disease and chronic inflammatory bowel disease

AIM: To study the association between helicobacters and chronic liver diseases and chronic inflammatory bowel diseases. PATIENTS AND METHODS: Thirty-two patients with various chronic liver diseases and 137 patients with inflammatory bowel disease were enrolled. Antibodies to H. pylori, H. hepaticus, H. bilis, and H. pullorum were measured by enzyme immunoassay (EIA), and sera positive in a non-pylori helicobacter EIA were further examined by immunoblot assay. Detection of Helicobacter DNA in liver biopsies was done by denaturating gradient gel electrophoresis of PCR products (PCR-DGGE) and DNA sequence analysis. RESULTS: Six inflammatory bowel disease patients, four with ulcerative colitis and two with Crohn's disease, and one liver disease patient with autoimmune cholangitis had antibodies to non-pylori helicobacters by an immunoblot assay. Four immunoblot assay-negative patients, three with autoimmune and one with non-autoimmune liver disease, had Helicobacter DNA in liver biopsies; three of the polymerase chain reaction (PCR) products were closely related to non-pylori helicobacters. CONCLUSION: Evidence for non-pylori helicobacters was scant in Finnish patients with inflammatory bowel disease or chronic but not end stage liver disease. We cannot, however, rule out their role in these diseases.     

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determi...     

Campylobacter-triggered reactive arthritis: a population-based study

OBJECTIVE: To study the incidence and clinical picture of Campylobacter-associated reactive arthritis (ReA) and other reactive musculoskeletal symptoms in the population. METHODS: A questionnaire on enteric and extraintestinal, including specifically musculoskeletal, symptoms was sent to 870 consecutive patients with Campylobacter-positive stool culture and 1440 matched controls. Analysis of self-reported musculoskeletal symptoms with clinical examination was performed. RESULTS: Forty-five of the patients (7%) had ReA and eight (1%) had reactive tendinitis, enthesopathy or bursitis. No child had ReA. The arthritis was oligo- or polyarticular, and, in most cases, mild. HLA-B27 was positive in 14% of ReA patients. Of the 45 ReA patients, 37 had C. jejuni and 8 had C. coli infection. No controls had ReA. CONCLUSION: ReA is common following Campylobacter infection, with an annual incidence of 4.3 per 100000. At the population level, acute ReA is mild, more frequent in adults, and not associated with HLA-B27. Besides C. jejuni, C. coli can trigger ReA.     

Evaluation of Blood Tests to Predict Normal Gastric Mucosa

Background: To determine the accuracy of blood tests in predicting normal gastric mucosa confirmed by histological examination of gastric biopsy specimens. Methods: In total, 207 consecutive patients referred for upper endoscopy were included. Two biopsy specimens each from the antrum and corpus were assessed histologically for the presence of Helicobacter pylori, gastritis, and atrophy. Serum samples were studied for H. pylori antibodies by enzyme immunoassay (Pyloriset EIA-G and EIA-A) and by a rapid latex agglutination test (Pyloriset Dry); pepsinogen I was measured by an immunoenzymometric assay (Gastroset PGI), gastrin by radioimmunoassay, and parietal cell antibodies by indirect immunofluorescence. Results: In 101 (49%) of 207 patients, the gastric mucosa on histologic examination was normal. In the 63 patients aged 45 years or less, H. pylori IgG serology was negative in all 47 patients with normal gastric mucosa and none had low serum pepsinogen I levels. Among 144 patients over age 45 years, 72 had negative H. pylori IgG serology. Combining the serum pepsinogen I assay with the results of H. pylori IgG serology, 12 patients with normal serology but low serum pepsinogen I were found. Thus, 60 patients, 52 of whom showed normal gastric histology, had normal IgG serology and serum pepsinogen I. In the remaining eight patients with normal blood tests, the histologic changes were very mild. Conclusions: Although negative H. pylori IgG serology alone in younger patients, and in combination with normal serum pepsinogen I levels in older patients, reliably predicted the presence of normal gastric mucosa, gastroscopy is still recommended for patients over 45 years.     

Helicobacter antibodies in Finnish centenarians.

BACKGROUND: The prevalence of helicobacter antibodies increases with age and, in many developed countries, is highest in people born before 1940. Data on very old subjects are, however, limited. In this study we wanted to determine whether the age-related increase in the seroprevalence of H. pylori infection continues even in the oldest age group alive in Finland, the centenarians. METHODS: Sera from 173 subjects (93% of all centenarians alive in Finland in 1991) were available for the present study. IgG and IgA antibodies against H. pylori were determined by an in-house enzyme immunoassay. To estimate the influence of atrophic gastritis on the prevalence of helicobacter antibodies, serum pepsinogen I (PG I) concentrations and parietal cell antibodies (PCAs) were measured by an enzyme immunoassay and indirect immunofluorescence, respectively. RESULTS: The prevalence of helicobacter antibodies in Finnish centenarians was 66%. Low PG I values (<28 microg/l) were found in 36% and positive PCAs in 16% of the subjects studied. The prevalence of PCAs was especially high (50%) in H. pylori-negative subjects with low PG I values, suggesting severe gastric atrophy. CONCLUSIONS: The age-related increase in H. pylori seroprevalence did not continue in the oldest age group alive in Finland. This may be explained partly by a relatively high frequency of atrophic gastritis (as suggested by low PG I values) in H. pylori-negative centenarians, but other factors--such as selective H. pylori-related mortality--may also have contributed to the fairly low seroprevalence (66%) observed.     

Helicobacter antibodies in 1973 and 1994 in the adult population of Vammala,Finland.

Changes in Helicobacter pylori seroprevalence were studied determining IgG and IgA antibodies of 408 randomly selected adults aged 15-74 years living in Vammala, Finland in 1973 and of 504 similarly selected subjects in 1994. Seroprevalence increased by age at both time points. The age-adjusted seroprevalence rate was clearly lower in 1994 than in 1973 (31 vs. 56%, P = 0.001). Paired serum samples of 224 subjects collected in 1973 and 1994 showed that the antibody status remained unaltered in 92%; 4% seroconverted and 4% seroreverted within the 21 years. The decrease in the seroprevalence rate in the population and the persistence of individual antibody status over two decades support a difference in H. pylori infection rates among birth cohorts over time rather than continuous acquisition of new infections with advancing age. Thus the risk of helicobacter infection in Vammala, Finland has been highest in childhood and continuously decreased at least for the last five decades.