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PubMed1997

Significance of Helicobacter pylori infection as a risk factor in gastric cancer: serological and histological studies.

We conducted a case-control study to examine the association of Helicobacter pylori infection as a risk factor in gastric cancer in the Japanese population. Serum IgG antibodies for Helicobacter pylori were determined in 55 consecutive patients with gastric cancer and in 75 age- and sex-matched mass survey subjects and 57 age- and sex-matched cancer-free patients with conditions considered at a high risk for development of gastric cancer (precancerous condition). We examined the histology in all subjects and particular focus was placed on the extent of Helicobacter pylori-associated gastritis. The seroprevalence of Helicobacter pylori in gastric cancer patients (82%) and those with a precancerous condition (89%) was significantly higher (P < 0.005) than that in the mass survey subjects (60%). Positive relative risk associations were found for patients with gastric cancer (odds ratio, 3, with 95% confidence intervals of 1.69-5.33) and those with a precancerous condition (odds ratio, 5.66, with 95% confidence intervals 2.66-12.03). Significant differences were found when comparisons were made among the case-control groups who were H. pylori-positive and had inflammatory cell infiltration (P = 0.0127). The characteristics of Helicobacter pylori in histologically examined gastric mucosa showed differences between Helicobacter pylori-infected and uninfected persons in all groups. However, for none of these groups was there a significant differences between background mucosa for Helicobacter pylori-infected persons with or without gastric cancer. Helicobacter pylori seroprevalence is strongly associated with an increased risk of gastric cancer and with a precancerous condition; histological investigation did not define additional factors that might be associated with increased cancer risk.

Adult↗
PubMed1999

Acute myocardial infarction and Helicobacter pylori seropositivity.

Infectious agents including Helicobacter pylori, have been linked to coronary heart diseases on epidemiological and pathogenetic grounds. Classical risk factors fail to explain all the epidemiological variations of the disease. Our aim was to investigate the association of acute myocardial infarction with Helicobacter pylori infection in a case-control study by comparing a group of male patients with a control group of blood donors matched for sex and age. We investigated the classical cardiovascular risk factors in all patients. We studied 44 consecutive male patients, aged 40-65 years, admitted for acute myocardial infarction to the Coronary Care Unit at Novi Ligure Hospital in northern Italy. Helicobacter pylori infection was assessed by measurement of antibodies (IgG) against Helicobacter pylori in blood. Volunteer blood donors attending Molinette Hospital Blood Bank in Turin, northern Italy served as controls. Among the patients we investigated the presence of hypertension, cholesterol and glucose levels in serum, fibrinogen in plasma, smoking habits, and social class. Helicobacter pylori infection was present in 34 of 44 (77%) patients and in 183 of 310 (59%) controls (P<0.05); the odds ratio was 2.36 (95% confidence interval 1.08-5.31). Classical cardiovascular risk factors did not differ among patients with and without Helicobacter pylori infection. In conclusion, patients with acute myocardial infarction had a significantly higher prevalence of Helicobacter pylori infection than the control population. The classical risk factors for cardiovascular diseases were equally distributed among patients irrespective of their Helicobacter pylori status.

Adult↗
PubMed2005

The role of Helicobacter spp. in the pathogenesis of primary biliary cirrhosis and primary sclerosing cholangitis.

Helicobacter species DNA has been detected in liver tissue of patients affected by primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC). To investigate a potential causative relation between Helicobacter species and PBC/PSC, we compared the presence of Helicobacter species-specific DNA in liver tissue of patients with PBC/PSC (n=18/n=13) with those of a control group of patients with various liver diseases with known cause (n=29). A PCR with Helicobacter genus-specific 16S rRNA primers was performed on DNA isolated from paraffin embedded liver tissue. Control patients had hepatitis-B (n=9), alcoholic cirrhosis (n=14), or non-cirrhotic metabolic liver disease (n=6). There was no significant difference between the incidence of Helicobacter spp.-specific DNA in PBC/PSC (9/31; 29%) and the control group (10/29; 34%). Sequence analysis confirmed Helicobacter spp. DNA. Because Helicobacter spp. DNA can be found in approximately one-third of all samples tested, it is unlikely that PSC and PBC are caused by Helicobacter infection.

Adult↗
PubMed2004

Endoscopic balloon dilation for benign gastric outlet obstruction with or without Helicobacter pylori infection.

BACKGROUND: Endoscopic balloon dilation has been used to treat patients with gastric outlet obstruction caused by peptic stricture. This study assessed the role of endoscopic balloon dilation in patients with gastric outlet obstruction with or without Helicobacter pylori infection. METHODS: Consecutive patients seen between January 1996 and September 2001 with benign gastric outlet obstruction (defined as stenosis preventing the passage of a 9-mm diameter endoscope, vomiting, succussion splash, and recent weight loss) were prospectively studied. Exclusion criteria were the following: refusal to undergo dilation, and gastric outlet obstruction because of malignancy. At endoscopy, antral biopsy specimens were obtained for histopathologic evaluation and for a rapid urease test for Helicobacter pylori infection. Patients then underwent dilation with through-the-scope balloons. After balloon dilation, patients with Helicobacter pylori infection were treated to eradicate the infection. RESULTS: Fifty-one patients (33 men, 18 women; median age 65 years; IQR 44-79 years) were studied; 33 consented to endoscopic balloon dilation. Symptom resolution occurred in 25 patients (14 Helicobacter pylori positive, 11 Helicobacter pylori negative). During a median follow-up of 24 months (IQR 16-40 months), 3 of 14 patients in the Helicobacter pylori positive group and 6 of 11 in the Helicobacter pylori negative group developed further ulcer complications (p=0.039). CONCLUSIONS: After endoscopic dilation for gastric outlet obstruction, eradication of Helicobacter pylori infection is associated with fewer ulcer complications.

Adult↗
PubMed1999

Pathology, diagnosis and epidemiology of the rodent Helicobacter infection.

Since the first isolation of Helicobacter pylori from humans in 1983, 18 Helicobacter species have been identified during the last decade in domestic and laboratory animals. Several Helicobacter species have been isolated from the gastrointestinal tracts of various mammalian species and birds. Helicobacter hepaticus, H. muridarum, H. bilis, H. rodentium and Flexispira rappini have been isolated from mice. Among these species, only H. hepaticos has been clearly recognized as a pathogen. Indeed, it displays the pathogenic potential to elicit hepatitis in several strains of mice; moreover in A/JCr mice, it is strongly associated with hepatic cancer. Among the five murine helicobacter species, apart from H. hepaticus, F. rappini has not been found associated with lesions, H. muridarum has been observed in gastric glands of mice with chronic gastritis, and H. bilis has been reported in the liver of mice with chronic hepatitis. When associated with H. rodentium, H. bilis is able to induce diarrhea in SCID mice. In no case has pathogenicity of a single species been clearly proven. In rats, H. trogontum and H. muridarum have been isolated from the intestine, without any information concerning their respective pathogenicity. H. cinaedi and H. cholecystus have been identified from the intestine and the gallbladders of hamsters, respectively. The diagnosis of Helicobacter species by polymerase chain reaction (PCR) is a rapid, specific and sensitive technique. One of the most promising diagnostic techniques of these infections seems to be the PCR detection of Helicobacter sp. from feces based on the 16S rRNA sequences, then a restriction enzyme analysis to identify the actual species. Several drug regimens have also been evaluated to eradicate H. hepaticus from mice. Helicobacter infections, particularly H. hepaticus and H. bilis, seem to be widespread in laboratory mouse colonies and have also been detected from commercial breeders.

Animals↗
PubMed1998

Helicobacter pylori and upper gastrointestinal bleed in heart valve surgery.

OBJECTIVE: This study was designed to evaluate objectively the incidence of Helicobacter pylori infection and upper gastrointestinal (GI) bleeding in patients following heart valve replacement surgery. Since the discovery of Helicobacter pylori, its association with gastritis, peptic ulceration and upper GI bleed have been extensively studied. Anticoagulation of patients with mechanical heart valve prostheses is a prerequisite for the prevention of valve thrombosis and thrombo-embolic events. However anticoagulation can have its complications, notably that of upper GI bleeding. METHODS: Patients were assessed in routine postoperative outpatient clinics following cardiac valve replacement surgery. This assessment comprised initially of a questionnaire reflecting the symptomatology of upper GI bleeding and its subsequent management. With informed consent, a small sample of blood was obtained by stilette. The Helicobacter pylori status was assessed by measuring the presence of antibodies (immunoglobins) to Helicobacter pylori in a commercially available test kit, the Rapid Helisal Test. In this preliminary study 150 consecutive patients were scrutinised and their responses to the questionnaire were collected and compared with the Helisal test. RESULTS: From the 150 patients studied, 37 patients were found to be positive to the Helisal test for Helicobacter pylori infection, representing 24.6% of all the cohorts. Of these 37 patients, eight gave a positive history of upper GI bleed; five requiring hospital admission with three requiring urgent upper GI endoscopy. Although these eight patients represent only 4.4% of the total group, it is significant to note that this represents 21.6% of those patients found to be Helicobacter pylori positive. There were no GI complications in any of those tested negative. There was an increasing incidence of Helicobacter pylori infection in the older age group of patients. CONCLUSIONS: Helicobacter pylori infection is a common infection with serious consequences in heart valve surgery. For those requiring anticoagulation, the incidence of serious consequential upper GI bleed is significantly higher in the presence of this infection. Preoperative or immediate postoperative eradication of the organism is mandatory in those patients requiring indefinite anticoagulation.

Adult↗
PubMedDate not supplied

Manometric and pH-metric features in gastro-oesophageal reflux disease patients with and without Helicobacter pylori infection.

BACKGROUND: The role of Helicobacter pylori in the pathogenesis and evolution of gastro-oesophageal reflux disease is still debated. AIM: To investigate the impact of Helicobacter pylori infection on the oesophageal function and on intra-gastric and intra-oesophageal pH in patients with gastro-oesophageal reflux. METHODS: Fifty patients with non-complicated-gastro-oesophageal reflux disease classified according to Savary-Miller in: grade O, n=24; grade 1, n=19; grade 2, n=6; grade 3, n=1. Of these patients, 24 were Helicobacter pylori positive and 26 negative. Patients underwent, on two different days, stationary oesophageal manometry and 24-hour gastro-oesophageal pH-metry. RESULTS: No difference was observed between Helicobacter pylori infected and non-infected individuals with regard to lower oesophageal sphincter function, oesophageal peristalsis and gastrooesophageal reflux. These parameters were more impaired in individuals with erosive gastro-oesophageal reflux disease but this result was not dependent on the Helicobacter pylori status. Helicobacter pylori did not influence the pattern of gastric pH; however, considering only individuals with non-erosive gastro-oesophageal reflux disease, gastric pH was significantly higher in infected individuals, who, histologically, also showed a corpus predominant gastritis. CONCLUSIONS: In patients with gastro-oesophageal reflux disease, Helicobacter pylori does not affect the oesophageal motility or the gastro-oesophageal reflux. These parameters are strictly related to the severity of gastro-oesophageal reflux disease as assessed at endoscopy. In patients with non-erosive gastro-oesophageal reflux disease, a corpus predominant Helicobacter pylori gastritis could be responsible for the less severe gastro-oesophageal reflux.

Adult↗
PubMed2000

Incidence of secondary Helicobacter pylori resistance to antibiotics in treatment failures after 1-week proton pump inhibitor-based triple therapies: a prospective study.

BACKGROUND: Antibiotic-resistant Helicobacter pylori strains are becoming increasingly prevalent, although it is not clear to what extent the new resistant organisms will spread. AIM: To evaluate the incidence of secondary Helicobacter pylori resistance to metronidazole, clarithromycin and/or amoxycillin after one-week proton pump inhibitor based triple therapy failure in patients who were, before therapy infected with Helicobacter pylori strains susceptible to these antibiotics. PATIENTS AND METHODS: Enrolled in the study were 97 consecutive Helicobacter pylori-positive subjects infected by Helicobacter pylori strains susceptible to metronidazole, clarithromycin and amoxycillin. Activity of tested antibiotics was determined by means of the E-test. Patients were treated for seven days with a proton pump inhibitor, omeprazole 20 mg twice daily or pantoprazole 40 mg once daily, plus clarithromycin 250 mg twice daily and metronidazole 250 mg four times daily; or with a proton pump inhibitor plus amoxycillin 1 g twice daily and clarithromycin 500 mg twice daily. Two months after completion of therapy, endoscopy and gastric biopsies for histology, rapid urease test and culture were repeated. RESULTS: Four patients were dropped from the study Overall Helicobacter pylori cure rates expressed as both intention-to-treat and per-protocol analyses, were, respectively 80% (40/50) and 81.6% (40/49) with proton pump inhibitor, clarithromycin and metronidazole and 76.6% (36/47) and 81.8% (36/44) with proton pump inhibitor amoxycillin and clarithromycin. No significant differences were observed between the two treatments. Subjects in whom treatment failed were significantly younger and had less active ulcer than cured patients. Of treatment failures, 70.6% (12 out of 17 subjects) de veloped a secondary resistance to metronidazole (35.33% and/or clarithromycin (64.7%). Secondary antibiotic resistance occurred in 77. 8% of treatment failures treated with proton pump inhibitor, clarithromycin and metronidazole and in 62.5% of those treated with proton pump inhibitor, amoxycillin and clarithromycin. Considering all patients treated, the overall incidence of secondary metronidazole and/or clarithromycin resistance after therapy was reported in 12.9% of subjects (12 out of 93 treated patients). CONCLUSIONS: Secondary Helicobacter pylori resistances to metronidazole and/or clarithromycin occurred in large percentages in patients with treatment failure after the one-week proton pump inhibitor-based triple therapies, proton pump inhibitor, clarithromycin and metronidazole and proton pump inhibitor, amoxycillin and clarithromycin. It is likely that new antibiotics or treatment strategies will be needed in the near future to successfully treat Helicobacter pylori infection.

Adult↗
PubMed2001

Gastric permeability is not increased in children colonized by CagA-positive strains of Helicobacter pylori.

BACKGROUND: Sucrose permeability has been used as a marker to detect gastric lesions in children. As CagA status of Helicobacter pylori is an important factor in determining the evolution of the gastric lesion, CagA-positive strains being more frequently associated with severe mucosal lesions, the aim of this study was to determine the prevalence of CagA-positive strains in Helicobacter pylori-colonized children and to evaluate whether the sucrose permeability test might discriminate between colonization by CagA-positive or negative strains. PATIENTS AND METHODS: A series of 38 children (11.1+/-3.6 years) who required upper endoscopy for diagnostic purposes were included in the study. Endoscopy was carried out after the sucrose permeability test, and gastric biopsies were obtained for histologic examination, Helicobacter pylori detection by Giemsa staining and CLO-test, and determination of CagA status of the colonizing Helicobacter pylori strains by polymerase chain reaction. RESULTS: Helicobacter pylori was detected in 26 subjects (68.4%) and of these, 16 (61.5%) were colonized by CagA-positive strains. The intensity of the histologic findings was significantly associated with the presence of Helicobacter pylori and with CagA status of the infecting strains (chi2=21.2, p=0.0017). However no significant difference in the urinary excretion of sucrose between children not colonized and children with CagA- negative or positive strains was observed (0.027% [0.012-0.035%]; 0.027% [0.016-0.047%] and 0.026% [0.016-0.038], median [range], respectively; Kruskal-Wallis analysis of variance F=0.75, p=0.69). CONCLUSIONS: These results indicate that in Chile, about 60% of the Helicobacter pylori infected children are colonized by CagA-positive strains, in association with more intense lesions of the gastric mucosa, but that gastric permeability to sucrose does not discriminate between colonization by CagA-negative and positive strains of Helicobacter pylori.

Abdominal Pain↗
PubMed2002

Lower concentrations of clarithromycin suppress urease activity, motility, and binding to gastric epithelial cells in Helicobacter pylori isolates.

BACKGROUND: Our previous study showed that histological scores of gastric mucosal inflammation and Helicobacter pylori density decreased even in patients who failed to eradicate Helicobacter pylori after antimicrobial therapy including clarithromycin. This may reflect indirect suppressive effects of lower concentrations of clarithromycin on Helicobacter pylori, as suggested in other Gram-negative rod infections. AIMS: To investigate whether clarithromycin suppresses virulence factors of Helicobacter pylori at sub-minimal inhibitory concentration. METHODS: Six clarithromycin-susceptible Helicobacter pylori isolates and 7 clarithromycin-resistant isolates were obtained from patients with peptic ulcer disease. These isolates were analysed for urease activity, motility, and ability to bind to gastric epithelial cells after they were incubated with or without clarithromycin at sub-minimal inhibitory concentrations. RESULTS: Incubation of Helicobacter pylori isolates with clarithromycin at sub-minimal inhibitory concentrations reduced urease activity motility, and binding to gastric epithelial cells in a dose-dependent manner. These findings were observed both in clarithromycin-susceptible and resistant strains. CONCLUSIONS: Suppressive effects of clerithromycin on virulence factors of Helicobacter pylori at sub-minimal inhibitory concentrations may be associated with observed attenuation of gastric inflammation and Helicobacter pylori density in patients who failed in bacterial eradication after triple therapy including clarithromycin.

Anti-Bacterial Agents↗
PubMed1997

Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis.

In a prospective study of consecutive patients with reflux esophagitis and/or hiatal hernia and Barrett's esophagus, the prevalence of Helicobacter pylori was assessed. Antral biopsy specimens were studied and a serum sample for detection of IgG antibodies against Helicobacter pylori was taken. As a reference group patients presenting with a normal esophagus, stomach, and duodenum were taken. Reflux esophagitis was diagnosed in 118 patients, hiatal hernia without esophageal inflammation in 109, and Barrett's esophagus in 13. Helicobacter pylori was present in 74 (30%) of these patients and in 204 (51%) of the reference group. Prevalence of Helicobacter pylori was significantly lower in all groups compared with the reference group (P < 0.001). There was no difference when patients with esophagitis, Barrett's esophagus, or hiatal hernia were compared. Patients with esophagitis and Helicobacter pylori in their antrum are significantly older than esophagitis patients without concomitant Helicobacter infection, 61.5 (SD, 17) versus 53 (SD, 17) years (P < 0.001). It is concluded that the prevalence of Helicobacter pylori infection in patients with gastroesophageal reflux disease is significantly lower than in the reference group, irrespective of the severity of esophagitis. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis.

Antibodies, Bacterial↗
PubMed1997

High prevalence of Helicobacter pylori in liver cirrhosis: relationship with clinical and endoscopic features and the risk of peptic ulcer.

In 153 consecutive patients with cirrhosis we assessed: (1) the prevalence of IgG to Helicobacter pylori and compared it with that found in 1010 blood donors resident in the same area; and (2) the relationships of IgG to Helicobacter pylori with clinical and endoscopic features and with the risk of peptic ulcer. The IgG to Helicobacter pylori prevalence of cirrhotics was significantly higher than in blood donors (76.5% vs 41.8%; P < 0.0005) and was not associated with sex, cirrhosis etiology, Child class, gammaglobulins and hypertensive gastropathy. In both groups, the prevalence of IgG to Helicobacter pylori was significantly higher in subjects over 40. Among patients with cirrhosis a significantly higher prevalence of Helicobacter pylori was found in patients with previous hospital admission (P = 0.02) and/or upper gastrointestinal endoscopy (P = 0.01) and patients with peptic ulcer (P = 0.0004). Multivariate analysis identified increasing age and male sex as risk factors for a positive Helicobacter pylori serology and no independent risk factors for peptic ulcer. The high prevalence of Helicobacter pylori-positive serology found in the present series is related to age and sex and might also be explained by previous hospital admissions and/or upper gastrointestinal endoscopy. Our results do not confirm the role of Helicobacter pylori as risk factor for peptic ulcer in patients with liver cirrhosis.

Adult↗
PubMed2001

Involvement of the corporal mucosa and related changes in gastric acid secretion characterize patients with iron deficiency anaemia associated with Helicobacter pylori infection.

BACKGROUND: Recent studies have reported an association between iron deficiency anaemia and Helicobacter pylori. Helicobacter pylori could cause iron deficiency anaemia by altering iron absorption. We observed that most patients with Helicobacter pylori infection and iron deficiency anaemia present a chronic superficial pangastritis. AIM: To investigate whether Helicobacter pylori-positive patients with iron deficiency anaemia have peculiar histological and functional features when compared with non-anaemic Helicobacter pylori-positive subjects. PATIENTS: Fifty-one patients with iron deficiency anaemia, in whom chronic superficial Helicobacter pylori gastritis was the only gastrointestinal finding, and 103 non-anaemic Helicobacter pylori-positive controls were included in the study. Thirty-seven patients were randomly matched with 37 controls of the same sex and age. METHODS: Gastroscopy, with antral (n=3) and body (n=3) biopsies, was performed. Gastrin and pepsinogen I levels and antiparietal cell antibodies were evaluated. Intragastric pH was also measured. RESULTS: Gastritis involved the corporal mucosa in 90% of patients compared to 42.7% of controls (P < 0.0001). The mean inflammatory score in the gastric body was significantly higher among patients than in controls (2.2 vs. 0.6; P=0.012). Gastrin was significantly higher in patients than in controls (mean 60.2 vs. 29 pg/mL; P=0.0069). Intragastric pH was higher in patients than in controls (median 5.7 vs. 2; P=0.0026). CONCLUSIONS: These data suggest that patients with iron deficiency anaemia and Helicobacter pylori infection have a peculiar pattern of gastritis with corporal involvement and related changes in intragastric pH.

Adolescent↗
PubMed2003

Does N-acetyl cystein affect the sensitivity and specificity of Helicobacter pylori stool antigen test?

BACKGROUND: N-acetyl cystein, a mucolytic agent, might make Helicobacter pylori antigens shed more easily to stool, and might therefore contribute to the diagnostic accuracy of the Helicobacter pylori stool antigen test. The aim of this study is to investigate if N-acetyl cystein contributes to the diagnostic accuracy of the Helicobacter pylori stool antigen test by increasing the sensitivity and specificity of the test. MATERIALS AND METHODS: 107 patients were separated into treatment and placebo groups. The AC group (n = 53) was given 5 ml of acetyl cystein (4%) t.i.d. and the Placebo group (n = 54) was given placebo, for 3 days. Helicobacter pylori status was determined by both histology and CLOtest. Stool samples were assayed using a specific ELISA kit for Helicobacter pylori stool antigen. RESULTS: The sensitivity, specificity, positive predictive value, negative predictive value and diagnostic accuracy of Helicobacter pylori stool antigen test were 76%, 79%, 90%, 55%, and 77%, respectively, in AC group; and 85%, 89%, 93%, 76% and 86%, respectively, in placebo group. CONCLUSIONS: N-acetyl cystein did not increase, and actually decreased, the sensitivity and specificity of the Helicobacter pylori stool antigen test according to our results. We believe that this finding can be taken into consideration when setting up the exclusion criteria for future studies, which will use Helicobacter pylori stool antigen tests.

Acetylcysteine↗
PubMed2005

Diagnosing Helicobacter pylori in vivo by confocal laser endoscopy.

BACKGROUND & AIMS: Confocal laser endomicroscopy enables subsurface microscopic imaging of living tissue during ongoing endoscopy. This case report describes the in vivo detection of Helicobacter pylori by endomicroscopy. METHODS: Endomicroscopy (Pentax, Tokyo, EC-3870CIFK) was performed by using two different contrast stains: Topical Acriflavine in addition to intravenously applied fluorescein netted the surface and allowed identification of focal accumulation of Helicobacter pylori at the surface and in deeper layer of the gastric epithelium. Biopsies were performed at the antrum and corpus for urease testing and histology. In addition, biopsies were cultured for Helicobacter pylori. Cultured bacteria were re-assessed ex vivo using confocal microscopy with and without acriflavine staining. RESULTS: Helicobacter pylori infection could be detected in a 70-year-old male by endomicroscopy. Accumulated, as well as single bacteria, could be observed and the distinct shape and flagella of Helicobacter pylori could be identified. Helicobacter pylori infection was proved by histology. Furthermore, ex vivo examination of cultures proved the presence of Helicobacter pylori and the active uptake of acriflavine into the bacteria. CONCLUSIONS: Endomicroscopy is a new diagnostic approach, which enables the immediate diagnosis of Helicobacter pylori in vivo during standard video endoscopy.

Acriflavine↗
PubMed2006

Faecal antigen tests in the confirmation of the effect of Helicobacter eradication therapy.

BACKGROUND: The frequent occurrence of Helicobacter pylori infection requires significant health care resources after eradication therapy. Therefore the non-invasive testing methods are required to alleviate the increased work-load of health care personnel and to allow an easy control of eradication therapy. Conventionally, the effect of eradication therapy has been confirmed with 13C-urea breath test 4-6 weeks after a completed eradication. AIM: To assess the applicability of Helicobacter pylori stool antigen tests as alternatives to the breath test in the control of the effect of eradication therapy. METHODS: Fifty patients were diagnosed Helicobacter-positive by endoscopy and histology as well as by rapid urease test from mucosal specimen. Four weeks after an eradication therapy the patients were subjected to 13C-urea breath test as well as to faecal Helicobacter pylori antigen tests with mono- and polyclonal primary antibodies. RESULTS: The monoclonal and polyclonal stool tests had 94% and 88% sensitivity, and 100% and 97% specificity, respectively, in the detection of Helicobacter pylori infection as compared to the 13C-urea breath test. The non-invasive test results were completely parallel in patients with various grades of mucosal atrophy or intestinal metaplasia. CONCLUSIONS: Monoclonal faecal Helicobacter pylori antigen test is slightly superior to the polyclonal test regarding the sensitivity in the detection of stool Helicobacter antigens. Due to their sufficient sensitivity and specificity, and to their practicability and cost-effectiveness, they can be recommended for non-invasive testing of Helicobacter pylori infection as alternatives to the 13C-urea breath test.

Antibodies, Bacterial↗
PubMed2006

Helicobacter cynogastricus sp. nov., isolated from the canine gastric mucosa.

A Gram-negative, microaerophilic helical rod, isolated from the gastric mucosa of a dog and designated strain JKM4(T), was subjected to a polyphasic taxonomic study. The tightly coiled organism, measuring 10-18 mum long and up to 1 mum wide, was motile by means of multiple sheathed flagella located at both ends of the cell and by a periplasmic fibril running along the external side of the helix. Strain JKM4(T) grew preferably on biphasic culture plates or on very moist agar. Coccoid forms predominated in cultures older than 4 days as well as in growth obtained on dry agar plates. The strain grew at 30 and 37 degrees C, but not at 25 or 42 degrees C and exhibited urease, oxidase and catalase activities. On the basis of 16S rRNA gene sequence analysis, the novel isolate was identified as a member of the genus Helicobacter and showed > 97 % similarity to Helicobacter felis, Helicobacter bizzozeronii and Helicobacter salomonis, three species previously isolated from the canine gastric mucosa. Protein profiling of strain JKM4(T) using SDS-PAGE revealed a pattern different from those of other Helicobacter species of mammalian gastric origin and from Helicobacter canis. Additionally, the urease gene sequence of strain JKM4(T) was different from those of urease genes of H. felis, H. bizzozeronii, H. salomonis and "Candidatus Helicobacter heilmannii". It is thus proposed that strain JKM4(T) (=LMG 23188(T)) represents a novel species within this genus, Helicobacter cynogastricus sp. nov.

Animals↗
PubMed2005

Multiple displacement amplification of isolated DNA from human gallstones: molecular identification of Helicobacter DNA by means of 16S rDNA-based pyrosequencing analysis.

BACKGROUND: Molecular typing of Helicobacter spp. in clinical biopsy specimens has become increasingly important. By means of nested polymerase chain reaction (PCR) amplification and Southern blot analysis of the PCR amplicons, we have shown that Helicobacter spp. DNA is present in human gallstones. In this study we have investigated the possibility of using multiple displacement amplification (MDA) of isolated gallstone DNA and pyrosequencing analysis for the molecular identification of Helicobacter spp. MATERIALS AND METHODS: DNA isolated from the nucleus of 33 human gallstones and one control strain were used in a MDA assay. Subsequently, pyrosequencing analysis was performed either directly on MDA-DNA using primers flanking the Helicobacter spp. 16S rDNA variable V3 region or on PCR amplicons derived from broad-range primers flanking the 16S rDNA variable V3, V4, and V9 regions. RESULTS: Pyrosequencing analysis of 16S rDNA derived from MDA-DNA revealed that Helicobacter spp.-like DNA was present in 25 of 33 (approximately 76%) gallstones. Using an H. pylori-specific Southern blot analysis, Helicobacter spp.-like DNA was present in 20 of 33 [approximately 61%] of the gallstones. Using MDA-DNA directly in pyrosequencing analysis, Helicobacter spp.-like DNA was present in 13 of 33 [approximately 39%] gallstones. CONCLUSIONS: We conclude that multiple displacement amplification combined with pyrosequencing enables a rapid and accurate molecular typing of Helicobacter spp. from small and precious biopsy specimens.

Adult↗