IgG ELISA antibodies and detection of Helicobacter pylori in elderly patients. Italian Helicobacter pylori Study Group.
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Adolescent↗
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Common presence of Helicobacter DNA in the gallbladder of patients with gallstone diseases and controls.
BACKGROUND: Several species of Helicobacter colonise the biliary tract of animals and cause hepatobiliary diseases. Helicobacter species have also been identified in the gallbladder of a high proportion of Chilean patients with gallbladder cancer. AIM: To determine the presence of Helicobacter species, particularly Helicobacter pylori and Helicobacter bilis, in the gallbladder of patients with non-malignant gallbladder diseases and control patients. PATIENTS AND METHODS: DNA was extracted from gallbladder samples from 122 consecutive patients undergoing cholecystectomy. The presence of Helicobacter genus-specific or Helicobacter pylori and Helicobacter bilis species-specific DNA was determined by polymerase chain reaction and sequence analysis. The presence of Helicobacter pylori-specific immunoglobulin G in the serum (n=84) and bile (n=104) samples was determined by enzyme linked immunosorbent assay. RESULTS: Helicobacter DNA was detected in 61 (50.0%) gallbladder samples: 29 of 60 (48.3%) patients with symptomatic gallstone, six of 10 (60.0%) patients with asymptomatic gallstones, 11 of 15 (73.3%) patients with other biliary diseases, and 15 of 37 (40.5%) control patients, respectively. Among them, 39 samples were positive for Helicobacter pylori but none were positive for Helicobacter bilis. Sequence analysis of Helicobacter genus-positive samples showed that 56 samples were Helicobacter pylori and five were Helicobacter species 'Liver 3' strain. Overall, there was no significant difference in the detection rate of Helicobacter DNA or the levels of serum and bile Helicobacter pylori-specific immunoglobulin G in the various biliary disease groups compared with control patients. Neither was there any significant difference in the blood biochemistry and liver function tests between patients with positive and negative Helicobacter DNA detection. CONCLUSION: Helicobacter species' DNA are commonly present in the gallbladder of patients with gallstone diseases and in controls, implying that Helicobacter infection alone may not play a significant role in the formation of gallstones. However, our results do not exclude the possibility of Helicobacter infection as a cofactor in the development of gallstones.
Antibodies, Bacterial↗
Histological and immunohistochemical detection of different Helicobacter species in the gastric mucosa of cats.
Detailed histopathological evaluation of the gastric mucosa of Helicobacter-infected cats is complicated by the difficulty of recognizing Helicobacter organisms on hematoxylin and eosin (HE)-stained sections and the ability of multiple Helicobacter species to infect cats. In this study, the presence and localization of different species of Helicobacter in the stomachs of cats was investigated using silver staining and immunohistochemistry. Five groups containing 5 cats each were established (group 1: urease negative and Helicobacter free; groups 2, 3, 4, and 5: urease positive and infected with Helicobacter heilmannii, unclassified Helicobacter spp., Helicobacter felis, and Helicobacter pylori, respectively). Gastric samples were evaluated by HE and silver staining and by immunohistochemistry with 3 different anti-Helicobacter primary antibodies. Helicobacter were detected by Steiner stain in all infected cats at the mucosal surface, in the lumen of gastric glands, and in the cytoplasm of parietal cells. In silver-stained sections, H. pylori was easily differentiated from H. felis, H. heilmannii, and unclassified Helicobacter spp., which were larger and more tightly coiled. No organisms were seen in uninfected cats. Helicobacter antigen paralleled the distribution of organisms observed in Steiner-stained sections for 2 of the 3 primary antibodies tested. The antisera were not able to discriminate between the different Helicobacter species examined. A small amount of Helicobacter antigen was present in the lamina propria of 3 H. pylori-, 3 H. felis-, and 1 H. heilmannii-infected cat. Minimal mononuclear inflammation was present in uninfected cats and in those infected with unclassified Helicobacter spp. and H. heilmannii cats. In H. felis-infected cats, lymphoid follicular hyperplasia with mild pangastric mononuclear inflammation and eosinophilic infiltrates were present. The H. pylori-infected cats had severe lymphoid follicular hyperplasia and mild to moderate mononuclear inflammation accompanied by the presence of neutrophils and eosinophils. These findings indicate that Steiner staining and immunohistochemistry are useful for detecting Helicobacter infections, particularly when different Helicobacter species can be present. Monoclonal antibodies specific for the different Helicobacter species could be important diagnostic aids. There appear to be differences in the severity of gastritis in cats infected with different Helicobacter species.
Animals↗
Association of Helicobacter with cholangiohepatitis in cats.
Infection with Helicobacter spp. is increasingly linked with hepatobiliary inflammation and neoplasia in people and in a variety of animals. We sought to determine if Helicobacter species infection is associated with cholangiohepatitis in cats. Deoxyribonucleic acid was extracted from tissue blocks from cats with cholangiohepatitis (32), noninflammatory liver disease (13), and cats with normal liver histology (4). Deoxyribonucleic acid was polymerase chain reaction-amplified with 2 sets of Helicobacter genus-specific primers, gel purified, and sequenced. Polymerase chain reaction-positive hepatic tissue was further examined with Steiner's stain, immunocytochemistry for Helicobacter species, and eubacterial fluorescent in situ hybridization. Gastric tissues of cats with known Helicobacter infection status served as controls for deoxyribonucleic acid extraction and sequence comparison. Helicobacter species were detected in 2/32 cats with cholangiohepatitis, and 1/17 controls. Sequences had 100% identity with Helicobacter species liver, Helicobacter pylori, and Helicobacter fenelliae/cinaedii in a cat with suppurative cholangitis, Helicobacter species liver, Helicobacter pylori, and Helicobacter nemistrineae in a cat with mild lymphocytic portal hepatitis, and Helicobacter bilis in a cat with portosystemic vascular anomaly. In contrast, sequences from gastric biopsies showed highest homology (99-100%) to "Helicobacter heilmannii," Helicobacter bizzozeronii, Helicobacter felis, and Helicobacter salomonis. Fluorescent in situ hybridization revealed a semicurved bacterium, with Helicobacter-like morphology, in an intrahepatic bile duct of the cat with suppurative cholangitis. This study has identified Helicobacter deoxyribonucleic acid in 2/32 cats with cholangiohepatitis and 1/13 cats with noninflammatory liver disease. Deoxyribonucleic acid sequences of hepatic Helicobacter species were distinct from those found in the stomach and are broadly consistent with those identified in cat intestine and bile, and hepatobiliary disease in people and rodents.
Animals↗
Comparative chemical and biological characterization of the lipopolysaccharides of gastric and enterohepatic helicobacters.
BACKGROUND: The lipopolysaccharide of Helicobacter pylori plays an important role in colonization and pathogenicity. The present study sought to compare structural and biological features of lipopolysaccharides from gastric and enterohepatic Helicobacter spp. not previously characterized. MATERIALS AND METHODS: Purified lipopolysaccharides from four gastric Helicobacter spp. (H. pylori, Helicobacter felis, Helicobacter bizzozeronii and Helicobacter mustelae) and four enterohepatic Helicobacter spp. (Helicobacter hepaticus, Helicobacter bilis, 'Helicobacter sp. flexispira' and Helicobacter pullorum) were structurally characterized using electrophoretic, serological and chemical methods. RESULTS: Structural insights into all three moieties of the lipopolysaccharides, i.e. lipid A, core and O-polysaccharide chains, were gained. All species expressed lipopolysaccharides bearing an O-polysaccharide chain, but H. mustelae and H. hepaticus produced truncated semirough lipopolysaccharides. However, in contrast to lipopolysaccharides of H. pylori and H. mustelae, no blood group mimicry was detected in the other Helicobacter spp. examined. Intra-species, but not interspecies, fatty acid profiles of lipopolysaccharides were identical within the genus. Although shared lipopolysaccharide-core epitopes with H. pylori occurred, differing structural characteristics were noted in this lipopolysaccharide region of some Helicobacter spp. The lipopolysaccharides of the gastric helicobacters, H. bizzozeronii and H. mustelae, had relative Limulus amoebocyte lysate activities which clustered around that of H. pylori lipopolysaccharide, whereas H. bilis, 'Helicobacter sp. flexispira' and H. hepaticus formed a cluster with approximately 1000-10,000-fold lower activities. H. pullorum lipopolysaccharide had the highest relative Limulus amoebocyte lysate activity of all the helicobacter lipopolysaccharides (10-fold higher than that of H. pylori lipopolysaccharide), and all the lipopolysaccharides of enterohepatic Helicobacter spp. were capable of inducing nuclear factor-Kappa B(NF-kappaB) activation. CONCLUSIONS: The collective results demonstrate the structural heterogeneity and pathogenic potential of lipopolysaccharides of the Helicobacter genus as a group and these differences in lipopolysaccharides may be indicative of adaptation of the bacteria to different ecological niches.
Antibodies, Bacterial↗
Role of Helicobacter pylori infection in pernicious anaemia.
BACKGROUND: Pernicious anaemia is associated with atrophic body gastritis and considered an autoimmune disease. Whether Helicobacter pylori is involved in the induction of pernicious anaemia is uncertain. AIMS: To investigate the prevalence of Helicobacter pylori infection in pernicious anaemia patients and to ascertain whether the Helicobacter pylori-positive patients had distinctive clinical and gastric morphofunctional characteristics. PATIENTS AND METHODS: A series of 81 consecutive pernicious anaemia patients underwent serological, functional and endoscopic/histological investigations. RESULTS: A total of 49 (60.5%) patients were Helicobacter pylori-positive (males 61.2% vs females 38.8%). No difference was observed in clinical and morphofunctional characteristics between Helicobacter pylori-positive and negative patients, whereas distinctive functional/histological features between histologically Helicobacter pylori-positive (n=8) and serologically Helicobacter pylori-positive (n=41) cases were detected. In the histologically Helicobacter pylori-positive group, Pepsinogen I was higher [13 (058) vs 5 (0-26) ng/ml; p=0.0025)] and positivity for anti-parietal cell antibodies was lower [42.9% vs 76.9, p=0.0867]. Antral histological variables of the gastritis score were significantly higher in the histologically Helicobacter pylori-positive than in the serologically Helicobacter pylori-positive patients, but this latter group had a higher score of body atrophy (2.63+/-0.12 vs 1.71+/-0.29; p=0.0051). Body inflammation was also significantly higher in the histologically Helicobacter pylori-positive group (chronic inflammation: 1.43+/-0.2 vs 1.05+/-0.06; p=0.0271; inflammation acitivity: 0. 57+/-0.3 vs 0.15+/-0.06, p=0.0220). Antral mucosa was normal in 24/41 (58.5%) of the serologically Helicobacter pylori-positive patients, but only in 1/8 (12.5%) of the histologically Helicobacter pylori-positive patients (p=0.0232). CONCLUSIONS: Almost two thirds of pernicious anaemia patients have evidence of Helicobacter pylori, but only those with an active Helicobacter pylori infection have distinctive functional and histological features. These findings support the hypothesis that Helicobacter pylori infection could play a triggering role in a subgroup of pernicious anaemia patients.
Adult↗
Prevalence of Helicobacter pylori infection in coronary artery disease and effect of its eradication on coronary lumen reduction after percutaneous coronary angioplasty.
BACKGROUND: Gastric infection caused by Helicobacter pylori has recently been associated with increased risk of coronary artery disease. AIM: To: 1) determine seroprevalence of Helicobacter pylori and its cytotoxin associated gene A in patients with/without coronary artery disease (group A), 2) assess influence of Helicobacter pylori eradication on coronary artery lumen reduction after percutaneous coronary angioplasty (group B) and 3) determine influence of Helicobacter pylori eradication on plasma cytokines, lipids and coagulation factors in patients subjected to percutaneous coronary angioplasty (group B). PATIENTS AND METHODS: Group A included 100 patients with coronary artery disease (subgroup 1) and 100 patients without (subgroup II). For Helicobacter pylori seroprevalence, plasma anti-Helicobacter pylori and anti-cytotoxin associated gene A IgG were examined. Group B included 40 patients with significant single-vessel coronary arterial disease and Helicobacter pylori infection confirmed by 13C-urea breath test and serologically using anti-Helicobacter pylori and anti-cytotoxin associated gene A IgG. Six months after percutaneous coronary angioplasty and triple anti-Helicobacter pylori therapy, the Helicobacter pylori status reassessed by urea breath test was negative in all but two patients of subgroup I subjected to Helicobacter pylori therapy. Coronary angiography and laboratory tests were repeated in both subgroups of group B included in the trial and reduction in coronary artery lumen in these subgroups was compared to baseline after percutaneous coronary angioplasty considered as 100%. RESULTS: Helicobacter pylori seropositivity reached 81.5% of coronary artery disease (subgroup I) and was significantly higher than that in controls without coronary artery disease (subgroup II) (51%), the odds ratio being 4.3 for Helicobacter pylori in coronary artery disease. Cytotoxin associated gene A IgG detection was also significantly higher (47.3%) in coronary artery disease than in controls (28%) giving the odds ratio about 2.3. Mean coronary artery lumen reduction in patients undergoing percutaneous coronary angioplasty + Helicobacter pylori eradication therapy (subgroup I) was significantly (p<0.05) smaller compared to percutaneous coronary angioplasty + placebo-treated subgroup II (22% vs 41%). CONCLUSIONS: 1) There is a significant link between coronary artery disease and infection with Helicobacter pylori, especially expressing CagA proteins, 2) Helicobacter pylori eradication significantly attenuates reduction in coronary artery lumen in coronary artery disease patients after percutaneous coronary angioplasty possibly by elimination of chronic inflammation and decline in proinflammatory cytokine release, and 3) Infection of Chlamydia pneumoniae in these percutaneous coronary angioplasty patients is not affected by eradication therapy.
Adult↗
Helicobacter infection in hepatocellular carcinoma tissue.
AIM: To investigate whether Helicobacter species (Helicobacter spp.) could be detected in hepatocellular carcinoma (HCC) tissue. METHODS: Liver samples from 28 patients with hepatocellular carcinoma (HCC) diagnosed by histopathology were studied. Twenty-two patients with other liver diseases (5 with liver trauma, 7 with cavernous liver hemangioma, 6 with liver cyst and 4 with hepatolithiasis), 25 patients with gastric cancer, 15 with colonic cancer and 15 with myoma of uterus served as controls. Two pieces of biopsy were obtained from each patient. One was cultured for Helicobacter spp. and extraction of DNA, the other was prepared for scanning electron microscopy (SEM) and in situ hybridization. The samples were cultured on Columbia agar plates with microaerobic techniques. Helicobacter spp. in biopsy from the studied subjects was detected by polymerase chain reaction (PCR) with Helicobacter spp. 16S rRNA primers. Amplified products were identified by Southern hybridization and sequenced further. Besides, other genes (vacA, cagA) specific for Helicobacter pylori (H pylori) were also detected by PCR. Helicobacter spp. in biopsies was observed by SEM. Transmission electron microscopy (TEM) was performed to identify the cultured positive Helicobacter spp. The presence of Helicobacter spp. was detected by in situ hybridization to confirm the type of Helicobacter. RESULTS: The positive rate of Helicobacter cultured in HCC and gastric cancer tissue was 10.7% (3/28) and 24% (6/25), respectively. Helicobacter microorganisms were identified further by typical appearance on Gram staining, positive urease test and characteristic colony morphology on TEM. The bacterium was observed in adjacent hepatocytes of the two HCC samples by SEM. The number of cocci was greater than that of bacilli. The bacterium was also found in four gastric cancer samples. PCR showed that the positive rate of HCC and gastric cancer samples was 60.7% and 72% respectively, while the controls were negative (P<0.01). The PCR-amplified products were identified by Southern hybridization and sequenced. The homology to 16S rRNA of H pylori was 97.80%. The samples were verified by in situ hybridization for Helicobacter spp. 16S rRNA-mRNA and proved to be H pylori positive. There was no statistical significance between HCC and gastric cancer (P>0.05), but the positive rate of HCC and controls had statistical significance (P<0.01). Only 3 HCC samples and 2 gastric cancer samples of the cagA genes were detected. None of the samples reacted with primers for vacA in the two groups. As for the genotype of H pylori, type II had preference over type I. CONCLUSION: Helicobacter infection exists in liver tissues of HCC patients. Helicobacter spp. infection is related with HCC, which needs further research.
Base Sequence↗
Influence of Helicobacter pylori infection on severity of oesophagitis and response to therapy in the elderly.
BACKGROUND: The prevalence both of Helicobacter pylori infection and oesophagitis is higher in the elderly, than in adult and young populations. However the relationship between Helicobacter pylori infection and the clinical behaviour of oesophagitis has not yet been clarified. AIM: To evaluate the influence of Helicobacter pylori infection on the severity and clinical outcome after treatment of oesophagitis in elderly patients. METHODS: A total of 271 elderly patients (134 male, 137 female, mean age = 79.2 years, range 65-96) with grade 1 to 3 oesophagitis were studied. At baseline, the patients were divided into 3 groups according to Helicobacter pylori infection: Group 1 = 88 Helicobacter pylori-negative patients; Group 2 = 59 Helicobacter pylori-positive patients and Group 3 = 124 Helicobacter pylori-positive patients who underwent a one-week proton pump inhibitor-based triple therapy for the eradication of Helicobacter pylori infection. All patients were treated with proton pump inhibitors for two months; patients in Group 3 were also treated for one week with proton pump inhibitors plus two antibiotics. After two months, endoscopy and histology were repeated. RESULTS: At baseline, 32.5% of patients were Helicobacter pylori-negative and 67.5% were Helicobacter pylori-positive. No baseline differences in severity of oesophagitis were found between Helicobacter pylori negative and positive patients. After proton pump inhibitor therapy, the complete resolution of oesophagitis was observed in 80.7% of Group 1, 76.3% of Group 2 and 75.8% of Group 3 (p=ns). Dividing patients also according to the severity of oesophagitis, no difference in healing rates between the three Groups were observed. CONCLUSIONS: In this elderly population, Helicobacter pylori infection did not influence the severity of oesophagitis at baseline or the response to short-term treatment with proton pump inhibitors. Furthermore, Helicobacter pylori eradication therapy did not influence the healing rate of oesophagitis.
Aged↗
Evidence against colonic mucosa colonisation by Helicobacter pylori. Lack of a specific antibody response in homogenates of rectal endoscopic biopsies.
Aim of this study is to provide indirect evidence that human colonic mucosa harbour Helicobacter pylori. The antibody response of IgG and IgA class against Helicobacter pylori was examined in autologous homogenate of gastric and rectal endoscopic biopsies from 26 patients and in rectal samples of a further 36. All had a documented (histology and/or serology) Helicobacter pylori status. Helicobacter pylori specific IgG and IgA were measured by an in-house ELISA. In Helicobacter pylori positive patients having both gastric and rectal homogenate, mean level of Helicobacter pylori IgG and IgA was higher in gastric than in rectal samples (0.810 +/- 0.668 optical density vs 0.329 +/- 0.509 optical density for IgG, p = 0.007 and 0.660 +/- 0.477 vs 0.116 +/- 0.229 for IgA, p < 0.001, respectively). In each patient, level of the two isotypes was clearly higher in gastric than in autologous rectal sample. In the overall study population, mean level of Helicobacter pylori IgG in rectal homogenate was not significantly (p = 0.16) different between Helicobacter pylori positive (48/62, 77%, 0.243 +/- 0.388 optical density) and negative (14/62, 23%; 0.095 +/- 0.088) patients. In same material, levels of Helicobacter pylori IgA were very low and undetectable either in Helicobacter pylori positive or negative patients. Although Helicobacter pylori IgG are detectable in rectal homogenates of Helicobacter pylori positive patients, present data suggest that these antibodies may not be local in origin but rather reflect circulating response. These observations do not support the view that large bowel mucosa is colonised by Helicobacter pylori.
Adult↗
Identification of murine helicobacters by PCR and restriction enzyme analyses.
Three murine helicobacter species have recently been identified: Helicobacter hepaticus, Helicobacter muridarum, and Helicobacter bilis. Infections with H. hepaticus and H. bilis have been associated with hepatitis and hepatic neoplasia. In this study, oligonucleotide primers were designed from regions of the 16S rRNA gene that are conserved among members of the Helicobacter genus. The assay amplified the expected 374-bp product from all three rodent Helicobacter species and was able to detect as little as 5 pg of H. hepaticus, H. bilis, or H. muridarum DNA. The specificity of the reaction was determined by testing cecal DNA from uninfected mice and mice with documented Helicobacter infections and by testing DNA from other bacterial genera. A product of the expected size was generated with cecal DNA from Helicobacter-infected mice but not with DNA from uninfected mice. With the exception of that of "Flexispira rappini, " which is closely related to the Helicobacter genus, DNA from other bacterial genera was not amplified with the Helicobacter genus-specific primers. MboI, MaeI, and HhaI restriction enzyme analyses of the amplified product were able to differentiate among the murine Helicobacter species but could not differentiate H. bilis from "F. rappini." To distinguish H. bilis, a reverse primer based on H. bilis 16S rRNA sequence was designed. PCR with the H. bilis-specific reverse primer (Hbr) and the Helicobacter genus-specific forward primer (H276f) amplified H. bilis DNA but not DNA from "F. rappini" or other rodent helicobacters. Examination of a large number of murine cecal tissues with this combination of PCR assays and restriction enzyme analyses indicated that H. hepaticus and H. bilis infections are widespread in laboratory mouse and rat colonies.
Animals↗
Evaluation of immunological rapid urease testing for detection of Helicobacter pylori.
The aim of this study was to evaluate in clinical specimens the immunological rapid urease test (IRUT), a new diagnostic system for detection of Helicobacter pylori which employs a monoclonal antibody against Helicobacter pylori urease. Helicobacter pylori urease adsorbed on a solid-phase tip coated with a monoclonal antibody against Helicobacter pylori urease after 15 min of incubation with a gastric mucus sample solution was measured by the pH change of the urea solution inside the tip. The detection limit of Helicobacter pylori urease using this system was determined and compared with that of a commercially available rapid urease test. Clinical evaluation of the system was performed in 155 patients. The IRUT could detect 0.25 milli-international units (mIU) of Helicobacter pylori urease per milliliter in less than 20 min. If a patient with at least one positive result in a standard test for Helicobacter pylori was considered to be Helicobacter pylori positive, the sensitivity, specificity, positive and negative predictive values of the system were calculated as 95.2%, 98.9%, 98.4% and 96.8%, respectively. However, 10 of 19 Helicobacter pylori-positive patients in whom the pH change was less than 0.1 had negative results in at least one of the standard tests, whereas the IRUT correctly detected Helicobacter pylori in all but 3 of these 19 patients. The IRUT accurately determined the Helicobacter pylori status of 75 (98.7%) of 76 patients who had completed treatment. This system has high sensitivity for the detection of Helicobacter pylori, especially in patients with low urease activity.
Adult↗
Effect of Helicobacter pylori infection on gastric cell proliferation and genomic instability in a paediatric population of southern Italy.
BACKGROUND: The incidence of gastric cancer is high in areas with a high prevalence of Helicobacter pylori infection. Cell transformation and tumour progression occur over a long period of time and markers of genomic instability usually precede morphological changes. AIM: To evaluate the effect of Helicobacter pylori infection on cell proliferation, DNA status and oncogene expression in children. PATIENTS AND METHODS: Morphometric and immunohistochemical techniques were used to analyse DNA content, p53 and c-myc oncogene expression and cell proliferation on gastric biopsies of 53 children (27 Helicobacter pylori-negative and 26 Helicobacter pylori-positive). RESULTS: Gastric mucosa was normal in 11% of Helicobacter pylori-positive and in 33% of Helicobacter pylori-negative subjects. Most children had chronic non-atrophic gastritis regardless of Helicobacter pylori infection, and only a minority of children affected by Helicobacter pylori had mild atrophic gastritis. Cell proliferation was significantly higher in children with Helicobacter pylori-positive gastritis than in those with Helicobacter pylori-negative gastritis. No metaplasia, dysplasia, p53 overexpression or altered DNA content was found in any child. Interestingly, 46% of children with and 29% without Helicobacter pylori infection had c-myc overexpression closely related to the cell proliferation rate. CONCLUSION: Helicobacter pylori infection in children may coexist with a normal gastric mucosa, and it is not associated with genomic instability markers in cases of chronic gastritis.
Adolescent↗
Chinese tea consumption and lower risk of Helicobacter infection.
BACKGROUND: Our first study had shown that Chinese tea has anti-Helicobacter activity. The present study investigated the relationship between patients'Helicobacter status and the history of Chinese tea consumption. METHODS: Chinese patients who had their first upper endoscopy were recruited. Before the procedure, patients completed questionnaires about their current Chinese tea consumption habits and those when they were around 10-25 years old. This information was used to calculate the tea consumption indices (TCI). Gastric biopsies (two from the antrum and two from the corpus) were taken for histological examination for Helicobacter. RESULTS: Eighty patients were recruited. Eight patients were rejected because of either an incomplete questionnaire, absence of gastric biopsy or a suspected history of treatment for Helicobacter infection. Of the 72 patients, 42 (58.3%) were Helicobacter positive. The age, sex ratio and indications for endoscopy were similar in both Helicobacter-positive and -negative groups. Classifying patients using either current, past or total TCI, patients with high tea consumption had significantly lower Helicobacter infection rate than those with low tea consumption (45% compared to 74%, 42% compared to 67% and 40% compared to 83%, respectively). Helicobacter-negative patients had higher overall TCI than Helicobacter-positive patients (28.2:17.3). When current and previous histories were analyzed separately, Helicobacter-negative patients also had a trend towards higher TCI currently (16.6:11.0) and in their 20s (11.6:6.1). CONCLUSIONS: There is a significant inverse relationship between Chinese tea consumption and Helicobacter infection. Chinese tea consumption may decrease the chance of Helicobacter infection.
Adult↗
Lack of association between Helicobacter sp colonization and gallstone disease.
Recently, Helicobacter sp has been identified in resected gallbladder tissue and in collected bile from Chilean patients with chronic cholecystitis. Therefore, it an association between bile Helicobacter sp and gallbladder cancer has been proposed. Interestingly, both Helicobacter colonization and gallstone disease (GD) happen very frequently in Chile. However, whether there is an association between Helicobacter colonization and GD has not been completely studied. The aim of this study was to determine the incidence of Helicobacter in human gallbladder tissues with GD. The study included 95 Mexican patients undergoing cholecystectomy. Collected gallbladder specimens were assessed to identify Helicobacter sp using histology, immunohistochemistry, and polymerase chain reaction (PCR) analysis using Helicobacter-specific 16-S ribosomal RNA primers. Of the 95 specimens examined in detail, all had stones as follows: 56 (59%) had chronic cholecystitis; 7 (7.4%), acute cholecystitis: 15 (16%), both chronic and acute cholecystitis, 10 (9.5%), cholesterolosis, and 7 (7.4%), lymphoid hyperplasia. Specimens were considered positive for Helicobacter when histology was positive. Only 1 of the 95 specimens was positive for Helicobacter by immunohistochemistry analysis; 1 of 32 cases, by PCR. These results suggest a low incidence of Helicobacter in the gallbladder epithelium of Mexican patients with GD. However, we can not discard the existence of uncommon Helicobacter sp in gallbladder epithelium and its association with gallstone pathogenesis. Additionally, this study suggests no apparent association between GD and Helicobacter colonization in a Mexican population.
Adult↗
Gastric function in dogs with naturally acquired gastric Helicobacter spp. infection.
The association of Helicobacter pylori with gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship of Helicobacter spp. infection to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter infection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquired Helicobacter spp. infection were studied before and after (4 and 29 days) the attempted eradication of Helicobacter spp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific-pathogen-free, Helicobacter-free Beagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection with Helicobacter felis- and H bizzozeronii-like organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin-stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P = .09) toward higher meal-stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin-stimulated maximal acid output (mmol HCI/kg0.75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P < .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA with Helicobacter-specific primers indicated persistence of Helicobacter DNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression of Helicobacter spp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquired Helicobacter spp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastric Helicobacter spp. in dogs.
Animals↗
Isolation and characterization of novel Helicobacter spp. from the gastric mucosa of harp seals Phoca groenlandica.
Since the recent discovery of Helicobacter cetorum in cetaceans and its role in the development of gastritis, speculation has existed as to whether pinnipeds have Helicobacter spp. associated gastritis and peptic ulcer disease. The gastric mucosa of 4 stranded harp seals Phoca groenlandica from the Massachusetts coastline were assessed for Helicobacter spp. by culture and PCR. We cultured 2 novel Helicobacter spp. from the pyloric antrum of 1 of the 4 harp seals studied, and identified these by PCR in 2 of the 4 seals. Both gram-negative bacterial isolates were catalase- and oxidase-positive. However, a fusiform helicobacter with flexispira morphology was urease-positive, and a spiral-shaped helicobacter was urease-negative. Slender, spiral and fusiform-shaped bacteria were detected in the gastric mucosa by the Warthin-Starry stain. Histopathologic analysis revealed mild diffuse lymphoplasmacytic gastritis within the superficial mucosa of the pyloric antrum of both infected seals. The 2 bacterial isolates were classified by 16S rRNA analysis; they clustered with other enteric helicobacters and represent 2 novel Helicobacter spp. The urease-negative bacterial isolate clustered with H. canis and the urease-positive isolate clustered with an isolate from a sea lion and isolates from sea otters. This cluster of pinniped isolates has 97 % similarity to a number of Helicobacter species, but appears to be most closely related to other helicobacters with flexispira morphology. These findings suggest that the novel Helicobacter spp. may play a role in the etiopathogenesis of gastrointestinal diseases in pinnipeds. To our knowledge, this represents the first isolation and characterization of a novel Helicobacter spp. from pinnipeds.
Animals↗
Peptic diseases and Helicobacter pylori infection after pancreatogastrostomy.
BACKGROUND/AIMS: To investigate the correlation between peptic diseases and Helicobacter pylori after pancreatogastrostomy. Pylorus-preserving pancreatodudenectomy is associated with an increased risk of postoperative peptic diseases. They are thought to be associated with Helicobacter pylori. Little is known about the long-term effects of instillation of alkaline pancreatic juice on the gastric mucosa and Helicobacter pylori infection. METHODOLOGY: We periodically checked the histology and Helicobacter pylori infection of gastric mucosae in 16 patients who had undergone pancreatogastrostomy and pylorus-preserving pancreatodudenectomy. Helicobacter pylori infection and gastritis were assessed according to the culture grade and the updated Sydney System. RESULTS: A stomal ulcer occurred in one patient without Helicobacter pylori. Another 2 patients with Helicobacter pylori infection contracted gastric ulcers. They were cured with anti-ulcer drugs in a short period of time. Gastroesophageal reflux disease occurred in one patient without Helicobacter pylori. None of the patients' Helicobacter pylori infectious states changed postoperatively. Culture grade of Helicobacter pylori significantly decreased after pancreatogastrostomy. The severity of gastritis tended to ameliorate after pancreatogastrostomy. CONCLUSIONS: Pancreatogastrostomy appears to decrease the grade of Helicobacter pylori infection. Peptic diseases are rather frequent minor grade complications. However, they are unlikely to be associated with Helicobacter pylori.
Aged↗