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PubMed1998

Epidemiology of peptic ulcer disease in cirrhotic patients: role of Helicobacter pylori infection.

OBJECTIVE: The aim of this study was to investigate the clinical and epidemiological factors associated with the appearance of peptic ulcer in patients with cirrhosis and, in particular, the role of Helicobacter pylori infection. METHODS: A total of 201 of 220 consecutive patients included in a prospective study that aimed to evaluate the effect of dietary intervention on cirrhotic complications and survival underwent upper gastrointestinal endoscopy. At entry, an epidemiological and clinical questionnaire was completed and the presence of peptic ulcer disease or esophageal varices at endoscopy was prospectively collected. Sera were obtained and stored at -70 degrees C until analyzed, being tested afterward for Helicobacter pylori antibodies using a commercial ELISA kit. RESULTS: Eleven of 201 patients had borderline anti-Helicobacter pylori IgG titers and were excluded from further analysis. In the remaining 190 patients, point prevalence of peptic ulcer was 10.5% and lifetime prevalence 24.7%. Multivariate analysis selected male sex (OR 2.3; 95%CI 1.09-4.89) and Helicobacter pylori seropositivity (OR: 1.7, 95%CI 1.02-2.81) as the variables independently related to peptic ulcer disease. CONCLUSIONS: Male sex and seropositivity for Helicobacter pylori are the major risk factors for peptic ulcer in cirrhosis.

Female↗
PubMed2000

A survey of internal medicine residents' knowledge about Helicobacter pylori infection.

OBJECTIVE: Despite recently published national guidelines, many physicians have only limited knowledge about Helicobacter pylori infection. We conducted this study to assess internal medicine residents' knowledge about H. pylori. METHODS: Two hundred and nineteen residents in seven accredited internal medicine training programs completed a self-administered questionnaire on personal demographics and practices related to testing for-and treating-H. pylori infection. RESULTS: Noon conferences (82%), ward teaching (66%), journals (70%), and sponsored symposia (27%) were their major sources of H. pylori-related information. Forty-eight percent had used office-based tests for the infection. Testing for (and treatment of) Helicobacter pylori infection was recommended by 97% (97%) for newly diagnosed duodenal ulcer, but by only 61% (63%) for a past history of duodenal ulcer. Many recommended testing in unproven conditions and might not have offered treatment to an infected patient. A proton pump inhibitor-based triple-drug regimen was the treatment of first choice of 55%; 20% recommended proton pump inhibitor-based dual regimens. Sixty-six percent and 80%, respectively, underestimated the rates of resistance to clarithromycin and metronidazole. In the absence of gastrointestinal symptoms, 22% would have ordered Helicobacter pylori testing but only 33% of these would undergo treatment if positive. CONCLUSIONS: Internal medicine residents usually test for Helicobacter pylori infection in appropriate conditions, but may not always treat the infection when the result is positive. Most use efficacious treatment regimens although many have inaccurate knowledge of resistance rates, which may adversely influence prescribing. Education should focus on practical issues surrounding Helicobacter pylori testing and treatment such as those contained in the American College of Gastroenterology's 1998 practice guidelines.

Adult↗
PubMed1991

Helicobacter-associated duodenitis and gastric metaplasia in duodenal ulcer patients.

Biopsy specimens were taken from the duodenal bulb and the distal duodenum in 45 duodenal ulcer patients before and after treatment with histamine-2 antagonists, prostaglandin analogues or antacids. After four weeks of treatment, the ulcer had healed in 31 patients. The treatment did not lead to a reduced frequency of helicobacter-associated duodenitis or gastric metaplasia of the duodenal epithelium. We found gastric metaplasia in 52.3% of all biopsy specimens from the duodenal bulb, chronic active duodenitis in 71.9% and helicobacter-like structures in 15.9%. The helicobacter organisms were found only in areas of gastric metaplasia, and an accompanying chronic active duodenitis was found in 94.1%. In the distal duodenum, we observed chronic active duodenitis in 15.0% of the specimens. Here the inflammation was not associated with gastric metaplasia or helicobacter-like structures. These observations support the hypothesis that Helicobacter pylori colonizes the duodenal mucosa only in areas of gastric metaplasia, and that such colonization may lead to an active duodenitis.

Antacids↗
PubMed2002

Identification of novel Helicobacter spp. from a beluga whale.

The gastric fluid and feces of three belugas from the Mystic Aquarium were assessed for the presence of Helicobacter spp. Gastric fluid and feces from the two clinically healthy belugas were negative for helicobacter, and endoscopy performed on these animals revealed no lesions. However, a helicobacter isolate and PCR product similar to helicobacter strains previously recovered from dolphins were identified, respectively, from the feces and gastric fluid of a beluga manifesting intermittent inappetence and lethargy. Esophageal and forestomach ulcers were noted on endoscopy. This is the first report of novel Helicobacter spp. being identified from whales.

Animals↗
PubMed1999

Cloning and expression of an immunogenic membrane-associated protein of Helicobacter hepaticus for use in an enzyme-linked immunosorbent assay.

Helicobacter hepaticus is a bacterial pathogen that causes chronic active hepatitis and inflammatory bowel disease in mice. The purpose of this study was to develop a recombinant antigen-based enzyme-linked immunosorbent assay (ELISA) to detect H. hepaticus-infected mice. A genomic library of H. hepaticus was constructed and was screened with sera from H. hepaticus-infected mice. A 459-bp open reading frame that coded for an 18-kDa immunoreactive protein, MAP18, was identified. The gene had high identity with genes coding for outer membrane proteins of other bacteria, and the predicted amino acid sequence of MAP18 had a putative membrane-trafficking signal sequence and a putative signal peptidase II cleavage site. The recombinant protein was expressed in Escherichia coli as a glutathione S-transferase (GST) fusion protein, GST-MAP18, and purified by affinity chromatography. The 44-kDa fusion protein was detected on Western blots probed with sera from H. hepaticus-infected mice but was not detected on blots probed with sera from mice infected with Helicobacter muridarum or Helicobacter bilis or with sera from mice free of Helicobacter infection. The GST-MAP18 fusion protein was used as an antigen in an ELISA to detect anti-H. hepaticus antibodies in sera from infected mice. This ELISA was compared to an H. hepaticus-specific ELISA that uses a detergent extract of H. hepaticus as the antigen. Sera from mice naturally and experimentally infected with H. hepaticus, H. bilis, or H. muridarum and sera from mice free of Helicobacter infection were evaluated. Both ELISAs performed with a high specificity (98%); however, the detergent extract-based ELISA performed with a higher sensitivity (89%) than the recombinant protein-based ELISA (sensitivity, 66%). These data indicate that H. hepaticus carries a gene that encodes an immunogenic 18-kDa membrane-associated protein; however, antibodies to this protein are not detected in all infected mice.

Amino Acid Sequence↗
PubMed2001

Emergence of diverse Helicobacter species in the pathogenesis of gastric and enterohepatic diseases.

Since Helicobacter pylori was first cultivated from human gastric biopsy specimens in 1982, it has become apparent that many related species can often be found colonizing the mucosal surfaces of humans and other animals. These other Helicobacter species can be broadly grouped according to whether they colonize the gastric or enterohepatic niche. Gastric Helicobacter species are widely distributed in mammalian hosts and are often nearly universally prevalent. In many cases they cause an inflammatory response resembling that seen with H. pylori in humans. Although usually not pathogenic in their natural host, these organisms serve as models of human disease. Enterohepatic Helicobacter species are an equally diverse group of organisms that have been identified in the intestinal tract and the liver of humans, other mammals, and birds. In many cases they have been linked with inflammation or malignant transformation in immunocompetent hosts and with more severe clinical disease in immunocompromised humans and animals. The purpose of this review is to describe these other Helicobacter species, characterize their role in the pathogenesis of gastrointestinal and enterohepatic disease, and discuss their implications for our understanding of H. pylori infection in humans.

Animals↗
PubMed2006

Rapid onset of ulcerative typhlocolitis in B6.129P2-IL10tm1Cgn (IL-10-/-) mice infected with Helicobacter trogontum is associated with decreased colonization by altered Schaedler's flora.

Infection with Helicobacter trogontum, a urease-positive helicobacter isolated from subclinically infected rats, was evaluated in B6.129P2-IL10(tm1Cgn) (interleukin-10(-/-) [IL-10(-/-)]) and C57BL/6 (B6) mice. In a first experiment, IL-10(-/-) mice naturally infected with Helicobacter rodentium had subclinical typhlocolitis but developed severe diarrhea and loss of body condition with erosive to ulcerative typhlocolitis within 1 to 3 weeks of experimental infection with H. trogontum. A second experiment demonstrated that helicobacter-free IL-10(-/-) mice dosed with H. trogontum also developed severe clinical signs and typhlocolitis within 2 to 4 weeks, whereas B6 mice colonized with H. trogontum were resistant to disease. In a third experiment, using helicobacter-free IL-10(-/-) mice, dosing with H. trogontum resulted in acute morbidity and typhlocolitis within 8 days. Acute typhlocolitis was accompanied by signs of sepsis supported by degenerative hemograms and recovery of Escherichia coli and Proteus spp. from the livers of infected mice. Quantitative PCR data revealed that H. rodentium and H. trogontum may compete for colonization of the lower bowel, as H. trogontum established higher colonization levels in the absence of H. rodentium (P < 0.003). H. trogontum-induced typhlocolitis was also associated with a significant decrease in the levels of colonization by five of eight anaerobes that comprise altered Schaedler's flora (P < 0.002). These results demonstrate for the first time that H. rodentium infection in IL-10(-/-) mice causes subclinical typhlocolitis and that infection with H. trogontum (with or without H. rodentium) induces a rapid-onset, erosive to ulcerative typhlocolitis which impacts the normal anaerobic flora of the colon and increases the risk of sepsis.

Animals↗
PubMed1994

Recombinant antigens prepared from the urease subunits of Helicobacter spp.: evidence of protection in a mouse model of gastric infection.

Urease is an important virulence factor for gastric Helicobacter spp. To elucidate the efficacy of individual urease subunits to act as mucosal immunogens, the genes encoding the respective urease subunits (UreA and UreB) of Helicobacter pylori and Helicobacter felis were cloned in an expression vector (pMAL) and expressed in Escherichia coli cells as translational fusion proteins. The recombinant UreA and UreB proteins were purified by affinity and anion-exchange chromatography techniques and had predicted molecular masses of approximately 68 and 103 kDa, respectively. Western blotting (immunoblotting) studies indicated that the urease components of the fusion proteins were strongly immunogenic and were specifically recognized by polyclonal rabbit anti-Helicobacter sp. sera. The fusion proteins (50 micrograms) were used, in combination with a mucosal adjuvant (cholera toxin), to orogastrically immunize mice against H. felis infection. Gastric tissues from H. felis-challenged mice were assessed by the biopsy urease test and by histology. In mice immunized with recombinant H. felis UreB, 60% of animals (n = 7) were histologically negative for H. felis bacteria after challenge at 17 weeks. This compared with 25% (n = 8) for mice immunized with the heterologous H. pylori UreB antigen. Neither the homologous nor the heterologous UreA subunit elicited protective responses against H. felis infection in mice. The study demonstrated that a recombinant subunit antigen could induce an immunoprotective response against gastric Helicobacter infection.

Animals↗
PubMed2005

Gastric helicobacter infection induces a Th2 phenotype but does not elevate serum cholesterol in mice lacking inducible nitric oxide synthase.

Persistent Helicobacter felis infection in (C57BL/6 x 129SvEv)F1 mice induces chronic gastritis. Expression of inducible nitric oxide synthase (iNOS) is upregulated in response to Helicobacter infection. In this study, 20 10-week-old iNOS-/- mice and 20 wild-type [(C57BL/6 x 129SvEv)F1] mice were infected with H. felis by oral gavage and were assessed histologically and serologically at 32 weeks postinfection. Equal numbers of uninfected controls were sham inoculated. The mice were scored for severity of gastric inflammation, hyperplasia, glandular atrophy, and mucous metaplasia in the corpus and for the level of helicobacter colonization. The immunoglobulin G1 (IgG1), IgG2a, and IgG2c antibody responses to H. felis were determined. As a secondary measure, serum cholesterol levels were assessed. iNOS-/- mice have a propensity for increased serum cholesterol, and although controversial, several human epidemiologic studies have demonstrated an association between Helicobacter infection and several risk factors for cardiovascular disease, including elevated serum cholesterol. Nevertheless, no differences in serum cholesterol levels were observed between the H. felis-infected and -uninfected iNOS-/- mice in this study. The uninfected animals had minimal to no gastric pathology. The gastric pathology scores for the infected animals were reduced significantly in the iNOS-deficient mice relative to those for the wild-type mice (all P <0.01). Helicobacter-infected iNOS-/- mice had chronic lymphoid infiltration and negligible to mild glandular atrophy and mucous metaplasia in the fundic mucosa, while H. felis-infected wild-type mice had severe atrophic and metaplastic mucosal changes. The atrophic gastritis in the infected wild-type mice, particularly the female mice, was also accompanied by greater granulocytic infiltration, antral hyperplasia, and diminished antral colonization, unlike that in the infected iNOS-/- mice. iNOS-/- mice developed significantly lower Th1-associated IgG2c antibody responses to H. felis (P <0.0003); the Th2-associated IgG1 responses were similar (P=0.09), suggesting a greater effect of the iNOS defect on Th1 responses. H. felis colonization was significantly greater in the iNOS-deficient mice. These findings are indicative of an impaired Th1 component of the H. felis-induced inflammatory response when the influence of iNOS is removed.

Animals↗
PubMed1997

Helicobacter westmeadii sp. nov., a new species isolated from blood cultures of two AIDS patients.

A slowly growing anaerobic Helicobacter species was isolated from the blood cultures of two human immunodeficiency virus-positive patients admitted to Westmead Hospital, Westmead, Australia, with fevers. The morphology of the isolates was consistent with Helicobacter cinaedi or Helicobacter fennelliae. The results of culture growth conditions, biochemical tests, gas chromatography data, ribotyping, and 16S rDNA sequencing showed that these isolates represent a new Helicobacter species, for which the name Helicobacter westmeadii has been proposed.

AIDS-Related Opportunistic Infections↗
PubMed2005

Comparison of Helicobacter spp. in Cheetahs (Acinonyx jubatus) with and without gastritis.

Chronic gastritis causes significant morbidity and mortality in captive cheetahs but is rare in wild cheetahs despite colonization by abundant spiral bacteria. This research aimed to identify the Helicobacter species that were associated with gastritis in captive cheetahs but are apparently commensal in wild cheetahs. Helicobacter species were characterized by PCR amplification and sequencing of the 16S rRNA, urease, and cagA genes and by transmission electron microscopy of frozen or formalin-fixed paraffin-embedded gastric samples from 33 cheetahs infected with Helicobacter organisms (10 wild without gastritis and 23 captive with gastritis). Samples were screened for mixed infections by denaturant gel gradient electrophoresis of the 16S rRNA gene and by transmission electron microscopy. There was no association between Helicobacter infection and the presence or severity of gastritis. Eight cheetahs had 16S rRNA sequences that were most similar (98 to 99%) to H. pylori. Twenty-five cheetahs had sequences that were most similar (97 to 99%) to "H. heilmannii" or H. felis. No cheetahs had mixed infections. The ultrastructural morphology of all bacteria was most consistent with "H. heilmannii," even when 16S rRNA sequences were H. pylori-like. The urease gene from H. pylori-like bacteria could not be amplified with primers for either "H. heilmannii" or H. pylori urease, suggesting that this bacteria is neither H. pylori nor "H. heilmannii." The cagA gene was not identified in any case. These findings question a direct role for Helicobacter infection in the pathogenesis of gastritis and support the premise that host factors account for the differences in disease between captive and wild cheetah populations.

Acinonyx↗
PubMed2002

Helicobacter pylori does not play a part in the dyspeptic complaints of rheumatology patients receiving long term treatment with non-steroidal anti-inflammatory drugs.

BACKGROUND: The presence of dyspeptic symptoms is a common finding in patients treated with non-steroidal anti-inflammatory drugs (NSAIDs). Some studies seem to support the involvement of Helicobacter pylori infection in the dyspeptic symptoms reported by these patients, and suggest that eradication may be useful. OBJECTIVE: To determine the variables related to dyspepsia in rheumatology patients requiring NSAID treatment, assessing in particular the role of Helicobacter pylori infection. METHODS: One hundred and eighty six consecutive patients with a rheumatological disorder requiring NSAID treatment (68 male, 118 female; mean (SD) age 55 (15) years) were included in a cross sectional study; dyspeptic symptoms were measured by a previously validated scale. Helicobacter pylori infection was determined by serology. Variables related to the severity of symptoms and the need for antisecretory drugs were determined by multivariate analysis. RESULTS: No relation was found between Helicobacter pylori infection and dyspepsia or any of its surrogate markers (antisecretory drug use or NSAID intolerance). Female sex and treatment with antisecretory drugs were found to be independent predictors for the appearance and severity of dyspeptic symptoms. The only independent predictive variables of the requirement for antisecretory drugs were age, previous ulcer disease, taking NSAIDs with a medium or high anti-inflammatory potential, and the symptoms score. CONCLUSION: Helicobacter pylori infection does not seem to play any part in the gastric symptoms of patients treated long term with NSAIDs.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2006

Helicobacter pylori seropositivity and stool antigen in patients with hyperemesis gravidarum.

The objective of this paper is to investigate whether Helicobacter pylori is an etiologic factor in hyperemesis gravidarum. Thirty one patients with hyperemesis gravidarum and twenty nine pregnant controls without hyperemesis gravidarum were included in this prospective study. All pregnant women were examined both for Helicobacter pylori serum immunoglobulin G antibodies (HpIgG Ab), showing chronic infection, and Helicobacter pylori stool antigens (HpSA), showing active gastrointestinal colonization. Chi-square and Student t tests were used accordingly for statistical analysis. Helicobacter pylori seropositivity was 67.7% in the patients with hyperemesis gravidarum and 79.3% in the control group (chi(2) = 1.02, P = .31). HpSA was detected in 22.6% of patients with hyperemesis gravidarum, whereas 6.9% of patients in the control group. The difference was not statistically significant (chi(2) = 2.89, P = .08). In this study, no relation was found between Helicobacter pylori and hyperemesis gravidarum. The low social status of women in both groups could be one of the reasons for the high prevalence of Hp infection.

Adolescent↗
PubMed2002

Helicobacter species are not detectable by 16S rDNA PCR in bile from Dutch patients with common bile duct stones.

BACKGROUND: Some Helicobacter species colonize the intestinal tract. To explore the possible relation between Helicobacter spp. and gallbladder disorders, we have investigated their presence in bile of patients with biliary obstruction and dilatation of the bile ducts. METHODS: Bile was sampled from 31 Dutch patients with biliary obstruction identified by jaundice and dilatation of the bile ducts on ultrasound. Samples (n = 31) were obtained immediately following cannulation of the common bile duct (CBD) by endoscopic retrograde cholangiopancreatography (ERCP) (n = 29) or by peri-operative puncture of the gallbladder (n = 2). DNA was isolated from bile by binding to diatoms. Helicobacter spp. were detected by a sensitive (detection limit 1 CFU per reaction tube) 16S rDNA PCR with genus-specific primers. Duplicate samples were spiked with Helicobacter pylori DNA and subjected to PCR in order to check for inhibition. RESULTS: 28 patients had CBD stones (bile collected by ERCP (n = 26) or operatively (n = 2)), 2 had a pancreatic head tumor, and in 1 no abnormalities were found. In 1 of 21 amplifiable bile samples (10/31 inhibited) from Dutch patients with CBD stones, H. pylori 16S rDNA was found. CONCLUSION: Our data indicate that CBD stones in Dutch patients are not associated with the presence of Helicobacter spp. in bile.

Adult↗
PubMed2005

Development of a microelectronic chip array for high-throughput genotyping of Helicobacter species and screening for antimicrobial resistance.

A microelectronic array assay was developed to specifically genotype Helicobacter pylori versus Helicobacter heilmannii and to determine antimicrobial resistance. Helicobacter 16S rRNA and 23S rRNA genes were specifically generated with Helicobacter genus-specific primers, respectively. The single-nucleotide polymorphisms (SNPs) in 16S rRNA, 268T specific in the H. pylori sequence, and 263A specific in H. heilmannii were used as molecular markers for identification of H. pylori and H. heilmannii, respectively. A triple-base-pair resistant mutation, AGA965-967TTC in 16S rRNA, is known to be responsible for H. pylori tetracycline resistance and was detected to identify resistant strains. H. pylori macrolide resistance was determined by the identification of 3 defined mutations in the 23S rRNA gene using the same method. The assay could be directly used to detect H. pylori in feces. The assay performs multiple determinations, including identification of Helicobacter species and antibiotic resistances, on the same microelectronic platform and is highly amenable to the development of other DNA-based assays.

Base Sequence↗
PubMed2006

Progressive proliferative and dysplastic typhlocolitis in aging syrian hamsters naturally infected with Helicobacter spp.: a spontaneous model of inflammatory bowel disease.

Helicobacter spp. have been implicated in a variety of gastrointestinal tract diseases, including peptic ulcer disease, gastric cancer, and inflammatory bowel disease (IBD), in humans and animals. Although most models of IBD are experimentally induced, spontaneous or natural models of IBD are rare. Herein, we describe a long-term study of chronic, progressive lesions that develop in the distal portion of the large bowel of unmanipulated Syrian hamsters naturally infected with Helicobacter spp. Twenty-four Syrian hamsters of three age groups (group A, 1 month [n = 4], group B, 7-12 months [n = 12], group C, 18-24 months [n = 12]), underwent complete postmortem examination. Results of microbial isolation and polymerase chain reaction and restriction fragment length polymorphism analyses confirmed the presence of Helicobacter spp. infection in the distal portion of the large bowel of all animals. Additionally, confounding pathogens, such as Clostridium difficile, Lawsonia intracellularis, and Giardia spp. that can cause proliferative enteritis, were absent in the hamsters of this study. Histopathologic scores for inflammation (P < 0.01), hyperplasia (P < 0.01), and dysplasia (P < 0.05) were significantly higher in the ileocecocolic (ICC) junction of animals in group C, relative to group A. Dysplastic lesions of various grades were detected in 5 of 11 hamsters in group C. Interestingly, the segment of the bowel that is usually colonized by Helicobacter spp. in hamsters had the most severe lesions. One hamster of group C developed a malignant fibrous histiocytoma, whereas another hamster developed a round cell sarcoma originating from the ICC junction. Thus, lesions in the distal portion of the large bowel of aging hamsters naturally colonized with Helicobacter spp. warrants developing the hamster as an animal model of IBD and potentially IBD-related cancer.

Animals↗
PubMedDate not supplied

[Changes in ultra rapid urease test and histopathological examination for Helicobacter pylori by antisecretory drugs].

BACKGROUND: One of the major problems when evaluating dyspeptic patients at public hospitals is the large interval between the consultation and the endoscopy, leading to the prescription of antisecretory drugs, what can be responsible for false results on examinations. AIM: To evaluate changes in ultrarapid urease test and histopathological examination for Helicobacter pylori by antisecretory drugs. METHODS: In a prospective double-blind study, 50 patients with dyspeptic complaints and endoscopic diagnosis of peptic ulcer, erosive gastritis, esophagitis or duodenitis with a positive urease test, were randomized to a 7-day course of treatment with either omeprazole 20 mg or ranitidine 300 mg a day. Before and after treatment, two biopsy specimens each were obtained from the antrum and corpus and an ultrarapid urease test and a histopathological examination for Helicobacter pylori were performed. RESULTS: There were no significant changes in the results of ultrarapid urease test and histopathological examination for Helicobacter pylori after treatment with ranitidine. With omeprazole, we observed a decrease in positive results in ultrarapid urease test and histopathological examination for Helicobacter pylori in the antrum, but not in the corpus. CONCLUSION: Omeprazole, used for 7 days can lead to negative results in ultrarapid urease test and histopathological examination for Helicobacter pylori in the antrum, and should not be employed in patients before the endoscopy is performed.

Adult↗
PubMedDate not supplied

Detection of Helicobacter pylori in gastric cancer.

BACKGROUND AND OBJECTIVES: Considering the high prevalence of stomach cancer in the northern region of Brazil and the recognized relationship between chronic gastric inflammation caused by Helicobacter pylori, and its carcinogenic potential, the objective we had with this study was to investigate the presence of the microorganism in macro and microscopic presentations of neoplasm in different regions of the stomach, and in non-malignant lesions concomitant to the adenocarcinoma in patients originating from the metropolitan area of Belém (State of Pará, Brazil). METHODS: Examinations were made on 172 patients divided into two groups: group I, formed by 75 patients with gastric carcinoma, and group II, formed by 97 patients with mild enanthematic gastritis, considered control group. The diagnosis was obtained during endoscopic examination and the respective biopsy. Gastric neoplasms were classified macroscopically in accordance with Borrmann's classification, and microscopically in accordance with Laurén's classification. In group I, 54 patients were male and 21 female while in group II, 22 patients were male and 75 female. The average age in group I was 61.2 years (range 27 to 86 years), while in group II it was 37.5 years (range 16 to 69 years). Thin sections were prepared and stained using the hematoxylin-eosin method. In the Helicobacter pylori research, the modified Gram stain was utilized. Statistical analysis was done by utilizing the chi-squared (chi 2) test, Mann-Whitney test (U), and Fisher's exact test. RESULTS: The results showed the detection of Helicobacter pylori were significantly greater in patients with mild enanthematic gastritis than in patients with gastric carcinoma. The presence of Helicobacter pylori in patients with gastric carcinoma and mild enanthematic gastritis was significantly greater in the antral region than in other gastric regions. Helicobacter pylori detection in patients with gastric carcinoma did not present a significant difference in relation to the macroscopic aspect of the tumor either intestinal or diffuse histological types. CONCLUSIONS: These data suggest the presence of the bacteria is predominant in the antral region and it does not show relation with the macroscopic types or histological intestinal or diffuse types of gastric carcinoma.

Adenocarcinoma↗