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PubMed2005

Bactericidal and morphological effects of NE-2001, a novel synthetic agent directed against Helicobacter pylori.

The antibacterial activities of NE-2001 were tested against 24 clinical isolates of Helicobacter pylori and compared with those of amoxicillin, clarithromycin, metronidazole, and furazolidone. The MIC(50) and MIC(90) of this synthetic compound on the isolates were 8 and 16 mug/ml, respectively. This action was highly selective against Helicobacter pylori; there was a >4-fold difference between the concentration of NE-2001 required to inhibit the growth of Helicobacter pylori and that required to inhibit the growth of common aerobic and anaerobic bacteria. Exposure of Helicobacter pylori (ATCC43504) to NE-2001 at the MIC (4 mug/ml), or at a greater concentration, resulted in an extensive loss of viability. The phenomenon was also observed at pH levels between 3.0 and 7.0. When two clinical Helicobacter pylori strains were successively cultured at subinhibitory concentrations of NE-2001, no significant changes in the bactericidal effects were found. The morphological alterations of Helicobacter pylori cells (ATCC43504), exposed to NE-2001 at various concentrations for 6 h, were observed using transmission electron microcopy. The bacterium displayed features such as swelling, vacuole-like structures in the cytoplasm, and cell destruction following exposure to NE-2001. The efficacy of NE-2001 was maintained when evaluated in eight clinical isolates resistant to metronidazole and five isolates resistant to both metronidazole and clarithromycin (MIC ranging between 4 and 16 mug/ml). The above-described results suggest that NE-2001 may have the potential to be developed as a candidate agent for the treatment of Helicobacter pylori infection.

Adult↗
PubMed1999

A novel urease-negative Helicobacter species associated with colitis and typhlitis in IL-10-deficient mice.

A spiral-shaped bacterium with bipolar, single-sheathed flagella was isolated from the intestines of IL-10 (interleukin-10)-deficient (IL-10(-/-)) mice with inflammatory bowel disease. The organism was microaerobic, grew at 37 and 42 degrees C, and was oxidase and catalase positive but urease negative. On the basis of 16S rRNA gene sequence analysis and biochemical and phenotypic criteria, the organism is classified as a novel helicobacter. Cesarean section-rederived IL-10(-/-) mice without helicobacter infection did not have histological evidence of intestinal inflammation. However, helicobacter-free IL-10(-/-), SCID/NCr, and A/JNCr mice experimentally inoculated with the novel urease-negative Helicobacter sp. developed variable degrees of inflammation in the lower intestine, and in immunocompetent mice, the experimental infection was accompanied by a corresponding elevated immunoglobulin G antibody response to the novel Helicobacter sp. antigen. These data support other recent studies which demonstrate that multiple Helicobacter spp. in both naturally and experimentally infected mice can induce inflammatory bowel disease. The mouse model of helicobacter-associated intestinal inflammation should prove valuable in understanding how specific microbial antigens influence a complex disease process.

Animals↗
PubMed1999

Serological discrimination of dogs infected with gastric Helicobacter spp. and uninfected dogs.

Characterization of the humoral immune responses of people to Helicobacter pylori infection has facilitated the investigation of the host response to bacterial virulence factors and the development of sensitive and specific diagnostic tests. Dogs are commonly infected with gastric Helicobacter spp., but the presence of multiple Helicobacter spp. and possible coinfection in individual dogs have complicated serological evaluation. Evaluation of the antigenic homology of Helicobacter spp. revealed that the major protein bands of Helicobacter felis and Helicobacter bizzozeronii, two Helicobacter spp. that infect dogs, were very similar to UreA (29 to 31 kDa), UreB (63 to 66 kDa), and HSP (58 to 60 kDa) of H. pylori, and sera from infected and uninfected dogs bound in a similar way to each antigen. Immunoblotting and an enzyme-linked immunosorbent assay (ELISA) with H. felis ATCC 49179 antigen were performed with 101 serum samples (from 78 infected dogs and 23 uninfected dogs). Samples from uninfected dogs (median = 8) had fewer bands on immunoblotting than samples from infected dogs (median = 16) (P < 0.05). Combinations of the presence of any two of the low-molecular-mass bands (19, 25, 30, 32, and 37 kDa) or the high-molecular-mass bands (86 and 94 kDa) were found almost solely in samples from infected dogs (P < 0.0001). Kinetic ELISA results were significantly higher for samples from infected dogs (median = 0. 0802 optical density unit [OD]/min) than for samples from uninfected dogs (median = 0.01428 OD/min). The combination of ELISA and immunoblotting results gave a specificity of 95.6% and a sensitivity of 79.8%. No correlation between ELISA results, colonization density, degree of inflammation, and presence of lymphoid follicles was observed. The results indicate substantial antigenic homology between H. felis, H. pylori, and H. bizzozeronii. The combination of ELISA and immunoblotting was a highly specific and moderately sensitive indicator of infection. The degree of seropositivity assessed by ELISA was not related to bacterial colonization density, the degree of gastric inflammation, or the presence of lymphoid follicles.

Animals↗
PubMed2001

Identification of novel Helicobacter species in pig stomachs by PCR and partial sequencing.

Evidence of infection with Helicobacter species in pig stomach was investigated by the use of a PCR with Helicobacter genus-specific primers. Forty pig stomachs, each of four different ulcer lesion grades, 0, 1, 2, and 3 in the pars esophagea area, were collected from a slaughterhouse in Minnesota. Of 160 stomach samples examined, 102 (63.8%) were positive by the PCR assay. The 40 samples each of lesion grades 0, 1, 2, and 3 showed 22.5, 52.5, 85.0, and 95.0% PCR-positive results, respectively. There was a significant trend (P < or = 0.01) in the proportions of PCR-positive cases relative to severity of the lesion. About 80% of the 16S rRNA gene was amplified, and PCR-restriction fragment length polymorphism (RFLP) patterns were analyzed. Of 102 PCR-positive samples, the PCR-RFLP patterns resulted in four different types, 32 samples being classified into type MN 1, 16 samples into type MN 2, 43 samples into type MN 3, and 11 samples into type MN 4. When the sequences of each RFLP type were compared to those reported in databases by using BLAST software, types MN 1, MN 2, MN 3, and MN 4 showed homologies of 97.3, 95.4, 96.7, and 99.5% with the 16S ribosomal DNA of Helicobacter flexispira taxon 3, Helicobacter sp. strains MIT 94-022 and MZ 640285, and Helicobacter suis, respectively. None of the 102 samples positive for the Helicobacter genus were positive with a primer set specific for Helicobacter pylori. Attempts to culture the organisms from selected stomachs in vitro were unsuccessful.

Abattoirs↗
PubMed2001

New Helicobacter species in humans.

During the last decade several new Helicobacter species have been isolated from human gastric mucosa, fecal samples, liver, and gallbladder. Gastric corkscrew-shaped Helicobacter species: H. heilmannii is usually seen in the gastric foveolae in 0.2-0.6% of histological sections from the gastric mucosa of patients with dyspepsia in Western Europe, but it has only been cultured once. It is genetically and morphologically closely related to H. bizzozeronii and H. salmonis which are common in dogs and cats. It causes constantly active chronic gastritis and is regularly associated with peptic ulcer. Intestinal Helicobacter species: H. cinaedi, H. fennelliae, H. pullorum, H. westmeadii, H. canadensis, and 'H. rappini' have been isolated from patients with enteritis and proctitis. H. fennelliae, H. cinaedi, H. westmeadii, and 'H. rappini' have been isolated also from patients with septicemia. Studies indicate that H. cinaedi is transmitted from hamsters and that H. pullorum is common in chickens. 'H. rappini' has been isolated from sheep, dogs, and mice, whereas no animal reservoir has been found for H. fennelliae. Except for the cases of septicemia, none of these Helicobacter species have yet been proven to cause human disease, but they are suspected to play a role in inflammatory bowel diseases. Hepatobiliary Helicobacter species include several Helicobacter species isolated from bile and liver of animals, but only H. bilis has been isolated from the human gallbladder and H. pylori from the human liver. H. bilis has been isolated from dogs, cats, mice, and rats. Nonpylori Helicobacter species are usually difficult to culture and may be more frequently causes of human disease than realized today.

Animals↗
PubMedDate not supplied

[Prevalence of Helicobacter pylori infection in children evaluated at "Hospital de Clínicas de Porto Alegre", RS, Brazil].

OBJECTIVES: To determine prevalence of Helicobacter pylori infection in a group of symptomatic patients between 2 and 18 years old who were submitted to gastric biopsy during upper endoscopy done in the period of 1990-97. To correlate the histological findings with clinical and endoscopical data. METHODS: A cross-sectional study done after review of clinical and histopathological data. Histopathological sections were reviewed by a pathologist, who did not know the clinical information and the previous histopathological reports. RESULTS: Among 181 patients evaluated, prevalence of Helicobacter pylori infection was 24.86% (45 positive cases). In pathological analysis, gastritis was found in 38/45 of the positive Helicobacter pylori patients and in 45/136 negative Helicobacter pylori. Gastric ulceration was found in 6/45 positive Helicobacter pylori and in 3/136 negative Helicobacter pylori. CONCLUSION: This study stated a significative association between Helicobacter pylori infection and pathological abnormalities in children evaluated in the "Hospital de Clínicas de Porto Alegre", RS, Brazil.

Adolescent↗
PubMed2003

Use of polymerase chain reaction and enzymatic cleavage in the identification of Helicobacter spp. in gastric mucosa of human beings from North Paraná, Brazil.

Helicobacter pylori is the most common gastric bacteria of human beings. Animal-borne helicobacter have been associated with gastritis, ulceration, and gastric mucosa-associated lymphoid-tissue lymphoma in people. We attempted to identify the species of Helicobacter spp. that infect human beings in north Paran , Brazil. Samples of gastric mucosa from 38 dyspeptic patients were analyzed by optic microscopy on silver stained slides, polimerase chain reaction (PCR), and enzymatic cleavage. Genus and species-specific primers to H. pylori, H. heilmannii, H. felis, and consensual primers to H. bizzozeronii or H. salomonis were used. The PCR products were submitted to enzymatic cleavage by VspI (Helicobacter spp. product) and HinfI (species products) enzymes. Thirty-two out of 38 patients evaluated had 3.2 to 5 m long bacteria that resembled H. pylori in Warthin-Starry stained slides and were positive to the genus Helicobacter by PCR. In 30 of these patients the bacteria were identified as H. pylori. Two samples positive by silver stain were negative to all species tested by PCR. None of the 38 samples was positive to animal-origin helicobacter species. These results show that PCR and enzymatic restriction are practical methods to identify the species of helicobacters present in gastric mucosa of human beings. People in north Paran appear to be infected mostly with H. pylori.

Adult↗
PubMed1994

Helicobacter pylori in patients with systemic sclerosis: detection with the 13C-urea breath test and eradication.

In patients with systemic sclerosis peristaltic abnormalities may delay gastric emptying, giving rise to bacterial overgrowth, including possibly Helicobacter pylori (HP). Infection with Helicobacter is an important risk factor for esophageal and gastric diseases, including esophagitis, gastritis and gastric cancer. The purpose of this prospective study was to assess gastric HP infection in patients with systemic sclerosis. In 12 patients with systemic sclerosis the newly introduced breath test with 13C-labelled urea was used for indirect detection of gastric urease activity due to HP infection. Five out of 12 patients gave Helicobacter-positive results (42%); 7 patients were negative for Helicobacter colonization (58%). Thus, the risk for gastric diseases caused by HP infection is enhanced in patients with systemic sclerosis compared with white healthy, asymptomatic persons examined in other studies. Helicobacter-positive patients were treated with 2 x 20 mg omeprazole and 4 x 500 mg amoxicillin over 14 days. Afterwards the 13C-urea breath test was repeated and showed negative results for Helicobacter in all systemic sclerosis patients treated. Dual therapy with omeprazole and amoxicillin therapy effectively eradicated HP. The 13C-urea breath test did not cause any side-effects and is therefore considered to be a non-invasive, non-toxic and safe method for the diagnosis and therapeutic control of Helicobacter-status.

Adult↗
PubMed1999

Helicobacter pylori infection and host cell responses.

It is well known that Helicobacter pylori is able to colonize the gastric mucosa, causing a chronic and persistent infection with complications, such as peptic ulcer and gastric cancer. This review places emphasis on some epidemiological aspects of Helicobacter pylori infection and its mode of transmission. At the same time, invasive and non-invasive methods of diagnosis of Helicobacter pylori infection are illustrated. More space is devoted to the host response following invasion of the stomach. In this respect, the role played by different growth factors and polyamines in the course of Helicobacter pylori disease is discussed also in relation to the result of eradicating treatment. On the other hand, an accurate description of the host immune responses against Helicobacter pylori organism and/or their components (e.g. lipopolysaccharides) is reported. Finally, since Helicobacter pylori has been classified as a class I carcinogen, current researches are focussed on the Helicobacter pylori-induced carcinogenesis.

Animals↗
PubMed2004

Vitamin B12 status and its association with Helicobacter pylori infection in alcohol dependent patients.

Both infection with Helicobacter pylori and alcohol abuse have been associated with low vitamin B12 serum levels. The interaction between both risk factors is unknown. The aim of this study was to determine whether Helicobacter pylori infection is associated with low vitamin B12 levels in alcohol dependent patients. Blood samples were obtained from adult alcohol dependent patients undergoing detoxification and analyzed for serum vitamin B12 levels. Helicobacter pylori infection was serologically measured. Patient characteristics, medication use and alcohol consumption at admission were assessed by interview. A total of 6 out of 89 patients included presented low vitamin B12 levels, all were sub clinical deficient (<250 pmol/L) and none were clinical deficient (<150 pmol/L). Infection with Helicobacter pylori was present in 29% of the patients. The average vitamin B12 levels in Helicobacter pylori seropositive and seronegative patients were 1,033 pmol/L (SD 741) and 971 pmol/L (SD 717), respectively. The relation between Helicobacter pylori infection and vitamin B12 deficiency was not of significance (OR=0.48; 95% CI [0.05-4.32]). In conclusion, Helicobacter pylori infection is not a risk factor for low vitamin B12 levels in alcohol dependent patients.

Adult↗
PubMed2006

Helicobacter species ribosomal DNA in the pancreas, stomach and duodenum of pancreatic cancer patients.

AIM: To determine whether gastric and enteric Helicobacter species are associated with pancreatic cancer. METHODS: Patients with exocrine pancreatic cancer (n = 40), neuroendocrine cancer (n = 14), multiple endocrine neoplasia type 1 (n = 8), and chronic pancreatitis (n = 5) were studied. Other benign pancreatic diseases (n = 10) and specimens of normal pancreas (n = 7) were included as controls. Pancreatic tissue specimens were analyzed by Helicobacter-specific PCR-assay and products were characterized by denaturing gradient electrophoresis and DNA-sequencing. From a subset of the pancreatic cancer patients, gastric and/or duodenal tissue as well as gallbladder and ductus choledochus tissue were analyzed. Gallbladder and choledochus samples were included as controls. Stomach and duodenum samples were investigated to analyze whether a gastric helicobacter might disseminate to the pancreas in pancreatic cancer patients. Pancreatic specimens were analyzed by Bacteroides-specific PCR for detecting the translocation of indigenous gut microbes to the diseased pancreas. RESULTS: Helicobacter DNA was detected in pancreas (tumor and/or surrounding tissue) of 75% of patients with exocrine cancer, 57% of patients with neuroendocrine cancer, 38% of patients with multiple endocrine neoplasia, and 60% of patients with chronic pancreatitis. All samples from other benign pancreatic diseases and normal pancreas were negative. Thirty-three percent of the patients were helicobacter-positive in gastroduodenal specimens. Surprisingly, H. bilis was identified in 60% of the positive gastroduodenal samples. All gallbladder and ductus choledochus specimens were negative for helicobacter. Bacteroides PCR-assay was negative for all pancreatic samples. CONCLUSION: Helicobacter DNA commonly detected in pancreatic cancer suggests a possible role of the emerging pathogens in the development of chronic pancreatitis and pancreatic cancer.

Adult↗
PubMed2003

Expression of TFF2 and Helicobacter pylori infection in carcinogenesis of gastric mucosa.

AIM: To investigate the expression of TFF2 and Helicobacter pylori infection in carcinogenesis of gastric mucosa. METHODS: The expression of TFF2 was immunohistochemically analyzed in paraffin-embedded samples from 119 patients with endoscopic biopsy and subtotal gastrectomy specimens of gastric mucosal lesions, including 16 cases of chronic superficial gastritis (CSG), 20 chronic atrophic gastritis (CAG), 35 intestinal metaplasia (IM), 23 gastric epithelial dysplasia (GED) and 25 gastric carcinoma (CA), and Helicobacter pylori infection was detected by Warthin-Starry staining. RESULTS: 1: TFF2 was located in the cytoplasm of gastric mucous neck cell. The expression of TFF2 was 100 %, 100 %, 0, 56.5 % and 0 in CSGs, CAGs, IMs, GEDs and CAs, respectively. 2: The value of TFF2 positive cell density in CSG with Helicobacter pylori infection was higher than that without Helicobacter pylori infection. (52.89+/-7.27 vs 46.49+/-13.04, P>0.05); But the value of TFF2 positive cell density in CAG and GED with Helicobacter pylori infection was significantly lower than that without Helicobacter pylori infection (18.17+/-4.09 vs 37.93+/-13.80, P<0.01 and 14.44+/-9.32 vs 24.84+/-10.22, P<0.05). CONCLUSION: Increase of TFF2 expression in CSG is perhaps associated with the protective mechanism after gastric mucosal injury. Decrease of TFF2 expression in CAG possibly attributes to the decrease in the number of gastric gland cell expressing TFF2. Re-expression of TFF2 in gastric epithelial dysplasia implies that TFF2 possibly contributes to the initiation of gastric carcinoma. The effect of Helicobacter pylori on the expression of TFF2 depends on the status of gastric mucosa.

Chronic Disease↗
PubMed1996

[A sero-epidemiological study on atrophic gastritis and Helicobacter pylori infection].

The aim of this study is to clarify the relationship between the incidence of atrophic gastritis and Helicobacter pylori infection. A case control study was conducted in 1995. Cases and controls were selected among those who took an annual health examination in a rural area of Fukuoka Prefecture. Cases are those who were not diagnosed as having atrophic gastritis in 1991 or 1992 but were diagnosed as having atrophic gastritis in 1995 by the examination of serum pepsinogens. Controls are those who were not diagnosed as having atrophic gastritis between 1991, or 1992 and 1995. Helicobacter pylori infection was evaluated by anti Helicobacter pylori IgG in 1995. The odds ratio for atrophic gastritis was calculated using Logistic regression analysis. The odds ratio of age and sex was not significant, but the odds ratio of Helicobacter pylori infection was significantly elevated (5.2, 95% confidence interval: 2.08-13.17). As for the influence of sex difference on the incidence of atrophic gastritis by Helicobacter pylori infection, the odds ratio among males was not significant (1.4, 95% confidence interval: 0.30-6.10), but the odds ratio among females was significantly high (9.8, 95% confidence interval: 2.82-34.11). These results suggest that Helicobacter pylori infection is associated with the incidence of atrophic gastritis. There may be a risk difference between males and females in the incidence of atrophic gastritis caused by Helicobacter pylori infection.

Adult↗
PubMedDate not supplied

Histological and functional recovery in patients with multifocal atrophic gastritis after eradication of Helicobacter pylori infection.

BACKGROUND/AIMS: To assess the effect of Helicobacter pylori eradication on gastric histology and physiology in patients with multifocal atrophic gastritis over 1-year period. PATIENTS: Fourteen consecutive patients with histological evidence of chronic gastritis and Helicobacter pylori infection diagnosed by histology and serology entered this study. Patients with pernicious anaemia, gastric ulcer or carcinoma, duodenal ulcer, reflux oesophagitis and regular intake of nonsteroidal anti-inflammatory drugs were excluded. METHODS: Patients underwent triple anti-Helicobacter treatment for one week, which resulted successful in all subjects on the basis of negative CLO test and histology as well as 50% decrease in IgG antibodies after 4 weeks and 6 months of treatment, respectively. Histological and functional investigations were performed at baseline, 6 and 12 months after Helicobacter pylori eradication. Histological assessment of inflammatory cell infiltrates was performed on multiple biopsy specimens of the corpus and fundus. Functional tests were 24-hour continuous gastric pH-metry, fasting serum gastrin assay and pepsinogen I levels. RESULTS: There was a progressive significant improvement (p < 0.01-0.001) in acute and chronic inflammatory cell infiltrates in the gastric mucosa throughout the 12-month period. Functional recovery with increase in gastric acidity (p < 0.01) and decrease in gastrin and pepsinogen I levels (p < 0.001) was more evident at the 6-month than at the 12-month checkpoint after Helicobacter pylori eradication (p = NS for gastric pH and p < 0.02 for the other two variables) between 6 and 12 months. CONCLUSIONS: Eradication of Helicobacter pylori infection significantly improves the inflammatory status of oxyntic mucosa and this promotes an almost complete functional recovery. However, the non-parallel behaviour of gastric acidity, which was maximal at 6-month checkpoint, and histological parameters which continued to improve throughout the entire 12-month observation period, seems to indicate that removal of acid-inhibitory substances induced by Helicobacter pylori infection was also responsible for the more rapid recovery of gastric secretory function.

Anti-Bacterial Agents↗
PubMedDate not supplied

[Relation of Helicobacter pylori and the stomach operated on for peptic ulcer].

OBJECTIVE: To review the present information about the relation of Helicobacter pylori with the operated stomach for peptic ulcer. BACKGROUND: The frequency of elective surgical operations for peptic ulcer has decreased in the last years as a result of the therapeutic efficacy of modern drugs while urgent operations have increased. Although the association of peptic ulcer and Helicobacter pylori is well known, the effects of this bacteria on the operated stomach and the effects of the operated stomach on the Helicobacter pylori are not clear. RESULTS: It seems to be that Helicobacter pylori may not be related with peptic ulcer complications that require surgical treatment. It may cause gastritis and mucosal atrophy on the operated patient, it seems not to provoke recurrent ulcer and it's relation with postoperative gastric cancer is not clear. Non-complete vagotomy favors the colonization by Helicobacter pylori and this is lower in patients that have been submitted to operations that cause biliary reflux (gastrectomy Billroth I, gastrectomy Billroth II, pyloroplasty or gastroenterostomy). CONCLUSIONS: Helicobacter pylori may cause alterations in the operated stomach and the operated stomach may favor Helicobacter pylori colonization or, on the contrary, cause its suppression. New studies are needed in order to know with precision the relationship of this bacteria with the operated stomach and to determine the possible usefulness of postoperative eradication treatment.

Adult↗
PubMed1999

[Prevalence of Helicobacter pylori infection in asymptomatic 5-7-year-old children of St. Gallen canton].

The prevalence of Helicobacter pylori infection in asymptomatic Swiss children is not known. The aim of this study was to determine the rate of Helicobacter pylori infection in preschool children of the Canton of St. Gallen, eastern Switzerland. A 13C-urea breath test was performed in 432 randomly selected 5- to 7-year-old children from February to September 1998. A total prevalence of 6.5% was found, with 3.9% for Swiss children and 19.2% for children of parents immigrated from countries or regions with a high prevalence of Helicobacter pylori infection. Children born in these countries and who immigrated later were Helicobacter pylori positive in 70%. In 20/21 brother and sister pairs, the status of Helicobacter pylori infection was concordant. The amount of living space per person and the educational level of parents were comparable for all Helicobacter pylori positive children (Swiss and immigrants). In conclusion, total prevalence of Helicobacter pylori infection in preschool children aged 5 to 7 is low in the eastern part of Switzerland, with a significantly higher rate in children of immigrant parents.

Breath Tests↗
PubMedDate not supplied

Effect of non-steroidal anti-inflammatory drugs on gastric and duodenal prostaglandin concentrations in patients with Helicobacter pylori infection.

BACKGROUND/AIMS: Both Helicobacter pylori and non-steroidal anti-inflammatory drugs are reported to affect gastroduodenal prostaglandin synthesis. However, their influence on gastric mucosal prostaglandins remains unclear. The aim of this study was to investigate the influence of nonsteroidal anti-inflammatory drugs on mucosal prostaglandin synthesis in patients with Helicobacter pylori infection. METHODOLOGY: We enrolled 87 Helicobacter pylori-infected patients in this study (gastric ulcer: 33, duodenal ulcer: 41, and non-ulcer dyspepsia: 13). Of them, 27 patients received non-steroidal anti-inflammatory drugs. Endoscopy was performed and biospy specimens from gastric body, antrum and duodenal bulb were assessed for Helicobacter pylori and prostaglandin concentration. RESULTS: A significantly lower mucosal prostaglandin E2 level at gastric body (142.2 +/- 28.1 ng/mg vs. 222.0 +/- 12.4 ng/mg, mean +/- SEM) and antrum (131.3 +/- 26.4 ng/mg vs. 226.0 +/- 19.0 ng/mg) was noted in Helicobacter pylori-infected gastric ulcer patients with non-steroidal anti-inflammatory drugs ingestion than in that of patients without non-steroidal anti-inflammatory drugs ingestion (p < 0.05). Using a multivariate analysis, we found that non-steroidal anti-inflammatory drug was an independent variable affecting gastric and duodenal mucosal prostaglandin E2 synthesis in patients with Helicobacter pylori-infected gastric ulcer. CONCLUSIONS: Non-steroidal anti-inflammatory drugs decrease gastroduodenal mucosal prostaglandin E2 synthesis in gastric ulcer patients with Helicobacter pylori infection.

Adolescent↗
PubMedDate not supplied

Correlation between endoscopic features of gastric antrum, histology and Helicobacter pylori infection in adults.

BACKGROUND: Helicobacter pylori induces histologic inflammation of mucosa variably correlated to different macroscopic features. Recent studies highlight that the presence of Helicobacter pylori could be assessed on the basis of the macroscopic pattern only, in particular nodularity. The present prospective study has correlated this and other endoscopic features, defined by Sydney classification of gastritis, both to Helicobacter pylori presence and histological patterns. RESULTS: Out of 532 patients, 364 were evaluable. The prevalence of Helicobacter pylori was 51.1% with a different distribution between the endoscopic features. Nodularity showed the highest positive predictive value in detecting the Helicobacter pylori presence (69.9%). The histological findings were: normal 26.9%, non atrophic gastritis 55.2%, atrophic gastritis 17.9%. There was a significant difference between abnormal endoscopic features in detecting the histologic gastritis, with endoscopic atrophy and nodularity showing the highest positive predictive value which reaches 96.7% and 91.8%, respectively. Helicobacter pylori infection and histologic gastritis were also present in 30.9% and 41.8%, respectively, of endoscopically normal subjects. Multivariate analysis has strictly correlated age with all abnormal endoscopic features, metaplasia with endoscopic atrophy, and chronic inflammation (gastritis) with nodularity. CONCLUSIONS: The single endoscopic features are poorly correlated with histologic changes and Helicobacter pylori status. Biopsies are mandatory in all cases. The causes of the different macroscopic findings are not yet fully understood.

Adolescent↗