Helicobacter pylori infection and erosive gastritis

One hundred and eleven patients were included in the study. Thirty seven had erosive gastritis, thirty four chronic gastritis and forty were controls without any gastrointestinal diseases confirmed by symptoms and upper gastrointestinal endoscopy. Patients with erosive gastritis were divided into non-steroidal anti-inflammatory drug (NSAID) users and non-users. H pylori status was determined by urease test, serology and/or histology. The prevalence of H pylori was compared between the various groups. The prevalence of H pylori infection in erosive gastritis, chronic gastritis and controls was 68%, 76% and 65%, respectively, the difference was not significant (P > 0.05), 8 out of 11 patients with erosive gastritis and NSAID use (73%) were positive for H pylori. Likewise 17/26 patients with erosive gastritis without NSAID use (65%) were positive for H pylori (P > 0.05). Body of the stomach (65%) was the commonest site for erosions compared to antrum (43%) or fundus (27%) (P < 0.02). H pylori infection does not predispose to erosive gastritis. NSAID use does not affect H pylori prevalence. Routine H pylori eradication is, therefore, not indicated in patients with erosive gastritis infection. Body of the stomach is the most predominant site for erosions.     

Histology of chronic gastritis with and without duodenitis in patients with Helicobacter pylori infection.

AIM: To compare the histological characteristics of Helicobacter pylori positive chronic gastritis in patients with and without associated duodenitis. METHODS: Gastric mucosal biopsy specimens were obtained from patients undergoing endoscopy for dyspepsia. Severity of gastritis and density of H pylori infection were graded according to the Sydney system. RESULTS: Of the 69 patients studied, 15 had normal histology, 22 had chronic gastritis only (77.3% H pylori positive), 21 had duodenitis (90.5% H pylori positive), and 11 had other diagnoses. In the H pylori positive patients, the median gastritis score was higher in the duodenitis group (6, range 3-9) than in the chronic gastritis only group (5, range 2-8), because of greater neutrophil activity scores in patients with duodenitis (median score 2 v 1). There were no differences in the density of H pylori infection, inflammation, atrophy, or intestinal metaplasia between patients with chronic gastritis only and those with duodenitis. CONCLUSIONS: These results suggest that H pylori positive patients with duodenitis have a more severe form of gastritis than those without associated duodenal inflammation. This is because of increased neutrophil activity, which seems to be independent of the density of H pylori infection.     

Relationship of CagA to serum gastrin concentrations and antral G, D cell densities in Helicobacter pylori infection.

The purpose of this study was to investigate whether the densities of antral gastrin and somatostatin-immunoreactive cells in Helicobacter pylori (H. pylori) infection were related to the bacterial expression of cytotoxin-associated gene A (CagA). 32 patients who had underwent diagnostic esophagogastroduodenoscopy were studied. On the histologic examination all patients had antral gastritis. We divided the subjects into three groups. Group I consisted of 6 patients who had chronic superficial gastritis, group II, 9 patients who had H. pylori-associated gastritis but with no expression of CagA, and group III, 17 patients who had H. pylori-associated gastritis with the expression of CagA. In group I and II, serum gastrin levels, and antral G cell and D-cell were measured. In group III, serum gastrin levels, and antral G cell and D-cell were measured, before and after the eradication of H. pylori. The results were as follows. Firstly, serum gastrin concentrations were significantly higher in the patients with H. pylori infection than in the negative controls. Nextly, there was no correlation between the changes in antral G or D-cell density and H. pylori infection. Thirdly, group III had a significant increase in serum gastrin concentrations and a significant decrease in antral D-cell density than group I. Forthly, eradication of H. pylori in group III showed a significantly increased antral D-cell density. Our results suggest that hypergastrinemia in H. pylori-associated gastritis is relevant to the presence of CagA, and the possible mechanism of hypergastrinemia may be related to antral D-cell deficiency, which is caused by H. pylori infection with the expression of CagA.     

The role of apoptosis and proliferation of epitheliocytes in morphogenesis of Helicobacter pylori-associated gastritis

77 patients with chronic Helicobacter gastritis verified endoscopically and exacerbation of duodenal ulcer were examined. H. pylori infection was identified by the rapid ureasa test (CLO-test) and Giemza staining. The patients received 7-day three-component therapy for eradication of H. pylori. Apoptosis and proliferation were studied in 16 patients in serial sections with the use of monoclonal antibodies. Eradication of H. pylori resulted in relief of inflammation and transformation of active gastritis in inactive one. H. pylori-associated gastritis is associated with activation of apoptosis of gastric mucosa epithelial cells and epitheliocytes proliferation. H. pylori eradication alters correlation between apoptosis of epitheliocytes and their proliferation: successful eradication of the infection decreases apoptosis, high proliferative activity of epitheliocytes persists reflecting enhancement of regeneration in gastric mucosa.     

Acute inflammation of the proliferative zone of gastric mucosa in Helicobacter pylori gastritis.

The neutrophilic infiltration has been regarded to represent the activity of Helicobacter pylori gastritis. It may involve the epithelium and/or lamina propria. The incidence and degree of the two types of infiltration do not correlate with each other frequently. We correlated the two types of neutrophilic infiltration with H. pylori infection and other pathologic parameters respectively in 300 randomly selected gastric biopsies as well as serial biopsies from a separate group of 95 patients who were treated for H. pylori infection. The "random biopsies" had chronic gastritis of various degrees, and the organisms were identified in 239 cases (79.7%); in the "treated group," the organisms disappeared completely in 62 cases (65.3%). Characteristically, the intraepithelial neutrophilic infiltration was predominantly localized to the proliferative zone of the gastric mucosa (zone 2) where the density of H. pylori was considerably lower than the surface epithelium. In the "random biopsies," both acute epithelial and interstitial neutrophilic infiltration correlated significantly (p < 0.01) with the H. pylori infection. In the "treated group," however, only acute epithelial inflammation correlated significantly (p < 0.01) with the eradication of infection while acute interstitial inflammation did not. Acute epithelial inflammation was no less frequently present in advanced chronic gastritis than in early chronic gastritis. Acute epithelial inflammation of the proliferative zone is a characteristic pathologic finding of H. pylori gastritis, and appears to be directly associated with the pathogenesis of H. pylori gastritis and its progression.     

Outcome of immunosuppressive therapy with Helicobacter pylori eradication therapy in patients with chronic idiopathic thrombocytopenic purpura

We initiated this study to investigate whether combining Helicobacter pylori eradication with immunosuppressive therapy provides an additional benefit to patients with idiopathic thrombocytopenic purpura (ITP) that has relapsed or has not responded to steroid and/or danazol therapy in patients who have H. pylori infection. Thirty- four patients with chronic ITP that had relapsed or failed to steroid and/or danazol therapy were assessed for H. pylori infection. Of the 21 confirmed cases, 12 patients were given H. pylori eradication therapy alone (EA), while 9 patients received eradication therapy combined with immunosuppressive therapy (EI). The response rate was not significantly different between patients in the EA and those in the EI group (41.7% in the EA group vs. 66.7% in the EI group, p=0.345). The median platelet count at 6 months after therapy was higher in the EI group patients (75 x 10(9)/L in the EI group patients vs. 18 x 10(9)/L in the EA group patients, p=0.028). The median response duration was also longer in the EI group patients (9 months in the EI group patients vs. 3 months in the EA group patients, p=0.049). These results show that a significant benefit is gained by the use of H. pylori eradication combined with immunosuppressive therapy over the use of eradication therapy alone for patients with chronic ITP.     

The role of screening for Helicobacter pylori in patients with duodenal ulceration in the primary health care setting.

BACKGROUND: It is known that at least 90% of duodenal ulcers are caused by infection with the bacterium Helicobacter pylori. Eradicating this organism usually results in complete resolution of the disease. Testing for H pylori was introduced relatively recently, and thus, many patients known to have uncomplicated peptic ulcer disease who continue to need long-term treatment with ulcer-healing drugs have never been tested for the infection or offered eradication therapy. In modern computerized practices, this subgroup of patients can readily be identified by reference to morbidity and repeat prescribing data. Eradication of H pylori infection in this group of patients has great potential benefit for the individuals concerned as well as cost-saving benefit for the National Health Service. AIM: The aim of this prospective study was to determine whether it is worthwhile screening for and treating H pylori infection in patients in a general practice population with previously diagnosed duodenal ulcer disease taking ulcer-healing drugs long term. METHOD: In 1994, in a practice of 7100 patients, morbidity and repeat prescribing data were used to identify 40 patients (0.6%) with proven duodenal ulcer disease taking ulcer-healing medication long term and with uncertain H pylori status. Twenty-nine of the 40 subjects agreed to undergo serology testing for H pylori antibodies. Of 20 (69%) who were positive, 18 (eight women, median age 63.8 years) were given eradication therapy. Seventeen patients received omeprazole 40 mg once daily and amoxycillin 500 mg three times daily for 14 days with metronidazole 400 mg three times daily for the first 7 days; for the remaining patient metronidazole was inadvertently omitted. [13C]Urea breath testing was carried out at the local hospital at least one month after therapy to determine whether eradication treatment had been successful. Subjects were also personally followed up by telephone after 1 and 4 months to assess the success of treatment subjectively. RESULTS: [13C]Urea breath testing showed that H pylori eradication was successful in all 17 patients (100%) who received the intended eradication regimen. Helicobacter pylori was not eradicated in the patient who received only omeprazole and amoxycillin. Four months after successful H pylori eradication, 13 of the 17 (76%) patients remained completely asymptomatic. Two of the four patients who had some recurrent dyspepsia had known gastro-oesophageal reflux and their ongoing symptoms after eradication therapy seemed, on close questioning, to be more attributable to this than to duodenal ulcer disease. CONCLUSION: Testing for and eradication of H pylori is worthwhile in general practice in those patients with previous proven duodenal ulceration who need long-term ulcer-healing medication. The high rate of eradication of H pylori achieved with the regimen used in this study compares very favourably with that of other treatment regimens. However, in patients with duodenal ulcers there may be coexisting pathology, and H pylori eradication does not necessarily result in complete disappearance of dyspeptic symptoms. Thus, when monitoring the outcome of treatment it is important to assess improvement of symptoms as well as objective evidence of eradication.     

Helicobacter pylori, gastritis, and peptic ulceration in the elderly.

AIMS: To determine the histopathological types of gastritis, presence of H pylori, and of peptic ulceration in patients aged 70 and over, compared with younger adults. METHODS: Gastric antral and corpus biopsy specimens from 112 elderly patients were classified and graded histologically according to the Sydney system. Details of recent antibiotic and non-steroidal anti-inflammatory drug use were recorded. Eighty four of the patients were positive for H pylori IgG antibodies and parietal cell antibodies. The results were compared with those from a series of 124 adult patients aged under 60. RESULTS: H pylori were visible at histological examination in only 57 of 87 (65.5%) elderly patients with chronic gastritis (excluding "special forms") compared with 72 of 79 (91.1%) of the younger patients with gastritis (p < 0.0002). Severe atrophy of the corpus mucosa was significantly associated with absence of H pylori (p < 0.002), and was present in eight of 30 elderly patients with helicobacter negative gastritis. Other explanations for absence of H pylori include recent antibiotic intake, more intestinal metaplasia, and lower bacterial load in elderly patients (p < 0.05). Autoimmune gastritis and NSAID use did not seem to be relevant. Serodiagnosis showed reduced sensitivity (81%) in patients who were helicobacter positive histologically, but was positive in 14 of 23 (61%) with H pylori negative gastritis histologically, suggesting either current infection that had been missed or previous infection. Peptic ulceration was significantly associated with NSAID use, but not with H pylori in the elderly. CONCLUSIONS: The spectrum of gastritis is different in the elderly, compared with younger adults, due to a significant group with chronic gastritis who are H pylori negative on histological examination. NSAID use, but not demonstration of H pylori (at histological examination) is associated with peptic ulceration in the elderly.     

Impact of Helicobacter pylori eradication on morphological changes in gastric mucosa

The purpose of the study was to examine gastric mucosal morphological changes in patients with gastroduodenal pathology after eradication therapy for Helicobacter pylori (H. pylori). A hundred and thirty-eight patients (40 females and 98 males) were examined. Of them, there were 122 patients with duodenal peptic ulcer, 8 with gastric peptic ulcer, 5 with erosive gastritis, 2 with chronic atrophic antral gastritis, and 1 with non-atrophic gastritis. Two months and a year after therapy, manifestations of gastric mucosal atrophy, the degree of inflammation, and its activity significantly diminished in patients with complete H. pylori eradication. Positive changes were observed mainly in the antral portion of the stomach. In patients with partial eradication, chronic inflammation and its activity became less. Two months and a year following therapy, positive changes in the gastric mucosa were absent in patients without H. pylori eradication.     

Helicobacter pylori in gastroduodenal diseases

OBJECTIVE: To determine the prevalence and disease association of Helicobacter pylori (H. pylori) in dyspeptic patients in southwest Nigeria. Setting: Obafemi Awolowo University Teaching Hospitals Complex, Ile-lfe, Nigeria. METHODS: Consecutive dyspeptic patients for upper gastrointestinal endoscopy from January 1996 to March 1997 were investigated for H. pylori in gastric biopsy by histopathology and culture. Patients without gastroduodenal ulcerations or neoplastic lesions constituted the nonulcer dyspeptic (NUD) group. RESULTS: 138 (92 males, 46 females) patients aged 4.5-85 years [mean (7) = 45+/-SD 17.8 years] who had upper gastrointestinal endoscopy were analyzed for presence of H. pylori. Eighty-three had histopathology alone, while 55 others had both histology and culture. Endoscopic diagnosis included duodenal ulcer (DU) (n=35, 23%); gastric ulcer (n=4, 3%); gastric cancer (n=14, 9%); NUD, including gastritis (n=49, 32%); duodenitis (n=47, 31%); and normal (n=16, 11%). Overall, H. pylori was positive in 107 of 138 (77.5%) patients. There was a significant association of H. pylori with DU and NUD (p<0.000). Three-quarters of cases of normal endoscopy harbored H. pylori. The finding of 80% and 85% H. pylori in gastritis and duodenitis, respectively, was of interest. CONCLUSIONS: These findings suggest that DU and NUD were the main clinical expressions of H. pylori infection in southwest Nigerian dyspeptic patients similar to what is found in developed nations. Of note is the high incidence of H. pylori in endoscopically normal patients.     

Preventing recurrent upper gastrointestinal bleeding in patients with Helicobacter pylori infection who are taking low-dose aspirin or naproxen

BACKGROUND: Many patients who have had upper gastrointestinal bleeding continue to take low-dose aspirin for cardiovascular prophylaxis or other non-steroidal antiinflammatory drugs (NSAIDs) for musculoskeletal pain. It is uncertain whether infection with Helicobacter pylori is a risk factor for bleeding in such patients. METHODS: We studied patients with a history of upper gastrointestinal bleeding who were infected with H. pylori and who were taking low-dose aspirin or other NSAIDs. We evaluated whether eradication of the infection or omeprazole treatment was more effective in preventing recurrent bleeding. We recruited patients who presented with upper gastrointestinal bleeding that was confirmed by endoscopy. Their ulcers were healed by daily treatment with 20 mg of omeprazole for eight weeks or longer. Then, those who had been taking aspirin were given 80 mg of aspirin daily, and those who had been taking other NSAIDs were given 500 mg of naproxen twice daily for six months. The patients in each group were then randomly assigned separately to receive 20 mg of omeprazole daily for six months or one week of eradication therapy, consisting of 120 mg of bismuth subcitrate, 500 mg of tetracycline, and 400 mg of metronidazole, all given four times daily, followed by placebo for six months. RESULTS: We enrolled 400 patients (250 of whom were taking aspirin and 150 of whom were taking other NSAIDs). Among those taking aspirin, the probability of recurrent bleeding during the six-month period was 1.9 percent for patients who received eradication therapy and 0.9 percent for patients who received omeprazole (absolute difference, 1.0 percent; 95 percent confidence interval for the difference, -1.9 to 3.9 percent). Among users of other NSAIDs, the probability of recurrent bleeding was 18.8 percent for patients receiving eradication therapy and 4.4 percent for those treated with omeprazole (absolute difference, 14.4 percent; 95 percent confidence interval for the difference, 4.4 to 24.4 percent; P=0.005). CONCLUSIONS: Among patients with H. pylori infection and a history of upper gastrointestinal bleeding who are taking low-dose aspirin, the eradication of H. pylori is equivalent to treatment with omeprazole in preventing recurrent bleeding. Omeprazole is superior to the eradication of H. pylori in preventing recurrent bleeding in patients who are taking other NSAIDs.     

Helicobacter pylori infection affects eosinophilic cationic protein in the gastric juice of patients with idiopathic chronic urticaria

BACKGROUND: Helicobacter pylori, the main cause of gastritis and peptic ulcer, has been associated with idiopathic chronic urticaria (ICU), an immunological skin disorder of unknown origin. Eosinophilic cationic protein (ECP) is a cytotoxic molecule secreted by the activated eosinophils involved in the pathogenesis of ICU. We assessed serum/gastric juice ECP levels and gastric mucosal eosinophil infiltration in ICU patients infected or not with H. pylori and evaluated the modification after bacterium eradication. METHODS: 33 patients with ICU and 25 dyspeptic controls underwent upper gastrointestinal endoscopy for histological evaluation and assessment of H. pylori infection. One-week triple therapy was given to H. pylori-positive patients. Serum and gastric juice ECP levels, eosinophil infiltration from gastric mucosal sections and urticaria symptoms were evaluated in all patients at enrollment and 8 weeks after eradication. RESULTS: 19 of 33 (57%) ICU patients and 16 of 25 (64%) controls were found to be infected with H. pylori. Serum ECP was significantly higher in ICU patients compared to controls, regardless of infectious status. Gastric juice ECP and gastric eosinophil infiltration were significantly higher in infected ICU patients when compared both to uninfected ICU patients and controls. H. pylori eradication determined a significant decrease in gastric juice ECP and gastric eosinophil infiltration only in ICU patients. Moreover, a total or partial remission of urticaria symptoms was observed only in ICU patients in whom the bacterium was eradicated. CONCLUSIONS: Although H. pylori infection affects gastric juice ECP and eosinophil infiltration of ICU patients, the role of the bacterium in the pathogenesis of this skin disorder still remains uncertain.     

Expression of HLA-DR, costimulatory molecules B7-1, B7-2, intercellular adhesion molecule-1 (ICAM-1) and Fas ligand (FasL) on gastric epithelial cells in Helicobacter pylori gastritis; influence of H. pylori eradication

There is evidence that Helicobacter pylori infection up-regulates the expression of HLA class II molecules by gastric epithelial cells (GEC). In this study we evaluated whether GEC are capable of expression of costimulatory molecules in H. pylori gastritis. The expression of FasL by GEC, before and after eradication of H. pylori, was also studied. Thirty patients (23 men) aged 27-81 years (53.67 +/- 13.99 years (mean +/- s.d.)) with dyspepsia were studied. Upper gastrointestinal endoscopy was performed and six biopsies were obtained (antrum, n = 3; corpus, n = 3) for Campylobacter-Like Organisms (CLO) test and histology; 23 (16 men) were H. pylori+ and seven (all men) were H. pylori- by both methods and served as controls. Helicobacter pylori eradication therapy was given to H. pylori+ patients and all patients were re-endoscoped after 116 +/- 9 days. Formalin-fixed paraffin-embedded tissue sections were stained by the ABC immunoalkaline phosphatase method. In H. pylori gastritis HLA-DR was expressed and correlated with disease activity (P < 0.01). No HLA-DR was observed in controls. In H. pylori-eradicated patients significant decrease of HLA-DR was found (antrum, P < 0. 001). ICAM-1 was expressed by GEC in 80% of H. pylori+ patients; ICAM-1 expression did not correlate with gastritis parameters and decreased significantly after eradication (antrum, P < 0.01). B7-1 and B7-2 were expressed on H. pylori+ samples and their expression decreased after eradication, albeit not significantly. Weak epithelial expression of both B7 molecules was observed in all the controls. FasL was steadily expressed by GEC in both H. pylori+ and H. pylori- patients and remained almost unchanged after eradication. These findings suggest that GEC may acquire antigen-presenting cell properties in H. pylori infection through de novo expression of HLA-DR and costimulatory molecules. This seems to be attenuated after eradication and resolution of mucosal inflammation. The same cells exhibit the capacity to control the inflammatory process, probably by inducing apoptotic cell death to Fas-bearing infiltrating lymphocytes.     

Decreased gastric proliferation of foveolar epithelial cells after the eradication of Helicobacter pylori.

Increased epithelial cell proliferation is associated with an increased risk of gastric carcinoma. Helicobacter pylori infection is an established risk factor for gastric cancer and the organism has recently been classified as a group I carcinogen by an IARC working group. In this study, we describe differences in gastric epithelial cell proliferation between a H. pylori eradicated group (n = 21) and a not eradicated group (n = 8) after anti-H. pylori eradication therapy to show that increased cell proliferation is associated with H. pylori infection. H. pylori infection was determined by rapid urease test and immunohistochemical method with anti-H. pylori polyclonal antibody. Gastric epithelial cell proliferation was assessed using immunohistochemical method using Ki-67 monoclonal antibody. Ki-67 positive cells in H. pylori associated chronic active gastritis were observed in the glandular neck and the upper portion of foveolar epithelium. Patients who cleared their H. pylori infections showed a significant decrease of Ki-67 labeling index after therapy (0.73 +/- 0.10 vs. 0.48 +/- 0.08, p < 0.01). By contrast, Ki-67 labeling index before and after treatment in patients who remained positive for H. pylori showed no significant difference (0.78 +/- 0.08 vs 0.74 +/- 0.10, p > 0.05). These results indicate that H. pylori infection increases the proliferation of gastric foveolar epithelium, which is reduced by the eradication therapy. We suggest that anti-H. pylori eradication therapy can prevent mucosal cell proliferation to be closely associated with gastric carcinogenesis.     

Helicobacter pylori infection in patients with Brunner's gland adenoma

Histopathologic and clinical data strongly suggest a causal relation between Helicobacter pylori infection and gastritis, peptic ulcer disease, or both. However, little has been written about the potential association between H. pylori infection and Brunner's gland adenoma. Therefore, we carried out a prospective study to determine the presence of H. pylori infection among patients with Brunner's gland adenoma. From November 1996 till October 1999, 19100 patients who had undergone upper gastrointestinal endoscopy at two clinical centers in Zagreb, Croatia, were candidates for participation in the study. Brunner's gland adenoma was diagnosed on the basis of histologic samples taken from the polyp (four patients) or after the entire polyp was made available upon endoscopic removal (three patients). When all endoscopic examinations had been performed, biopsy samples were taken from the antrum and body of the stomach, so that gastritis could be classified and H. pylori determined by histology. Biopsy samples were also taken from the duodenal bulb to verify duodenitis. Two other samples were taken from the antrum for rapid urease test. The patients were considered positive for H. pylori when both histology and rapid urease test were positive. Brunner's gland adenoma was diagnosed in seven patients (five women and two men; median age, 49 yrs). Five (71%) patients with diagnosed Brunner's gland adenoma had concurrent H. pylori infection. Duodenitis associated with gastric metaplasia was observed in six patients. Complete eradication of H. pylori was achieved in only two patients. Symptoms disappeared or markedly diminished in all patients with significant improvement during therapy or immediately upon endoscopic removal of the polyp. Although limited by a very small number of patients, our results suggest that concurrent H. pylori infection is very common in patients with Brunner's gland adenoma. However, the role of H. pylori infection in the pathogenesis and development of Brunner's gland hyperplasia remains unclear.     

Posttreatment follow-up of Helicobacter pylori infection using a stool antigen immunoassay.

The Helicobacter pylori stool antigen enzyme immunoassay (HpSA) was evaluated during posttreatment follow-up of patients in a country with a very high prevalence of H. pylori infection. From among 273 dyspeptic individuals (18 to 55 years) initially recruited from a shantytown in Lima, Peru, 238 participants who met the inclusion criteria and were suspected to be H. pylori positive based on (14)C urea breath test (UBT) results underwent endoscopy. Participants with endoscopy-proven infections received standard eradication therapy and were monitored by UBT and HpSA at 1 month following treatment and at 3-month intervals for 9 months posttreatment. A second endoscopy was performed if UBT results showed evidence of treatment failure or H. pylori recurrence. Biopsy results were considered the "gold standard" in all analyses. Among patients who underwent endoscopy, HpSA had a pretreatment sensitivity of 93%. Two-hundred thirty patients completed the treatment regimen, of whom 201 (93%) were considered to have had successful treatment outcomes based on a negative follow-up UBT. Thirty-two patients with UBT-defined treatment failures or H. pylori recurrences at any point during the 9-month follow-up underwent a second endoscopy. In the posttreatment setting, HpSA had an overall sensitivity of 73% and a specificity of 67%. Agreement between UBT and HpSA diminished throughout the follow-up. Among 14 participants in whom HpSA remained positive at 1 month following treatment despite UBT evidence of treatment success, 12 (86%) became HpSA negative within 3 months posttreatment. Although this study confirmed the validity of the HpSA in the initial assessment of dyspeptic patients, the test demonstrated a reduced overall accuracy in the detection of treatment failures and H. pylori recurrences during 9 months of posttreatment follow-up. Furthermore, in some patients it may take up to 3 months after successful eradication for antigen shedding to diminish to levels within the negative HpSA range.     

Long-term follow up of patients with gastritis associated with Helicobacter pylori infection.

The aim of this study was to evaluate the long-term prognosis for patients suffering from gastritis associated with Helicobacter pylori infection, and in particular the proportion of cases progressing to peptic ulcer. The study was carried out in one urban general practice. One hundred and three patients who had presented with dyspepsia over the 1973-80 period and who were found to have a macroscopically normal endoscopy were reassessed between seven and 14 years later. Gastric antral biopsies had been taken routinely at endoscopy and were subsequently re-examined for the presence of H pylori. The patients' medical records were examined to establish their consulting rates over the follow-up period and whether they suffered from any other medical conditions. Patients were interviewed to assess the course of their dyspeptic symptoms. Comparison of patients who were unequivocally H pylori positive with those who were negative revealed no significant differences in the consultation rate for gastroenterological symptoms, in the proportion of patients referred to a hospital consultant or for further gastroenterological investigations or in the proportion reporting that their symptoms had improved. However, a statistically highly significant relationship was found between H pylori infection and hypertension. The results of this study have shown that there is a good prognosis for non-ulcer dyspepsia whether or not H pylori infection is present. The association between H pylori gastritis and hypertension clearly merits further investigation.     

The histopathology of non-steroidal anti-inflammatory drug induced gastroduodenal damage: correlation with Helicobacter pylori, ulcers, and haemorrhagic events

AIMS: The spectrum of microscopic lesions resulting from the chronic use of non-steroidal anti-inflammatory drugs (NSAIDs), known as chemical gastritis, remains unclear, and the variable prevalence reported in different studies makes this issue a matter of lively debate. The aim of this study was to evaluate the prevalence and importance of chemical gastritis in patients regularly taking NSAIDs. Owing to the high prevalence of Helicobacter pylori infection, particularly in subjects over 60 years of age, and in view of a possible association with damage, the presence of H pylori infection in the same tissue sample was also determined in all patients. METHODS: One hundred and ninety seven subjects were enrolled, 118 of whom were receiving chronic treatment with NSAIDs and 79 of whom were controls, pair matched for age, sex, and clinical symptoms (ulcer-like dyspepsia or upper digestive tract haemorrhage). Antral biopsies taken during upper gastroduodenal endoscopy were assessed for chemical gastritis according to a modified version of Dixon's score, and for Helicobacter correlated chronic active gastritis, according to the updated Sydney system. RESULTS: Chemical gastritis was identified in 11 patients taking NSAIDs (9%) and in four controls (5%) (p < 0.05). Helicobacter pylori was detected in 53 patients taking NSAIDs (45%) and in 34 controls (43%). Patients taking NSAIDs had a significantly higher number of erosions and ulcers and worse endoscores than controls. The presence of H pylori did not appear to increase histological damage, ulcer prevalence, or haemorrhagic events. CONCLUSIONS: Chemical gastritis is present in a limited number of patients regularly taking NSAIDs, and is not strongly correlated with NSAID induced damage. In many cases of peptic ulcer or upper gastrointestinal bleeding in patients taking NSAIDs, the presence of chemical gastritis or H pylori infection cannot solely account for the development of mucosal damage.     

Chronic urticaria and Helicobacter pylori

Background: Helicobacter pylori (HP) have recently emerged as a novel eliciting factor for chronic urticaria (CU). The possible association between HP and CU has enormous potential, as eradicating HP could cure CU. Aims and Objectives: We conducted a study to assess the prevalence of HP infection and effect of bacterium eradication on skin lesions in patients of chronic idiopathic urticaria (CIU). Settings and Design: Four hundred sixty patients of CU attending the allergy clinic, SMS hospital, Jaipur during the period February 6, 2004, to February 6, 2006, were screened for possible eliciting factors. Patients with CIU were enrolled and others were excluded. Materials and Methods: Sixty-eight patients of CIU and similar number of age and sex matched controls, attending the allergy clinic, SMS Hospital, Jaipur were enrolled in the study. All patients underwent endoscopy with antral biopsy for urease and histopathology to identify HP-associated gastritis. Infected patients were given HP eradication therapy. Eradication of bacterium was confirmed by fecal antigen assay. Subjective response to treatment was judged using chronic urticaria quality-of-life questionnaire (CU-Q 2 oL) while objective response to treatment was judged by need for 'rescue medication' (antihistaminics). Statistical Analysis: Data were analyzed using Chi square and paired't' test for their level of significance. Results: HP associated gastritis was present in 48 (70.58%) patients, out of which 39 (81.25%) patients responded to eradication therapy. Ten (50.00%) patients without HP associated gastritis showed response to symptomatic therapy. Overall 49 (72.05%) patients responded and 19 (27.94%) showed no response. The value of chi2 was 28.571 (P = 0.003), which showed significant association between presence of HP and response to eradication regimen. Conclusion: The response of HP eradication therapy in infected patients of CIU is significant. HP should be included in diagnostic workup of patients with CIU.     

Fundic gland polyps are not induced by proton pump inhibitor therapy.

It is still unclear whether proton pump inhibitors (PPIs) could cause fundic gland polyps (FGPs) in patients without Helicobacter pylori infection. The frequency of FGPs in patients during PPI therapy has not been compared, however with a control group of patients who did not have H. pylori infection and were not undergoing PPI treatment. In a retrospective 12-month study, the frequency of FGPs in 2,251 patients without H. pylori infection receiving PPI therapy (duration of treatment at least 4 weeks) was compared with a control group of 28,096 patients who did not have H. pylori infection and were not receiving PPI therapy. FGPs were identified with an identical frequency in both groups (5.0% in the control and 5.2% in the PPI group). No significant differences were present between the groups with respect to the presence of gastritis or age or sex. Our study shows that a causal pathogenetic relationship between PPI therapy and FGPs is unlikely.