Ulcer recurrence after gastric surgery: is helicobacter pylori the culprit?

Objectives: Helicobacter pylori is the most important cause of recurrent peptic ulcer disease. However, its role in ulcer recurrence after peptic ulcer surgery is unclear. We aimed at studying the prevalence and distribution of H. pylori in patients who had undergone peptic ulcer surgery, and any association between H. pylori infection and ulcer recurrence in these patients.
Methods: Patients with previous vagotomy or partial gastrectomy presenting with dyspepsia or ulcer bleeding were recruited. Ulcer recurrence was documented by endoscopy. Biopsy specimens were taken from the gastric remnant and gastroenteric anastomosis in patients with previous partial gastrectomy, or from the antrum and corpus in vagotomized patients. H. pylori infection was detected by either a positive rapid urease test or the presence of the bacteria on histology.
Results: Ninety-three patients were studied; 73 patients (78%) had partial gastrectomy and 20 (22%) had vagotomy with drainage. H. pylori infection was documented in 36 patients (49%) in the gastrectomy group and in 13 (65%) in the vagotomy group. Thirty-six patients in the gastrectomy group had recurrent ulcers and 15 (42%) of them had H. pylori infection. Twelve patients in the vagotomy group had recurrent ulcers and eight (67%) of them were H. pylori positive. The prevalence of H. pylori infection did not differ between patients with or without ulcer recurrence.
Conclusion: H. pylori infection cannot account for ulcer recurrence after peptic ulcer surgery.     

The Diagnostic Yield of Various Tests for Helicobacter pylori Infection in Patients on Acid-Reducing Drugs

The diagnostic yield of various tests for Helicobacter pylori infection in patients on acid-reducing drugs, such as proton pump inhibitors (PPI) and histamine-2 receptor blocker (H2RB), was compared. Seventy-four consecutive patients on acid-reducing drugs were enrolled: 34 (46%) were on PPIs, 20 (27%) were on H2RBs and 20 (27%) were not on medications. For those patients on PPIs, RUT and histology results from antrum were negative in 28 (82%) and 17 (50%) patients, respectively (OR: 4.7; 95% CI: 1.4–16.6; P = 0.004), while those from the corpus were negative in was 28 (82%) and 18 (53%) patients, respectively (OR: 4.4, 95% CI: 1.3–15.5; P = 0.006). For patients on H2RBs, RUT and histology results from the antrum were negative in 12 (60%) and six (30%) patients, respectively (OR: 3.5; 95% CI: 0.8–16.1; P = 0.05), while those from the corpus were negative in 12 (60%) and nine (45%) patients, respectively (OR: 1.8; 95% CI: 0.4–7.8; P = 0.342). For those patients on PPIs, the diagnostic yield of both RUT and histology was reduced from both the antrum and corpus. In these patients, PCR for H. pylori is more sensitive than RUT and histology.     

Efficacy and Tolerability of Rifampicin-Based Rescue Therapy for Helicobacter Pylori Eradication Failure in Peptic Ulcer Disease

In vitro activity of rifampicin has been shown against H. pylori. It has also been reported that the prevalence of H. pylori is low in patients with tuberculosis treated with rifampicin. Clinical trials are required to establish the efficacy of rifampicin as a salvage therapy for eradication of H. pylori. We aimed to evaluate the efficacy of rifampicin-based salvage therapy for eradication of H. pylori in patients with peptic ulcer disease. Twenty-eight patients with peptic ulcer disease who either had failed eradication of H. pylori or had a recurrence of H. pylori following successful eradication were included in the prospective study. The inclusion criteria included one or more failed attempts at eradication and presence of H. pylori infection as evidenced by positivity of at least two of three tests: rapid urease test (RUT), ¹⁴C urea breath test (UBT), and histology. The subjects were treated with a 10-day regimen consisting of rifampicin, 450 mg od, tetracycline, 1 g bd, and esomeprazole, 40 mg bd. Four weeks after completion of therapy, H. pylori status was assessed by RUT, ¹⁴C, UBT, and histology. Liver function tests were done before and at the end of therapy. The study subjects included 25 males and 3 females with a mean age of 33.7 ± 8.92 years (range: 22–65 years). The median duration of symptoms was 42 months, with a range of 1–180 months. The median number of eradication attempts was two, with one prior attempt in 6 (21.4%), two attempts in 19 (67.9%), and three attempts in 3 (10.7%) patients. Successful H. pylori eradication as defined by concomitant negativity of RUT, UBT, and histology with special stains was achieved in 32.1% (9/28) of patients by intention-to-treat and 33.3% (9/27) of patients by per-protocol analysis. This pilot study suggests that rifampicin-based regimes have no role as salvage eradication therapy in refractory cases of H. pylori infection with peptic ulcer disease.     

Factors for improving the diagnostic efficiency of the rapid urease test from the gastric corpus

Objective: This study aimed to evaluate the optimal biopsy site for Helicobacter pylori detection by comparing the results of rapid urease test (RUT) between the gastric corpus and the antrum.

Methods: A biopsy specimen from each subject was obtained from the corpus and from the antrum. For each subject, the two specimens were separately immersed in two different RUT kits. Positive reaction times were measured at 20?minutes and 1, 3, and 24?hours. If either of the two RUT kits showed a positive reaction, H. pylori infection was confirmed.

Results: A total of 310 H. pylori-infected subjects were eligible for study inclusion. Compared with the antrum, positive RUT reaction times in the corpus were shorter when the degree of gastric atrophy was moderate or severe (p?=?.001 and p?p?=?.021) and severe gastric atrophy (OR?=?2.41; 95% CI?=?1.13–5.13; p?=?.023). Also, severe gastric atrophy was an independent factor associated with positive RUT reaction only in the corpus (OR?=?5.12; 95% CI?=?1.55–16.88; p?=?.007).

Conclusions: In subjects aged ≥50 years or with severe gastric atrophy, biopsy of the corpus mucosa optimized the efficiency of H. pylori detection through a faster positive RUT reaction.     

High acid secretion may protect the gastric mucosa from injury caused by ammonia produced by Helicobacter pylori in duodenal ulcer patients

The aim of the present study was to investigate the mechanism by which gastric atrophy does not tend to occur in patients with duodenal ulcer despite frequent Helicobacter pylori infection. This investigation was performed in 60 patients with duodenal ulcer and 63 age-matched gastritis patients. Endoscopic findings in the antrum and corpus were classified as normal, atrophic and superficial changes. Biopsy specimens were taken from the antrum and corpus. Ninety per cent of patients with duodenal ulcer and 63.5% of patients with gastritis had H. pylori infection (P<0.01). The incidence of normal findings in duodenal patients was 30% in antral regions and 50% in the corpus (P<0.05). Atrophic change was observed in 21.7% of patients in the antrum and 3.3% of patients in the corpus (P<0.01). The grade of inflammation in duodenal ulcer specimens was significantly higher in the antrum than in the corpus (P<0.01). >H. pylori density was significantly higher in the antrum than in the corpus in ulcer patients (P<0.01). No significant difference in endoscopic findings, >H. pylori density or the grade of inflammation was found between the antrum and corpus in patients with gastritis. The mean intragastric ammonia concentration was 10.3 mg/dL in duodenal ulcer patients and 6.2 mg/dL in gastritis patients (P<0.01). The mean pH was 3.5 and 4.6 in ulcer and gastritis specimens, respectively (P<0.01). Our data suggest that gastric mucosa injury is less frequently associated with duodenal ulcers than with gastritis due to the low >H. pylori density in the corpus and to the higher acid output that neutralizes the ammonia produced by H. pylori.     

Risk of Recurrence of Gastric Ulcer,Chronic Gastritis,and Grade of Helicobacter pylori Colonization: A Long-Term Follow-up Study of 25 Patients

Maaroos H-I, Kekki M, Vorobjova T, Salupere V, Sipponen P. Risk of recurrence of gastric ulcer, chronic gastritis, and grade of Helicobacter pylori colonization. A long-term follow-up study of 25 patients. Scand J Gastroenterol 1994;29:532-536.

Background: We describe here our observations on colonization of the gastric mucosa by Helicobacter pylori in a long-term follow-up of 25 patients with gastric ulcer (GU).

Methods: All patients were followed-up endoscopically for more than 10 years (mean, 16 years) and endoscopically verified to have GU in the angular or corpus area of the stomach. None had received treatment with H₂ blockers or omeprazole or had undergone any maintenance therapy or surgery. On the basis of the endoscopic findings on the activity of GU at follow-up endoscopies, the patients were divided into a group of subjects with 'low risk' of recurrence (15 patients who either had no (7 patients) or only a single recurrence (8 patients) at the first follow-up endoscopy but not thereafter) and into those with a 'high risk' of recurrence (10 patients who had at least 2 episodes of recurrence at follow-up endoscopies).

Results: A severe bilateral (antrum and corpus) colonization of the gastric mucosa by H. pylori at the first re-examination (1-6 years after the initial diagnosis of GU) was the most important characteristic feature in the patients with high risk of recurrence as compared with those with low risk. In the course of the follow-up, colonization of the corpus mucosa by H. pylori remained rather unchanged in both high- and low-risk subjects but decreased in grade in antrum particularly in those with low risk (no bacteria at the last endoscopy in 13 of 16 low-risk patients and in 2 of 8 high-risk patients). In both low-and high-risk groups corpus gastritis developed progressively into atrophic gastritis (11 of 25 patients had severe corpus atrophy at the last endoscopy). On the other hand, antral gastritis showed a tendency to heal (13 of 24 patients had normal or only slightly gastritic antrum at the last endoscopy).

Conclusions: The observations indicate that the H. pylori plays a role in and associates closely with the long-term course of angular or corpus GU disease and is related to the tendency of these ulcers to recur.     

The CLO test is unreliable in diagnosing H. pylori infection in post-surgical stomach; is there any role of H. pylori in peptic ulcer recurrence?

AIM: To evaluate the validity of the CLO test in detecting Helicobacter pylori in patients with gastric operation and to investigate the relationship of H. pylori with peptic ulcer recurrence in these patients. METHODS: In this prospective study, 110 consecutive patients, the majority of whom had undergone gastric operation for benign disease (n = 102), were included. Eighty patients (62 males), aged 38-87 years, had had a gastrectomy (10 Billroth I, 70 Billroth II), and 30 patients (27 males), aged 36-73 years, had had a vagotomy (13 vagotomy plus gastroenterostomy, 17 vagotomy plus pyloroplasty). H. pylori was sought on multiple biopsy specimens, using CLO test and histology (modified Giemsa stain). The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of the CLO test were estimated using histology as 'gold standard'. RESULTS: Overall, 21 gastrectomy patients (26%) were H. pylori-positive by CLO and 25 (31 %) were H. pylori-positive by histology. The estimated sensitivity, specificity, PPV and NPV of the CLO test, using histology as 'gold standard', were 68%, 91%, 77% and 86%, respectively. The CLO test was positive in 67% of vagotomy patients (20 of 30), while 50% (15 of 30) were H. pylori-positive by histology. The estimated sensitivity, specificity, PPV and NPV of the CLO test were 87%, 53%, 65% and 80%, respectively. H. pylori prevalence by histology was 50% in patients with vagotomy and 31% in those with gastrectomy (P = 0.0787). Recurrent ulcers were observed in 8/30 patients (27%) after vagotomy and in 10/72 patients (14%) after gastrectomy. Recurrent ulcer was documented in 6/15 H. pylori-positive patients with vagotomy (40%), and in one of 25 H. pylori-positive patients with gastrectomy (4%). This difference was significant (Fisher's exact test, P = 0.007, relative risk 5.091, 95% CI 0.819-31.64). CONCLUSION: The CLO test seems to be unreliable in diagnosing H. pylori in post-surgical stomach. The H. pylori prevalence is higher, although not significantly, in vagotomized patients compared with gastrectomized patients, and in this group is closely related to the presence of recurrent ulcer. So, at least in this group of patients, it is strongly recommended to look for and eradicate H. pylori.     

Impact of Non-steroidal Anti-inflammatory Drug and Aspirin Use on the Prevalence of Dyspepsia and Uncomplicated Peptic Ulcer Disease

Background: Non-steroidal anti-inflammatory drug and aspirin (here collectively called NSAIDs) use is the second most common aetiologic factor for peptic ulcer disease and a major factor for peptic ulcer complications. The role of NSAIDs in the pathogenesis of uncomplicated peptic ulcer is less well understood and the interaction between NSAIDs and Helicobacter pylori infection on ulcer development is controversial. The aim of the present study was to examine the role of NSAIDs in the occurrence and clinical features of uncomplicated peptic ulcer disease. Methods: A total of 1091 consecutive patients referred for open-access upper gastrointestinal endoscopy by general practitioners (GPs) were enrolled. The use of NSAIDs was gathered from a structured questionnaire completed by the patients and from patient files by GPs. The exclusion criteria were previous H. pylori eradication and gastric surgery, as well as symptoms and/or signs suggestive of acute gastrointestinal bleeding. Results: Of the whole study group (n = 1091), 76 (7%) patients had a peptic ulcer. Thirty patients had an NSAID-use-associated peptic ulcer and 46 patients a non-NSAID-use peptic ulcer. Of patients with chronic gastritis (n = 599), 71% were H. pylori-positive and 108 used NSAIDs. Of those with chronic gastritis, 23 had an NSAID-use-associated peptic ulcer and 38 a non-NSAID ulcer. Of patients with normal gastric histology (n = 492), 75 patients used NSAIDs, 7 had an NSAID ulcer and 8 a non-NSAID ulcer. The only independent risk factor for peptic ulcer in patients using NSAIDs was H. pylori infection (odds ratio (OR) 3.1, 95% confidence interval (CI) 1.3-7.3), whereas dyspepsia (OR 1.0, 95% CI 0.4-2.4), male sex (OR 1.4, 95% CI 0.6-3.4), age (OR 1.0 per decade, 95% CI 0.8-1.3) and anaemia (OR 2.9, 95% CI 0.9-8.7) were not risk factors. In patients not using NSAIDs, independent risk factors for peptic ulcer were dyspepsia (OR 4.3, 95% CI 2.1-8.8), male sex (OR 2.0, 95% CI 1.1-2.8), age (OR 1.2 per decade, 95% CI 1.0-1.5), anaemia (OR 6.2, 95% CI 2.6-14.9) and H. pylori infection (OR 7.5, 95% CI 3.4-16.6). When comparing patients using NSAIDs or not, the OR of patients on NSAIDs for peptic ulcer was 2.7 (95% CI 1.5-5.0) among patients with chronic H. pylori gastritis (n = 424) and 5.3 (95% CI 1.8-15.0) among patients with normal gastric mucosa (n = 492). Conclusions: The use of NSAIDs increases the risk of peptic ulcer 3- and 5-fold in H. pylori-positive and H. pylori-negative patients, respectively. Dyspepsia is a poor predictor of peptic ulcer among patients using NSAIDs, and serologic H. pylori testing and treatment for chronic NSAID users is recommended.     

Anti‐CagA and anti‐VacA antibodies in Helicobacter pylori‐infected patients with and without peptic ulcer disease in Serbia and Montenegro

Background: The expression of two Helicobacter pylori proteins, CagA and VacA, is associated with more severe pathogenesis and clinical outcomes of the infection. However, this association varies among geographical regions and ethnic groups. We therefore evaluated CagA and VacA seroprevalence in H. pylori‐positive dyspeptic patients in Serbia and Montenegro. Methods: In 173 consecutive dyspeptic patients referred to endoscopy (67M, mean age 49?±?15, 76 smokers), immunoblot assay was used to detect serum antibodies against CagA and VacA. Presence of H. pylori infection was assessed using a rapid urease test (RUT), routine histology and serology (anti‐IgG ELISA). Duodenal ulcer (DU) was diagnosed in 28, gastric ulcer (GU) in 3 and non‐ulcer dyspepsia (NUD) in the remaining 142 patients. Results: 129 (74.6%) patients were H. pylori‐positive, 27 (96.4%) with DU, 3 (100%) with GU and 99 (69.7%) with NUD (P?P?Conclusions: In Serbia and Montenegro there is high seroprevalence of CagA‐positive H. pylori strains in dyspeptic patients with and without peptic ulcer, while VacA‐positive strains are more closely related to peptic ulcer disease.     

Endoscopic characteristics and Helicobacter pylori infection in NSAID-associated gastric ulcer

Background and Aim: Helicobacter pylori infection and non‐steroidal anti‐inflammatory drugs (NSAIDs) are deeply involved in the etiology of gastric ulcers. The aim of our study was to clarify the endoscopic characteristics and H. pylori infection status of NSAID‐associated gastric ulcers. Methods: The study group comprised 50 patients (23 men, 27 women; mean age 66.5 years) with NSAID‐associated gastric ulcers and 100 sex‐ and age‐matched patients with gastric ulcer associated with other factors (control group). Ulcer morphology, size and number of lesions, onset site and incidence of hemorrhagic ulcers were investigated endoscopically in both groups. H. pylori infection was diagnosed by serology, histology and ¹³C‐urea breath test. Results: Multiple lesions (68% vs 20%, P < 0.001), occurrence in the antrum (56% vs 6%, P < 0.001), and hemorrhagic ulcer (34% vs 4%, P < 0.001) were significantly more prevalent in patients with NSAID‐associated gastric ulcers than in patients with non‐NSAID‐associated gastric ulcer. The H. pylori infection rate was significantly lower in NSAID‐associated gastric ulcer patients than in non‐NSAID‐associated gastric ulcer patients (48% vs 96%, P < 0.001). In the NSAID‐associated gastric ulcer group, the prevalence of H. pylori infection was significantly lower in patients with ulcers in the antrum than in those with ulcers in the angulus or corpus (25% vs 77.3%, P < 0.001). Conclusions: In contrast to non‐NSAID‐associated gastric ulcers, NSAID‐associated gastric ulcers frequently occur in the antrum with bleeding. The rate of H. pylori infection in NSAID‐associated gastric ulcers is significantly lower than that in non‐NSAID‐associated gastric ulcers.     

Helicobacter pylori eradication in the healing of atrophic gastritis: A one-year prospective study

Objective. Whether gastric atrophy or intestinal metaplasia heals after successful treatment of Helicobacter pylori (H. pylori) infection is still a matter of controversy. The aim of this article was to clarify whether, after one year, H. pylori eradication is associated with healing in glandular atrophy and intestinal metaplasia in the corpus and antrum. Material and methods. Ninety-two H. pylori-positive peptic ulcer patients with atrophic gastritis (panatrophy, antral or corpus predominant) participated in the baseline study, 1-year prospective follow-up data being available from 76 patients. Mean age was 58±12.6 years (mean±SD) and the male/female ratio 2/1. The patients participated in an H. pylori eradication study in which they randomly received active eradication therapy. Endoscopy was performed before H. pylori eradication therapy and after 8 and 52 weeks, with specimens examined according to the Sydney system. Results. Of the 92 patients, 8 (9%) had panatrophy, 58 (63%) had antral- and 26 (28%) had corpus-predominant atrophic gastritis. After H. pylori eradication, the mean atrophy score declined in patients with antral-predominant atrophy from 1.5 (mean) to 0.7 (p<0.05), in corpus-predominant atrophy from 1.7 to 0.2 (p=NS) and in patients with panatrophy from 1.2 to 0.8 (p=NS). Atrophy healing was seen in 55% of antral-predominant atrophy patients who had successful H. pylori eradication.The mean antral atrophic score in one year declined in patients with duodenal ulcer (from 1.0 mean to 0.4) whereas it remained the same (1.3) in those with gastric ulcer (p<0.05). Conclusions. Atrophy can diminish or even disappear, especially in the antrum, during a 1-year follow-up after eradication of infection. Atrophy progression seems milder in patients with duodenal ulcer than in patients with gastric ulcer.     

Differing Patterns of Helicobacter pylori Gastritis in Patients with Duodenal,Prepyloric, and Gastric Ulcer Disease

Background: We investigated the risk relationship between histotopographic patterns of Helicobacter pylori gastritis and peptic ulcer site. Methods: Three hundred and eighty-three infected patients were classified as having duodenal ulcer (n = 79), prepyloric ulcer (n = 39), gastric (angular) ulcer (n = 28), and no ulcer (n = 237). Antral and corpus biopsy specimens were taken. Sydney system-based scores for bacterial density and activity and degree of gastritis were added to antral and corpus sum scores (SS) (range, 0-9). These were used to categorize the phenotype of gastritis. In addition, the presence or absence of mucosal atrophy was taken into account. The relative risk for ulcer association with these conditions was calculated. Results: High-grade antral (SS &gt; 5) associated with mild to moderate corpus (SS &gt; 5) gastritis increased duodenal (RR = 4.9; confidence interval (CI), 2.8-8.5) and prepyloric ulcer risk (RR = 2.99; CI, 1.4-6.2). High-grade gastritis in the antrum (SS &gt; 5) and corpus (SS &gt; 5) increased gastric ulcer risk (RR = 3.7; CI, 1.6-8.3). Antral atrophy and/or intestinal metaplasia is associated with an increased gastric ulcer risk (RR = 3.3; CI, 1.4-7.8). Conclusion: The pattern of H. pylori gastritis may define a risk for peptic ulcer at various sites, but additional factors, not reflected in histology, also contribute to this risk.     

Changes in the histology and function of gastric mucosa and in Helicobacter pylori colonization during a long-term follow-up period after vagotomy in duodenal ulcer patients

BACKGROUND/AIMS: To investigate changes in the histology and the Helicobacter pylori (H. pylori) prevalence and density of the gastric mucosa, as well as in fasting serum gastrin and serum pepsinogen I, depending on completeness of vagotomy, and in cases of recurrent ulcer, during 14 years after operation in duodenal ulcer patients. METHODOLOGY: 122 vagotomized duodenal ulcer patients were studied twice on average 9 and 14 years after operation. The presence of recurrent ulcer and completeness of vagotomy were assessed simultaneously endoscopically and by endoscopic Congo red test. The histology of the gastric antrum and corpus mucosa was assessed in accordance with the Sydney system. The amount of H. pylori in the specimens was detected by microscopic counting; gastrin and pepsinogen I in serum were determined radioimmunologically. RESULTS: During the 14-year follow-up period, complete vagotomy patients were characterized by a smaller amount of active antrum gastritis and a larger amount of active chronic corpus gastritis involving corpus atrophy in 46% of cases 14 years after operation. Recurrent ulcer patients were characterized by a significantly higher prevalence of high-grade H. pylori colonization and active mucosal inflammation in the antrum as well as by a lower level of active mucosal inflammation and atrophy in the corpus and a higher serum pepsinogen I level compared with complete vagotomy cases. The data of incomplete vagotomy patients without recurrent ulcer became more similar to those recorded for recurrent ulcer patients. CONCLUSIONS: In duodenal ulcer patients, changes in the histology of the gastric antrum and corpus mucosa as well as in H. pylori prevalence and density and in serum pepsinogen I levels are different depending on completeness of vagotomy during 14 years after operation.     

Size of the peptic ulcer in Helicobacter pylori-positive patients: association with the clinical and histological characteristics

Objective. Based on a large trial of Helicobacter pylori-positive peptic ulcer patients, we studied whether the size of the ulcer, along with other clinical and histological characteristics, has any effect on healing. We also studied the clinical and endoscopic characteristics associated with size of the peptic ulcer. Material and methods. A total of 333 consecutive patients with H. pylori infection and peptic ulcer were enrolled (mean age 54.8±12.7 years). Location of the ulcer was recorded by gastroscopy and the presence of H. pylori was assured by rapid urease test, histology and by serum H. pylori IgG and IgA antibody measurement. The diameter of the ulcer was measured by placing the opened biopsy forceps (7 mm) beside it. Biopsy specimens were examined in accordance with the Sydney system. Results. Mean size of the peptic ulcer was 13.2±8.3 in corpus, 11.3±5.3 in antrum, 13.8±7.8 in angulus, 9.5±5.3 in prepylorus and 9.2±4.7 mm in duodenum (duodenal versus gastric type; p<0.05). Average size of the ulcers was 9.4±5.3 mm in patients with Forrest III type and 11.5±6.8 in other types (p<0.05). Patients who were ≥50 years of age, currently smoking, or who had corpus-predominant chronic gastritis or atrophic gastritis, had larger ulcers than others. Size of index ulcers, successful eradication of H. pylori and the presence of atrophic gastritis were independent factors for healing. The odds ratio was 11.5 (95% CI 3.3–40.5; p<0.01) for eradication of H. pylori, 3.5 (95% CI 1.1–11.2; p<0.05) for size of the index ulcer (≤10 mm versus >10 mm) and 3.4 (95% CI 1.2–9.8; p<0.05) for atrophic gastritis versus no atrophy. Conclusions. Size of the peptic ulcer, successful H. pylori eradication and atrophic gastritis were independent factors for the healing of peptic ulcers. A number of clinical and endoscopic variables (age, current smoking, corpus-predominant gastritis, Forrest classification) were associated with size of the peptic ulcer in H. pylori-positive patients.     

Association between peroxisome proliferator-activated receptor-γ gene polymorphism (Pro12Ala) and Helicobacter pylori infection in gastric carcinogenesis

Abstract

Objective. Helicobacter pylori infection is accompanied by inflammatory processes leading to peptic ulcer and gastric cancer in the minority of infected individuals. The interaction between H. pylori virulence factors, host defense mechanisms and environmental factors determine the outcome of clinical manifestations. One of the host factors involved in the processes of inflammation and carcinogenesis is the peroxisome proliferator-activated receptor-γ (PPAR-γ) molecule. The present case–control study aimed to determine polymorphism of PPAR-γ gene and its association with H. pylori infection and gastrointestinal diseases (peptic ulcer and non-cardia gastric cancer) in Iranian patients. Materials and methods. One hundred and fifty-five patients with upper gastrointestinal diseases (76 peptic ulcer and 79 non-cardia gastric cancer) and 152 matched controls were genotyped for PPAR-γ gene polymorphism (Pro12Ala) by the PCR–RFLP method. Infection with H. pylori was confirmed by histology, the rapid urease test (RUT) and ELISA assay (IgG anti-H. pylori). Results. The frequency of PPAR-γ G (Ala 12) allele was significantly higher in H. pylori positive patients with non-cardia gastric cancer than in controls (22.8% vs. 3.9%, p = 0.027; OR = 3.28; 95% CI = 1.21–8.89), But there was no significant difference without infection (p = 0.7). Moreover, the PPAR-γ polymorphism was not associated with peptic ulcer in the presence or absence of H. pylori infection. Conclusion. Our results indicated PPAR-γ G allele may be an important contributor to non-cardia gastric cancer in Iranian H. pylori infected patients.     

Diagnostic value of rapid urease test and urea breath test for Helicobacter pylori detection in patients with Billroth II gastrectomy: A prospective controlled trial

AimThe aim of this work was to assess the reliability of rapid urease test (RUT) and urea breath test (UBT) for detecting Helicobacter pylori (H. pylori) in patients with Billroth II (BII) gastrectomy, using histology as reference.MethodsIn this prospective controlled study, 31 consecutive patients with BII gastrectomy and 73 controls who had an indication for endoscopy were included. Their H. pylori status was assessed with biopsies for histology, RUT and UBT. Histology served as the gold standard. Only the biopsies from the gastric fundus were evaluated. Specificity, sensitivity, positive and negative predictive value, degree of agreement and k-statistics were used.ResultsRUT and UBT for detecting H. pylori in the control group had excellent agreement [97%, kappa (k) = 0.94 and 99%, k = 0.97 respectively] with biopsies. In BII patients, RUT from fundic biopsies had very good agreement (87%, k = 0.74) compared to histology from fundic biopsies, whereas the UBT was unreliable (agreement: 71%, k = 0.41) compared to histology.ConclusionThe RUT from fundic biopsies in BII patients is a reliable test for H. pylori detection, whereas the UBT is unreliable.     

Long-Term Effects of Helicobacter pylori Eradication on Intestinal Metaplasia in Patients with Duodenal and Benign Gastric Ulcers

This study was conducted to investigate whether or not the eradication of H. pylori could lead to the regression of intestinal metaplasia (IM) in patients with either duodenal ulcer (DU) or benign gastric ulcer (BGU). The initial antral IM grade was 0.21 in the 72 patients of the H. pylori-eradicated DU group, this decreased to 0.17, 0.14, 0.13, and 0.09 after periods of four weeks, one year, two years, and four years, respectively, but without statistical significance. In the corpus of the DU group, where IM grade was low (0.02), there was no detectable change in IM. The initial antral IM grade of 0.69 in the 41 patients of the H. pylori-eradicated BGU group decreased substantially to 0.61, 0.44, and 0.39 after periods of four weeks and one and two years, respectively, but again without statistical significance. The initial corporal IM grade of the BGU group of 0.27 decreased to 0.20, 0.15, and 0.06 after periods of four weeks and one and two years, again without statistical significance. In contrast, the IM grades of the noneradicated DU group (N = 20) and the BGU group (N = 16) showed nearly no change in the antrum and corpus. Gastritis grades of antrum and corpus in the H. pylori-eradicated DU or BGU group significantly decreased with respect to time (P = 0.0001), but there were no significant changes in the corresponding noneradicated groups. Although there was no statistical significance, IM decreased in the antrum and corpus of the stomach with BGU and in antrum of those with DU over a two to four-year period after H. pylori eradication, suggesting the possible reversibility of IM.     

Preferential location of idiopathic peptic ulcers

Objective: Helicobacter pylori infection-negative, nonsteroidal antiinflammatory drugs (NSAIDs)-negative peptic ulcers, which are termed idiopathic peptic ulcers (IPUs), have been increasing worldwide. In this study, we investigated the preferential locations of gastric ulcers according to their cause (e.g., H. pylori and NSAIDs), with special attention to IPUs.

Material and methods: A total of 361 patients consecutively diagnosed with a peptic ulcer over a period of one year were classified into four groups according to H. pylori-infection status and NSAIDs usage. The ulcer location was divided into the antrum, angularis, and body, and was compared among the four ulcer groups.

Results: The ulcers of 43 patients were classified as IPUs. Compared with simple H. pylori ulcers, IPUs more preferentially located in the antrum (14% vs. 52%, p?H. pylori eradication or those with severe atrophic gastritis were excluded, and 79% of these IPUs were located in the antrum. With duodenal ulcers taken together, the vast majority of (86%) these IPUs occurred in the duodenal bulb or the antrum. The proportion of antral ulcers in NSAISs users also differed depending on the presence of concomitant H. pylori infection (positive: 22% vs. negative: 62%, p?Conclusion: There was a striking difference in the ulcer location within the stomach depending on the cause of the ulcer, and IPUs predominantly occurred in the antrum. This information on the preferential locations of ulceration should provide endoscopists with some hints concerning the etiology of ulcers.     

ACCURACY OF ENDOSCOPIC DIAGNOSIS OF HELICOBACTER PYLORI IN PATIENTS WITH HEMORRHAGIC PEPTIC ULCERS

Background: Recent progress in Helicobacter pylori eradication has resulted in dramatic improvements in the incidence of peptic ulcers and decreased rates of ulcer relapse. Because bleeding is an important complication of ulcer diseases, accurate diagnosis of H. pylori infection is necessary. Methods: We studied the efficacy of diagnostic methods to detect H. pylori in hemorrhagic peptic ulcer patients. A total of 59 patients who had received emergency endoscopy because of symptoms such as hematemesis, melena or tarry stool, were examined. Endoscopic methods of H. pylori diagnosis (culture, histological assessment and rapid urease test) and serum anti‐H. pylori assays were used in the hemorrhagic peptic ulcer group and the control group. Results: The percentage of endoscopically determined H. pylori‐negative patients was significantly higher in the hemorrhagic ulcer group than the control group (P < 0.05). Out of the endoscopically determined H. pylori‐negative patients in the hemorrhagic ulcer group, 78.9% were serologically H. pylori‐positive. Conclusion: Endoscopic methods are not sufficient for the diagnosis of H. pylori infection in hemorrhagic ulcer patients. Therefore, serum anti‐H. pylori assessment should also be performed for such patients.     

Helicobacter pylori in gastric corpus of patients 20 years after partial gastric resection

AIM: To determine the long-term prevalence of Helicobacter pylori (H pylori) gastritis in patients after partial gastric resection due to peptic ulcer, and to compare the severity of H pylori-positive gastritis in the corpus mucosa between partial gastrectomy patients and matched controls. METHODS: Endoscopic biopsies were obtained from 57 patients after partial gastric resection for histological examination using hematoxylin/eosin and Warthin-Starry staining. Gastritis was graded according to the updated Sydney system. Severity of corpus gastritis was compared between H pylori-positive partial gastrectomy patients and H pylori-positive duodenal ulcer patients matched for age and gender. RESULTS: In partial gastrectomy patients, surgery was performed 20 years (median) prior to evaluation. In 25 patients (43.8%) H pylori was detected histologically in the gastric remnant. Gastric atrophy was more common in H pylori-positive compared to H pylori-negative partial gastrectomy patients (P<0.05). The severity of corpus gastritis was significantly lower in H pylori-positive partial gastrectomy patients compared to duodenal ulcer patients (P<0.01). There were no significant differences in the activity of gastritis, atrophy and intestinal metaplasia between the two groups. CONCLUSION: The long-term prevalence of H pylori gastritis in the gastric corpus of patients who underwent partial gastric resection due to peptic ulcer disease is comparable to the general population. The expression of H pylori gastritis in the gastric remnant does not resemble the gastric cancer phenotype.