Most Helicobacter pylori-Infected Patients Have Specific Antibodies, and Some Also Have H. pylori Antigens and Genomic Material in Bile: Is It a Risk Factor for Gallstone Formation?

Bile may contain a 130-kDa protein endowed withaminopeptidase activity and the ability to promotecholesterol crystallisation. As > 90% of H. pyloristrains have a similar peptidase activity, and half the isolates express a 110- to 140-kDa antigen, theCagA protein, we investigated a possible associationbetween H. pylori infection and gallstones, and thepresence in bile samples of factors related to H. pylori that could increase cholesterolcrystallization. The prevalence of H. pylori infectionwas 82.1% in 112 patients with gallstones and 80.3% in112 controls (NS). Fifteen bile samples out of 23specimens from infected patients (65.2%) containedanti-CagA antibodies. A ~60-kDa antigen only reactingwith an anti-CagA antibody was found in five bilesamples (21.7%) from 23 infected patients. One bilesample (4.1%) contained ureA and cagA genes of H.pylori. The homology of CagA with the N-terminalsequence of aminopeptidase N was very low. We concludedthat the presence of specific antibody to H. pylori in most bile samples tested and of an H. pyloriputative antigen in a discrete number of cases mayrepresent factors that increase the risk of gallstoneformation.     

Ammonia, Hydrogen Peroxide, and Monochloramine Retard Gastric Epithelial Restoration in Rabbit Cultured Cell Model

Ammonia (NH₃), hydrogen peroxide(H₂O₂) and monochloramine(NH₂Cl) produced by Helicobacter pyloriinfection might be responsible for mucosal injury. Theaim of this study was to evaluate the role ofNH₃, H₂O₂, andNH₂Cl in the restoration of rabbit primarycultured gastric mucosal cells with a wound repairmodel. Artificial wounds were made in confluentmonolayer gastric epithelial cell sheets by mechanicaldenudation, and changes in the size of the cell-freearea were analyzed quantitatively. Cell proliferation was assessed by bromodeoxyuridine staining. Incontrols, the wound healed within 48 hr. However,mucosal cell repair was inhibited by treatment withNH₃, H₂O₂, andNH₂Cl in a dose-dependent manner. These resultsindicate that NH₃,H₂O₂, and NH₂Clretarded the wound healing, which included epithelialcell migration and proliferation of gastric mucosa. Therefore, it is suggestedthat NH₃, H₂O₂, andNH₂Cl delays the healing process of pepticulcers.     

Low Prevalence of Helicobacter pylori Infection in Patients with Hamartomatous Fundic Polyps

Helicobacter pylori infection of the gastricmucosal surface was investigated in patients withhamartomatous fundic polyps or hyperplastic polyps andin patients without endoscopic evidence of disease(healthy subjects). Presence of H. pylori infection wasdetermined by culture, histologic examination, and theendoscopic phenol red test. Adherence of H. pylori wasevaluated with scanning electron microscopic examination of antral biopsy specimens. Bothprevalence of H. pylori infection (P < 0.001) and H.pylori adherence (P < 0.05) were less in patientswith hamartomatous fundic polyps than in healthy subjects and patients with hyperplastic polyps.However, the percentages of plasma cells in gastricmucosa that contained IgA and of gastric epithelialcells that expressed Lewis b did not differsignificantly among the three groups. These findings suggestthat defense mechanisms against the attachment of H.pylori other than IgA or Lewis b antigen are present inpatients with hamartomarous fundic polyps.     

Helicobacter pylori Eradication Ameliorates Primary Raynaud's Phenomenon

Raynaud's phenomenon is defined by anintermittent vasospasm of the arterioles of the distallimbs. Helicobacter pylori infection has been recentlyassociated with Raynaud's phenomenon. The aim of this study was to assess the effects of H. pylorieradication on Raynaud's attacks. Forty-six patientsaffected by primary Raynaud's phenomenon were evaluated.H. pylori infection was assessed by [¹³C]urea breath test. Eradication therapy was given toinfected patients for seven days. Discomfort and theduration and frequency of attacks of Raynaud'sphenomenon per week were assessed. Thirty-six subjectswere infected with H. pylori; the bacterium waseradicated in 83% of these after therapy. Attacks ofRaynaud's phenomenon completely disappeared in 17% ofthe patients with H. pylori eradication. Discomfort and the duration and frequency of attacks ofRaynaud's phenomenon were significantly reduced in 72%of the remaining patients. Conversely, attacks ofRaynaud's disease did not change significantly during the 12-week follow-up period either in the H.pylori-negative patients or in the infected subjects inwhom the bacterium was not eradicated by therapy. Thestudy shows that H. pylori eradication causes a significant decrease in clinical attacks ofRaynaud's disease. The reduction of vasoactivesubstances determined by the eradication of thebacterium may be the pathogenetic mechanism underlyingthe phenomenon.     

Recurrence of Helicobacter pylori Infection After Successful Eradication (Nature and Possible Causes)

Recurrence of Helicobacter pylori infectionafter successful eradication occurs and is associatedwith relapse of gastroduodenal diseases. The aims ofthis paper were to assess the incidence and identify the nature and possible causes of recurrence ofthe infection. A broad-based Medline search wasperformed to identify all related publicationsaddressing recurrence of the infection between 1986 and1995. The 12-month recurrence rate varied among thedifferent studies from 0 to 41.5%. A few studies showed18- to 24-month recurrence rates, which ranged between0 and 21.4%. Limited data, obtained using molecular fingerprinting techniques, have shown that inmost cases recurrence is due to recrudescence of theoriginal strain; a few cases appear to be due toreinfection with a new strain. Recrudescence is mostlikely during the first 12 months after apparenteradication. Despite the high sensitivity andspecificity of the available individual tests fordetecting H. pylori infection in untreated patients, notechnique alone is sensitive enough to monitoreradication when the four-week-rule definition foreradication is used. A combination of two or moretechniques increases sensitivity. Sensitivity andspecificity are increased when biopsies are taken from bothgastric antrum and corpus. The best treatments have thelowest recurrence rates and recurrence is rare when theeradication rate is over 90%. Individual susceptibility and reexposure to H. pylori are suggested astwo major causes of reinfection.     

Regional Differences on Production of Chemokines in Gastric Mucosa Between Helicobacter pylori-Positive Duodenal Ulcer and Gastric Ulcer

It is well known that antrum-predominantgastritis and pan-gastritis occurs in the patients withHelicobacter pylori-positive duodenal ulcer (DU) andgastric ulcer (GU), respectively. However, the role of chemokines in the pathogenesis of thesepathologies is unclear. We examined the regionaldifferences in mucosal chemokine production in patientswith DU and GU. The production of interleukin-8 (IL-8), growth-related gene (GRO) , andmacrophage inflammatory protein (MIP)-1 wasgreater in the antrum than in the corpus in DU patients.In the patients with GU, monocyte chemoattractantprotein (MCP)-1 levels in the mucosa adjacent to ulcer weregreater than those away for the ulcer in the corpus. Thereduction in chemokine production occurring inassociation with the eradication of H. pylori differed between DU and GU patients in the antrum (IL-8,P = 0.0394; GRO, P = 0.0149; MIP-1, P =0.0246; MCP-1, P = 0.0087). The data imply a differentpathogenesis may exist for the gastritis present in patients with DU and GU occurring in H.pylori-positive individuals.     

The Influence of Helicobacter pylori Infection on the Development of Gastric Ulcer in Symptomatic Patients after Bariatric Surgery

Background: There are few data relating to the role of H. pylori infection and surgical procedures on the occurrence of gastric ulcer following bariatric surgery. Methods: Subjects with upper gastrointestinal symptoms after bariatric surgery and receiving gastroscopic examinations were prospectively enrolled. All clinical data including age, sex, BMI before surgery, and surgical method were recorded. IgG antibodies against H. pylori were measured in preoperative serum by enzyme-linked immunosorbent assay (ELISA). Results: A cohort of 636 patients undergoing laparoscopic vertical banded gastroplasty (LVBG) or Roux-en-Y gastric bypass (LRYGBP) was recruited. The seropositivity of H. pylori in symptomatic and asymptomatic patients after surgery was 39% (32/82) and 39.7% (220/554) respectively. Endoscopic examinations revealed that 22 (26.8%) of 82 symptomatic patients had a gastric ulcer. Comparison of demographic characteristics between patients with ulcer (n=22) and patients without ulcer (n=60) showed no difference in distribution of gender, age, BMI, and seroprevalence of H. pylori (27.3%, 6/22 vs 43.3%, 26/60, P=0.212). Patients undergoing LRYGBP showed a higher rate of gastric ulcer (45.5%, 10/22) when compared to patients undergoing LVBG (20%, 12/60; P=0.027). Conclusion: Gastric ulcers in symptomatic patients following laparoscopic bariatric surgery are related to surgical procedures rather than exposure to H. pylori infection.     

The Influence of Helicobacter pylori Infection and Corpus Gastritis on the Postoperative Outcomes of Laparoscopic Vertical Banded Gastroplasty

Background: Helicobacter pylori (HP) infection is linked to weight control through gastric inflammation-induced deregulation of satiety-related hormone, and eradication of HP before a weight reduction operation has been advocated. We aimed to examine the impact of HP infection and corpus gastritis on preoperative patient characteristics, postoperative complications and weight loss following laparoscopic vertical banded gastroplasty (LVBG). Methods: A prospective cohort of 152 patients undergoing LVBG was enrolled. Gastric specimens at the corpus were obtained during LVBG operation and scored histologically according to the Sydney classification of gastritis. Excess weight loss, and early and late complications following LVBG, were recorded and correlated. Results: 63 and 89 patients were identified as HP positive and negative groups respectively. The prevalence of individual components of the metabolic syndrome was comparable in both groups except hypertension. The occurrence of early and late complications, either minor or major, in both groups was similar. The severity of gastritis was correlated positively with age and negatively with preoperative BMI and excess weight. Patients with higher neutrophil activity, chronic inflammation, and HP density experienced less excess weight loss at 24 to 48 months follow-up. The impact of gastritis on weight loss became less recognizable after 48 months follow-up. Conclusions: HP infection and gastric inflammation play a significant role in the amount of weight loss after LVBG. Further prospective studies should examine possible mechanisms and long-term effects on weight loss to determine the utility of preventive eradication of HP in different types of bariatric surgery.     

Gastric Ghrelin Expression Associated with Helicobacter pylori Infection and Chronic Gastritis in Obese Patients

Background: Helicobacter pylori is a major pathogen of stomach. Ghrelin is secreted from the stomach, and it plays a role in the coordination of eating behavior, and facilitates fat storage and weight regulation. The effects of H. pylori infection on gastric ghrelin production are still not well known. Recent exciting studies linked H. pylori infection to ghrelin, then to obesity. The aim of the present study is to investigate gastric ghrelin immunoreactivity associated with H. pylori infection, chronic gastritis and the clinical correlation in obese patients. Methods: The histologic findings of stomach were examined in 156 patients who were undergoing laparoscopic vertical-banded gastroplasty for obesity. Ghrelin immunoreactivity was evaluated immunohistochemically with an anti-ghrelin antibody, and the density of ghrelin-positive cells determined per total glands of the gastric mucosa. Relationship between density of ghrelin-positive cells, histopathology of chronic gastritis scored by the Sydney system and clinical correlation was analyzed. Results: H. pylori was present in 62 (39.7%) out of 156 patients. The density of ghrelin-positive cells was significantly lower for H. pylori-infected patients. There was a significant stepwise decrease in density of ghrelin-positive cells, with progression of histological severity of chronic inflammation, neutrophil activity and glandular atrophy in the corpus. Obese patients positive for H. pylori were associated with older age and abnormal plasma triglyceride level, but not with sex, body mass index, liver function tests or glucose level. There was no relationship between density of gastric ghrelin-positive cells and body mass index. Conclusion: H. pylori infection has a negative impact on density of gastric ghrelin-positive cells in obese patients. Impaired density of gastric ghrelinpositive cells is associated with neutrophil activity, chronic inflammation and glandular atrophy induced by H. pylori infection. The potential role of H. pylori infection and density of gastric ghrelin-positive cells on the development of obesity and their biological significance warrants further investigation.     

Comparison of Two Rapid Urease Tests for Detection of Helicobacter pylori Infection

Rapid urease tests are widely used at endoscopyto determine the presence of Helicobacter pyloriinfection. In this prospective study, we compared theaccuracy of two rapid urease tests, CLOtest andPyloriTek, using histology as the gold standard.Histologic staining was performed using both H&E andGiemsa, and all slides were reviewed by a singlepathologist who was blinded to the results of the rapidurease tests and endoscopic findings. One hundred twopatients were enrolled; their mean age was 59 years(range 16 to 95 years), and there were 45 males and 57females. Histology confirmed the presence of H. pylori infection in 39% of patients. Theproportions of false positives for CLOtest (8.0%) andPyloriTek measured at 1 hr (29.0%) were significantlydifferent (Z = 2.90, P = 0.0038). No significantdifference was seen between the proportions of falsenegatives. We conclude that the clinical usefulness ofPyloriTek urease test is limited by its lack ofspecificity.