Density of Gastric Helicobacter pylori Colonization Is Not Associated with Occurrence of Dyspeptic Symptoms

In most studies, the prevalence of Helicobacterpylori infection in patients with dyspeptic symptomsdoes not clearly differ from the prevalence inasymptomatic controls. However, the degree of H. pylori colonization might play a role for theoccurrence and severity of dyspeptic symptoms. BetweenAugust 1993 and July 1994, we screened 1500 apparentlyhealthy volunteers (1036 men, 464 women, 42 ± 12years) for H. pylori infection using the[¹³C] urea breath test. The noninvasive ureabreath test enables a semiquantitative assessment of theextent of H. pylori colonization in the stomach. Of the1500 volunteers, 526 (35.1%) complained of occasional orfrequent dyspeptic symptoms. No difference was observedin the H. pylori prevalence between asymptomaticsubjects (35.5%) and those with dyspeptic symptoms(35.9%; P > 0.95). A high density of H. pyloricolonization in the gastric mucosa was not associatedwith a higher frequency of dyspepsia (P > 0.80).According to these findings, an eradication therapy onthe basis of dyspeptic symptoms alone cannot berecommended as H. pylori is not a proven etiology ofdyspepsia.     

Helicobacter pylori-Positive Functional Dyspepsia in Elderly Patients Comparison of Two Treatments

The association of Helicobacter pylori andfunctional dyspepsia is not well defined. The role of H.pylori on dyspeptic symptoms is still controversial. Theaim of this study is to confirm the efficacy of H. pylori eradication by two differentcommonly used treatment regimens, as well as to examinethe improvement of the dyspeptic symptoms by eradicatingH. pylori. H. pylori functional dyspepsia is prevalent in people over 60 years old. In this age groupwe treated 126 patients with bismuth plus metronidazoleand amoxicillin (group A, 67 patients) versus omeprazoleplus amoxicillin (group B, 59 patients). Results were statistically analyzed utilizing theWilcoxon signed-rank test, McNemer test and chi-squaretest; P < 0.05 was considered significant. Two monthsafter the end of therapy we observed an eradication rate of 66.1% in group A vs 64.3% in group B.All treated patients showed improvement insymptomatology. Although there was no significantdifference between patients in whom H. pylori was or wasnot eradicated within the respective groups, when examiningall H. pylori-positive patients versus H.pylori-negative posttreatment patients, there was asignificant reduction (P < 0.05) in all four symptomsof functional dyspepsia measured. In conclusion, we suggestthat patients treated with H. pylori-eradicatingtherapeutic regimens have an improvement in functionaldyspepsia symptoms. We shall prefer the dual therapy as compared to the triple therapy. We believethat eradicating treatment to eradicate H. pylori in theelderly patients with H. pylori -related functionaldyspepsia will reduce health care costs by reducing the number of subsequent visits.     

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.     

Helicobacter pylori and Mucosal Atrophy in Patients with Gastric Cancer (A Special Study Regarding the Methods for Detecting Helicobacter pylori)

We assessed the sensitivities of several methodsfor detecting Helicobacter pylori (culture, histology,rapid urease test, and serology), and evaluated the H.pylori positivity considering the degree of atrophy in the background mucosa in 202 gastriccancer patients and 101 controls. The positivity of H.pylori determined by culture (81%) was significantlyhigher than that determined by serology (62%) in gastric cancer patients (P < 0.001). Thepositivities of H. pylori determined by biopsy and/orserology in intestinal (84%) and diffuse (95%) types ofgastric cancer were higher than that observed in controls (54%) (P < 0.001).Intestinal-type gastric cancer tended to occur in theatrophic mucosa, in which H. pylori positivity was notdifferent from that in controls after adjusting for thedegree of atrophy, whereas diffuse-type gastric cancerwas observed more often in the nonatrophic mucosa, inwhich H. pylori positivity was higher than that incontrols even after adjusting for the degree ofatrophy.     

Antibiotic Properties of Bovine Lactoferrin on Helicobacter pylori

To investigate a potential new treatment forgastric Helicobacter pylori infection, we have examinedthe use of the natural antibiotic lactoferrin, found inbovine milk, for activity against Helicobacter species both in vitro and in vivo. Lactoferrinwas bacteriostatic to H. pylori when cultured atconcentrations 0.5 mg/ml. Growth of H. pylori wasnot inhibited by another milk constituent, lysozyme, or by a metabolite of lactoferrin, lactoferricinB, but growth was inhibited by the iron chelatordeferoxamine mesylate. Lactoferrin inhibition of growthcould be reversed by addition of excess iron to the medium. Lactoferrin in retail dairy milk wasfound to be more stable intragastrically thanunbuffered, purified lactoferrin. Treatment of H.felis-infected mice with lactoferrin partially reversedmucosal disease manifestations. It is concluded thatbovine lactoferrin has significant antimicrobialactivity against Helicobacter species in vitro and invivo. Bovine lactoferrin should be further investigated for possible use in H. pylori infections inman.     

Helicobacter pylori Infection and Peptic Ulcer Disease in Cirrhosis

An increased frequency of peptic ulcer diseaseis noted in patients with cirrhosis, but the role of H.pylori in this disorder remains to be determined. Thediagnosis of cirrhosis was confirmed by a combination of clinical, biochemical, radiological, andhistological methods. The severity of cirrhosis wasassessed by Pugh's modification of Child's criteria.Upper gastrointestinal endoscopy was performedconsecutively to evaluate the presence of varices andgastroduodenal mucosa. H. pylori status was assessed byhistology, urease test, and serology. In all, 130patients with cirrhosis were recruited into the study;there were 86 males and 44 females with a mean (SD)age of 54.4 (12.7) years. The H. pylori prevalence was76.2% . There was no difference in age between the H.pylori-positive and -negative cirrhotics (P = 0.29). The H. pylori prevalence revealed no differenceamong cirrhotics with Child A (77.8%), Child B (72.9%),and Child C (78.6%) (P = 0.8), and neither was there adifference in H. pylori prevalence in cirrhotics with and without congestive gastropathy (77% vs73.7% , P = 0.84). The prevalence of H. pylori incirrhotics with and without varices did not show astatistical difference (75% vs 81.8%, P = 0.68). There also was no difference in the H. pyloriprevalence between cirrhotic patients with and withoutpeptic ulcers (84.4% vs 69.7% , P = 0.09). Inconclusion, the prevalence of H. pylori or peptic ulceris independent of the severity of cirrhotic liver disease. Theassociation between H. pylori infection and peptic ulcerdisease is weak in cirrhosis.     

Delayed Gastric Emptying by Helicobacter pylori Lipopolysaccharide in Conscious Rats

The present study was carried out to investigatethe possibility that lipopolysaccharide deprived fromHelicobacter pylori may alter gastric motility. Toaddress the question, we examined the effect of H. pylori lipopolysaccharide on gastricemptying in conscious rats. Gastric emptying wasevaluated by the phenol red method. Time-course anddose-related effects of intraperitoneal administrationof H. pylori lipopolysaccharide were investigated.Intraperitoneal injection of H. pylorilipopolysaccharide significantly suppressed gastricemptying of a liquid meal in a dose-dependent manner.The inhibitory action of H. pylori lipopolysaccharide wasobserved 2, 4, 8, or 12 hr after the injection. Theseresults suggest for the first time that H. pylorilipopolysaccharide may suppress gastric emptying in along-lasting fashion. It is also suggested that H. pylorimay influence gastric function through its cell wallstructure named lipopolysaccharide.     

High Prevalence of Helicobacter pylori in Liver Cirrhosis (Relationship with Clinical and Endoscopic Features and the Risk of Peptic Ulcer)

In 153 consecutive patients with cirrhosis weassessed: (1) the prevalence of IgG to Helicobacterpylori and compared it with that found in 1010 blooddonors resident in the same area; and (2) therelationships of IgG to Helicobacter pylori with clinical andendoscopic features and with the risk of peptic ulcer.The IgG to Helicobacter pylori prevalence of cirrhoticswas significantly higher than in blood donors (76.5% vs 41.8%; P < 0.0005) and was notassociated with sex, cirrhosis etiology, Child class,gammaglobulins and hypertensive gastropathy. In bothgroups, the prevalence of IgG to Helicobacter pylori was significantly higher in subjects over 40. Amongpatients with cirrhosis a significantly higherprevalence of Helicobacter pylori was found in patientswith previous hospital admission (P = 0.02) and/or upper gastrointestinal endoscopy (P = 0.01) andpatients with peptic ulcer (P = 0.0004). Multivariateanalysis identified increasing age and male sex as riskfactors for a positive Helicobacter pylori serology and no independent risk factors for pepticulcer. The high prevalence of Helicobacterpylori-positive serology found in the present series isrelated to age and sex and might also be explained byprevious hospital admissions and/or uppergastrointestinal endoscopy. Our results do not confirmthe role of Helicobacter pylori as risk factor forpeptic ulcer in patients with liver cirrhosis.     

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.     

Use of Chopsticks for Eating and Helicobacter pylori Infection

Epidemiological data suggests that ethnic groupsusing chopsticks for eating have a higher prevalence ofH. pylori infection. This study investigated thecarriage of H. pylori in chopsticks after eating. Used chopsticks and saliva were collected fromasymptomatic individuals whose H. pylori status wasdetermined by [¹³C]urea breath test andserology. Both the saliva specimens and chopsticks werecultured and processed by polymerase chain reaction(PCR) for the detection of H. pylori . Furthermore,chopsticks used by hospital staff in the cafeteria werepooled for the detection of H. pylori by bacteriologic culture and PCR. Sixty-nine volunteers wererecruited in the first study and 45 (65%) were diagnosedto have H. pylori infection. While all cultures werenegative, H. pylori was detected by PCR in the saliva from 15 (33%) infected subjects and in thechopsticks from one (2%). Among the 12 sets of pooledchopstick-washing studied, H. pylori was detected by PCRin two sets. This study showed that H. pylori was rarely detected in chopsticks after eating andhence, the risk of contracting this infection via theuse of chopsticks is low.     

Development of Helicobacter pylori Infection Model in BALB/c Mice with Domestic cagA-Positive and-Negative Strains in Taiwan

We aimed to develop an H. pylori-infected mousemodel using clinically stored strains in Taiwan and totest whether development of H. pylori infection in an invivo animal model is related to the status of the cagA gene. A total of 100 male BALB/cmice, 6-8 weeks old, including 80 in the experimentalgroup and 20 in the control group, were used. Twoclinically stored H. pylori isolates, a cagA-positive and a cagA-negative strain, were selected toinduce the H. pylori infection in half (N = 40) of themice in the experimental group. Bacterial isolates of0.8 × 10⁹ CFU/ml were orally inoculatedin each mouse of the experimental group for threeconsecutive days. Ten mice in the control group weresacrificed to confirm the initial absence of H. pylori.Eight weeks after inoculation of the experimental group and no inoculation of the remaining 10mice of the control group, each mouse was killed.Gastrectomy was then performed for rapid urease test(CLOtest) and histology. In the control group, none of 20 mice had positive results from the CLOtestor histology. In contrast, excluding eight of 80 micethat died before the eighth week, 90.3% (65/72) of themice challenged with H. pylori showed persistent presence of H. pylori by histology. Theseverity of gastritis at the eighth week was moreevident in H. pylori-infected mice than in control andnoninfected mice (P < 0.05). Although gastritis wasmore severe in mice inoculated with thecagA-positive strain than with the cagA-negative strain,the rates of H. pylori infection in mice were notdifferent between cagA-positive and -negative strains(91.4% vs 89.2%, P > 0.05). In summary, storedstrains of H. pylori can be applied to induce aninfection model in BALB/c mice. The less virulentcagA-negative strain can induce H. pylori infection inmice as effectively as the cagA-positive strain. Thehigh prevalence of cagA-positive strains in Taiwanesepatients may be related to factors other than only thecagA gene of the bacteria.     

Role of Helicobacter pylori Infection on Upper Gastrointestinal Bleeding in the Elderly (A Case-Control Study)

Nonsteroidal antiinflammatory drug (NSAID) useis known to be associated with a high incidence of uppergastrointestinal tract bleeding in the elderly. Theincreased prevalence of Helicobacter pylori (HP) infection, which also occurs with age, suggeststhat an interaction between NSAID use and HP infectionmay explain the higher incidence of ulcer complicationsin the elderly. The aim of the present study was to determine if a relationship existsbetween HP infection and NSAID use in elderly patientswith upper gastrointestinal bleeding. This was a case-control study on 146 elderly patients (73/group). The bleeding group consisted of 37 males and 36females (mean age 80.4 years, range 70-96) with symptoms(hematemesis, melena, anemia with loss of more than 3 ghemoglobin), and endoscopic stigmata of bleeding. The control group consisted of 73 age- andsex-matched patients with the same endoscopic diagnosisbut with no endoscopic stigmata of bleeding. NSAID usewas evaluated by interview at the time of endoscopy, and HP infection was confirmed in all cases byhistology and the rapid urease test. Statisticalanalyses were performed using the chisquare test andlogistic regression. In both groups, 46.57% of patients were affected with gastric ulcer, 36.98% withduodenal ulcer, and 16.43% with erosive gastritis. Thebleeding group had a significantly higher percentage ofNSAID users (53.42% vs 19.17%, P < 0.0001) and a lower percentage of HP-positive patients(47.94% vs 72.60%, P = 0.004). The NSAID use pattern wasas follows: occasional users (sporadic, as needed duringthe previous week): 53.8% of bleeding cases and 50% of controls; acute users (continuoustherapy for less than one month): 17.9% of bleedingcases and 28.5% of controls; and chronic users(continuous therapy for more than one month): 28.2% ofbleeding cases and 21.4% of controls. The logisticregression demonstrated that NSAID use was significantlyrelated to an increase risk of bleeding both in gastric(odds ratio: 4.98, 95% CI: 1.83-13.6) and duodenal ulcer patients (odds ratio: 10.2, 95% CI: 2.25-46.7) while HP-positivity presented a significantinverse relationship with bleeding only in subjects withgastric lesions (odds ratio: 0.20, 95% CI: 0.07- 0.55). NSAID use and HP infection were alsoshown to be independent, unrelated factors, with theoverall risk of bleeding in HP-positive NSAID usersidentified to be significantly less than in HP-negative NSAID users. In conclusion, in elderlypatients: (1) NSAID use increases the risk of uppergastrointestinal bleeding while HP infection wasassociated with a low risk for gastric bleeding; and (2)the two factors are independent variables, thereforethe HP-positive NSAID user has a lower risk than theHP-negative NSAID user.     

Prevalence of Helicobacter pylori Infection in Children from Urban and Rural West Virginia

Our objective was to evaluate the prevalencerate of Helicobacter pylori (HP) in children from urbanand rural areas of West Virginia. In all, 1164 bloodsamples were collected from children who attended a local health fair, pediatric clinics, andemergency departments of four different hospitalslocated in urban and rural counties. Socioeconomicstatus was determined in 303 children. Serum HP antibody (IgG) was measured by enzyme immunoassay (EIA).A total of 468 (40%) samples were HP positive. HPacquisition correlated with increasing age, familycrowding, and community location (urban/rural) but not with gender, water source used (city/well), orsocioeconomic status. The prevalence rate of HP in thechildren of West Virginia is higher than any datapreviously reported from the United States. The results correlated with only few socioeconomiccriteria, suggesting that other factors may contributeto the increased prevalence of HP infection in thechildren of West Virginia.     

Helicobacter pylori Stool Antigen Test (Clinical Evaluation and Cost Analysis of a New Enzyme Immunoassay)

Noninvasive tests for Helicobacter pylori areincreasingly used. Recently, an enzyme immunoassay forH. pylori detection in feces has been put on the market.Aim of this multicenter study was to evaluate the usefulness of this novel test as apredictor of H. pylori status in the pretreatmentsetting. Three hundred consecutive patients wereenrolled. None of the patients had received anyeradicating treatment in the last 12 months, and all underwentgastroscopy with biopsies of the antrum and body forhistology (H) and rapid urease test (RUT). H. pyloristatus was defined positive (or negative) if both H and RUT were positive (or negative). When H and RUTgave conflicting results, the patients were classifiedas H. pylori indeterminate. A stool specimen wascollected for each patient and tested by using a novel enzyme immunoassay for H. pylori detection(HpSAT). Sensitivity, specificity, and diagnosticaccuracy of the test were calculated, as was the cost ofeach assay. H. pylori status was positive in 159patients, negative in 131, and indeterminate in 10. HpSATgave evaluable results (positive or negative) in 293patients, and doubtful results in 7 (2.3%). Sensitivity,specificity, and diagnostic accuracy of HpSAT were 96.8%, 89.7%, and 93.6% respectively.Considering the H. pylori-indeterminate patients aspositive, the percentages were 95.8%, 98.7%, and 93.2%respectively. The cost for each assay was about US $27. These results suggest that HpSAT is anoninvasive, simple, reliable, fast, and cheap methodfor evaluating H. pylori status in the pretreatmentsetting.     

Bovine Milk Inhibits Both Adhesion of Helicobacter pylori to Sulfatide and Helicobacter pylori-Induced Vacuolation of Vero Cells

Adhesion of Helicobacter pylori to gastricmucosal cells is an initial important step incolonization and infection. To study adhesion, weinvestigated whether milk inhibits the adhesion ofHelicobacter pylori to sulfatide, an acidicglycosphingolipid that exists in human gastric mucosaand to which Helicobacter pylori adheres. As a measureof functional significance, we also studied whether milkinhibits Helicobacter pylori-induced vacuolation of Verocells. We used sulfatide-coated polystyrene plates andstudied the effect of bovine milk on the adhesion ofHelicobacter pylori to sulfatide. We used Vero cells for Helicobacter pylori -inducedvacuolation. Bovine milk 100- to 200-fold dilutedsignificantly inhibited both adhesion of Helicobacterpylori to sulfatide and Helicobacter pylori-inducedvacuolation in Vero cells. Bovine milk significantlyinhibited adhesion of Helicobacter pylori to MKN-45cells and Lewis b antigen-coated polystyrene plates. Inaddition, these results suggest that bovine milkcontains active substances that inhibit both adhesion ofHelicobacter pylori to mucosa and vacuole formation.Bovine milk may have a protective effect on the gastricmucosa in Helicobacter pylori-associatedgastritis.     

Potential Relevance of Agmatine as a Virulence Factor of Helicobacter pylori

The polyamine agmatine is able to increasegastric acid secretion. Therefore, we investigatedwhether Helicobacter pylori is able to form and releaseagmatine in vitro and in the human stomach in vivo , and if so, whether a relationship exists amongagmatine concentration in gastric juice, H. pyloriinfection, and gastroduodenal lesions. Agmatine wasdetermined by means of HPLC. In the supernatant of H. pylori cultures, agmatine concentrations up to1500 ng/ml (~12 M) were determined, depending on thenumber of the bacteria in the individual cultures.Agmatine concentration in gastric juice from H. pylori-positive patients was higher than inthat from H. pylori-negative patients. Gastrin in bloodwas elevated in H. pylori-positive patients comparedwith H. pylori-negative patients. Agmatine concentration in gastric juice and serum gastrin levelappeared to be related. In conclusion, H. pylori is ableto form and to release agmatine in vitro and in vivo.This may be assumed to be relevant in vivo, since higher amounts of agmatine are present ingastric juice from H. pylori-positive than from H.pylori-negative patients. Accordingly, agmatine producedby H. pylori may be a virulence factor of this bacterium and may be involved in the pathogenesis ofgastroduodenal lesions.     

Beneficial Effects of Helicobacter pylori Eradication on Idiopathic Chronic Urticaria

Helicobacter pylori, the most important cause ofgastritis and peptic ulcer, recently has been associatedwith several extradigestive diseases. The aim of thisstudy was to assess the prevalence of Helicobacter pylori infection and the effects of bacteriumeradication in 42 consecutive patients affected byidiopathic chronic urticaria. Helicobacter pylori wasassessed by [¹³C]urea breath test.Amoxicillin, clarithromycin, and lansoprazole were given to infectedpatients for seven days. Urticaria and gastrointestinalsymptoms were assessed on enrollment and aftereradication. Fifty-five percent of patients proved to beinfected by Helicobacter pylori. Prevalence ofgastrointestinal symptoms did not differ betweeninfected and uninfected patients. Eighty-eight percentof infected patients in whom the bacterium waseradicated after therapy showed a total or partial remission ofurticaria symptoms. Conversely, symptoms remainedunchanged in all uninfected patients. In conclusion,Helicobacter pylori affects a high percentage ofpatients with idiopathic chronic urticaria; however,typical gastrointestinal symptoms do not identifyinfection status. Bacterium eradication is associatedwith a remission of urticaria symptoms, suggesting apossible role of Helicobacter pylori in the pathogenesisof this skin disorder.     

Touch Cytology (A Reliable and Cost-Effective Method for Diagnosis of Helicobacter pylori Infection)

A variety of reliable methods are available fordetecting Helicobacter pylori (Hp) during uppergastrointestinal endoscopy. We evaluated the clinicalutility and cost-effectiveness of rapid urease test (RUT), touch cytology (TC), and histology (H).Two hundred thirty-eight consecutive patients (178without previous medical treatment and 60 formerlytreated with anti-Hp therapy) were tested for Hpinfection by RUT, TC, and H (H&E stain). Theinfection status for each patient was established by aconcordance of two test results. The time to carry outthe three tests and their cost were also calculated. Sensitivity of TC (100%) was significantlyhigher than that of RUT (86.8%; P < 0.001), but notthan that of H (94.9%). RUT was significantly morespecific than H (100% vs 95.6%; P < 0.05), but not than TC (96.4%). Hp infection was more frequentin the patients with chronic active gastritis than inthose with chronic nonactive gastritis (P < 0.001).No Hp infection was detected in absence of chronic antral inflammation. RUT resulted the cheapestmethod and H the most expensive; TC is faster andcheaper than H. When additional information about theseverity of mucosal damage or the presence of cell atypias is not necessary, histologicexamination can be omitted, and a cost-effectivestrategy for assessing Hp status might consist in takingtwo antral biopsies, the former for performing RUT andthe latter for preparing a slide by TC, whichshould be stained and examined only when the RUT resultis negative.     

Asymptomatic Helicobacter pylori Gastritis Is Associated with Increased Sucrose Permeability

Our aim was to investigate whether there arechanges in permeability to sucrose in asymptomaticHelicobacter pylori gastritis. Nineteen asymptomaticsubjects with Helicobacter pylori associated gastritis with no or mild mucosal atrophy and 19 age- andsex-matched normal controls were studied by peroral loadof sucrose (100 g). The fraction of the given oral doseof sucrose excreted in urine was increased in subjects with Helicobacter pylori gastritis(median 0.08% versus 0.04% in controls). Sucroseexcretion was not related to atrophy, intestinalmetaplasia, or inflammation in the gastric mucosa.However, sucrose permeability was related to the degreeof inflammatory (neutrophil) activity, since moderateactivity was associated with higher sucrose excretionthan mild activity (median 0.13% vs 0.07% ).Asymptomatic Helicobacter pylori gastritis was associatedwith an increased sucrose permeability, which could bea sign of gastric mucosal leakage. This could haveimplications for the diseases and complicationsassociated with Helicobacter pylori infection.