Systematic review: periprocedural hydration in the prevention of post-ERCP pancreatitis.

BACKGROUND: With an overall incidence of 3.5%, pancreatitis is the most frequent complication of endoscopic retrograde cholangiopancreatography (ERCP). Periprocedural hydration may prevent post-ERCP pancreatitis by maintaining pancreatic microperfusion, thereby inhibiting the pancreatic inflammatory response. However, the evidence for periprocedural hydration as a preventive measure is unclear. AIM: To conduct a systematic review to assess the evidence regarding periprocedural hydration as a preventive measure for post-ERCP pancreatitis. METHODS: We searched PubMed and EMBASE databases and adhered to the PRISMA guidelines. We included studies addressing periprocedural hydration as a preventive measure to reduce frequency and severity of post-ERCP pancreatitis. Study quality was assessed by using the MINORS and Cochrane Collaboration's tool. RESULTS: Six studies with a total of 1102 patients were included. Two randomised controlled trials reported a decreased incidence of post-ERCP pancreatitis after hydration: 0% vs. 17% (P = 0.016) and 5.3% vs. 22.7% (P = 0.002). A third trial and two case-controls studies did not report significant differences. Two retrospective studies found that patients with mild post-ERCP pancreatitis had received significantly more fluids during (mean 940 mL vs. 810 mL; P = 0.031) or after ERCP (median 2834 mL vs. 2044 mL; P < 0.02) compared to patients with moderate/severe disease. Adverse events of periprocedural hydration were not reported in any of the included studies. The different methodologies of the included studies precluded a formal data synthesis. CONCLUSIONS: There is some evidence to suggest that hydration affords protection against post-ERCP pancreatitis, but study heterogeneity precludes firm conclusions. Adequately powered randomised trials are needed to evaluate the preventive effect of periprocedural hydration.

Colonic work-up after incomplete colonoscopy: significant new findings during follow-up.

BACKGROUND AND STUDY AIMS: Cecal intubation is not achieved in 2 - 23 % of colonoscopies. The efforts made by physicians to visualize the remaining colon and the number of missed significant lesions are unknown. This study evaluates 1) the reasons for incomplete colonoscopy, 2) the rates of complete colonic evaluation after incomplete colonoscopy, and 3) the number of (pre-) malignant lesions missed by incomplete colonoscopy. PATIENTS AND METHODS: In this population-based cohort study index colonoscopies were performed between September and December 2005. Prospectively collected data from consecutive patients with an incomplete colonoscopy were analyzed. For up to 18 months after the index colonoscopy, any further examinations performed in these patients were identified retrospectively. These secondary examinations included: repeat colonoscopy, computed tomography (CT) colonography, barium enema, abdominal CT scan, and surgery involving the colorectum. RESULTS: Of 5278 colonoscopies, 511 were incomplete (9.7 %). The most frequent causes of incomplete colonoscopy were looping of the scope (20.4 %), patient discomfort (15.3 %), and obstructing tumor (13.9 %). Secondary examination was performed in 278 patients (54.4 %) after incomplete colonoscopy. Patients undergoing surveillance after colorectal cancer (CRC) (78.9 %) and those with anemia (73.1 %) most frequently received a secondary examination. Incomplete colonoscopies due to stenosis (78.9 %), severe inflammation (77.8 %) or an obstructing tumor (74.6 %) were most frequently followed by a secondary examination. In all of the follow-up examinations, CRC was diagnosed in 18 patients (3.5 %) and advanced adenoma in four patients (0.8 %). CONCLUSIONS: In 4.3 % of the patients, advanced neoplasia was missed by incomplete colonoscopy. Our data therefore suggest that additional imaging is obligatory to visualize the remaining colon adequately.

Practice and yield of early CT scan in acute pancreatitis: a Dutch Observational Multicenter Study.

BACKGROUND: Early computed tomography (CT) (within 4 full days after symptom onset) may be performed to distinguish acute pancreatitis (AP) from other intra-abdominal conditions or to identify early pancreatic necrosis. We analyzed practice and yield of early CT in patients with an established clinical diagnosis of AP in a Dutch cohort (EARL study). METHODS: Multicenter observational study. Etiology, disease course, CT timing, Balthazar CT score, and clinical management were evaluated. RESULTS: First documented hospital admissions of 166 patients were analyzed. Etiology was biliary (42.8%), unknown (20.5%), alcoholic (18.1%), post-endoscopic retrograde cholangiopancreatography (11.4%), and miscellaneous (7.2%). In 89.2% (148/166), the disease course was mild. Out of 18 patients with severe AP, 11 eventually developed (peri)pancreatic necrosis. At least one CT (range 1-12) was performed in 47% (78/166) of all patients and in 62.8% (49/78) it was acquired within 4 full days after symptom onset. Practice, timing, and Balthazar CT score of early CTs were not significantly different between mild and severe AP. None of the early CTs showed necrosis and no alternative diagnoses were established. In 89.8% (44/49), clinical management was not altered after early CT. In 10.2% (5/49), prophylactic antibiotics were started, but in absence of necrosis. CONCLUSIONS: A CT scan was frequently acquired early in the course of AP, but its yield was low and had no implications with regard to clinical management. It seems prudent that clinicians should be more restrictive in the use of early CT, in particular in mild AP, to prevent unnecessary radiation exposure and to save costs.

Colonoscopy-controlled intra-individual comparisons to screen relevant neoplasia: faecal immunochemical test vs. guaiac-based faecal occult blood test.

BACKGROUND: Guaiac-based faecal occult blood tests (g-FOBTs) are most commonly used in colorectal cancer (CRC) screening programmes. Faecal immunochemical tests (FITs) are thought to be superior. AIM: To compare performance of a g-FOBT and a quantitative FIT for detection of CRCs and advanced adenomas in a colonoscopy-controlled population. METHODS: We assessed sensitivity and specificity of both FIT (OC-sensor) and g-FOBT (Hemoccult-II) prior to patients' scheduled colonoscopies. RESULTS: Of the 62 invasive cancers detected in 1821 individuals, g-FOBT was positive in 46 and FIT in 54 (74.2% vs. 87.1%, P = 0.02). Among 194 patients with advanced adenomas, g-FOBT was positive in 35 and FIT in 69 (18.0% vs. 35.6%, P < 0.001). Sensitivity for screen relevant tumours (197 advanced adenomas and 28 stage I or II cancers) was 23.0% for g-FOBT and 40.5% for FIT (P < 0.001). Specificity of g-FOBT compared to FIT for the detection of cancer was 95.7% vs. 91.0%, P < 0.001) and for advanced adenomas (97.4% vs. 94.2%, P < 0.001). CONCLUSIONS: Faecal immunochemical test is more sensitive for CRC and advanced adenomas. Sensitivity of FIT for screen relevant tumours, early-stage cancers and advanced adenomas, is significantly higher. Specificity of g-FOBT is higher compared with FIT.

Nutritional management of patients with acute pancreatitis: a Dutch observational multicentre study.

BACKGROUND: Following a nil per os (NPO) regimen, most patients with acute pancreatitis (AP) can resume normal oral intake within 1 week. If not tolerated, it is recommended to initiate artificial feeding, preferably by the enteral route. AIM: To evaluate the nutritional management of patients with AP in a Dutch cohort (EARL study). METHODS: Observational study in 18 hospitals. Total days of NPO, tube feeding (TF) with/without oral feeding, total parenteral nutrition (TPN) and total starvation time were analysed. RESULTS: In mild AP, a majority of cases (80.7%, 117/145) were managed with an NPO regimen only. Twenty-seven patients (18.6%) with mild AP additionally received TF; one received TPN. Of those with severe AP, more than half of the patients (56.2%, nine of 16) were treated with TF besides an NPO regimen; four received TPN. TF was delivered preferably via the jejunal route. The median period of total starvation was 2 days for both mild and severe AP. Only 5.5% (nine of 164) of patients had a prolonged starvation time of more than 5 days. CONCLUSIONS: The total time of starvation was limited in a majority of patients admitted for AP. According to international guidelines, additional nutritional interventions were quickly undertaken with enteral feeding via the jejunum as the preferred route.

[The effect of Helicobacter pylori eradication on chronic use of acid-suppressant medication by patients in general practice; a randomised, double-blind study]. / Het effect van Helicobacter pylori-eradicatie op chronisch gebruik van maagzuursecretieremmende medicatie door patiënten in de huisartsenpraktijk; een gerandomiseerd, dubbelblind onderzoek.

OBJECTIVE: To study the feasibility of tapering long-term acid-suppressant drugs (ASD) use in chronic dyspeptic patients in relation to Helicobacter pylori eradication. DESIGN: Prospective randomised double-blind study. METHOD: Patients from 54 general-practitioner practices in the Amsterdam area were studied in the period 1 April 1997 - 30 September 1999 after selection on the basis of their use of acid suppressants for a period of at least 8 weeks. After gastroscopy the patients with a peptic ulcer (PUD) and H. pylori were treated with eradication therapy and patients without an ulcer but with H. pylori were randomised for eradication or placebo treatment. After a gradual reduction of acid suppressants over a 3-week period following the intervention, the patients kept a diary for 24 weeks of the quantities of acid suppressants and antacids they used. RESULTS: Of the 1083 patients approached, 434 were prepared to undergo the gastroscopy. Data for the follow-up period were available for 186 of the 227 H. pylori-positive patients. Of them 61% stopped ASD use during follow-up. The mean daily ASD dosage per patient decreased by 85% from 1.85 to 0.27 units (p < 0.05), with minimal antacids use. Of the 75 patients with peptic-ulcer disease 86% stopped ASD use. In patients with functional dyspepsia no difference in ASD use was observed after successful H. pylori eradication or placebo. Patients with mild reflux disease (GERD) used more ASD after H. pylori eradication than after placebo (p < 0.05). CONCLUSION. After H. pylori eradication many patients with PUD stopped ADS use, while GERD patients used more ASD than after placebo. A gradual withdrawal of long-term ASD use, supported by antacids and on-demand use of low-dosage ASD, facilitated reduction of ASD use during 6 months.

Helicobacter pylori and gastro-oesophageal reflux disease: association and clinical implications. To treat or not to treat with anti-H. pylori therapy?

BACKGROUND: It has been reported that patients are at risk of developing reflux oesophagitis after successful anti-Helicobacter pylori therapy, and the presence of the bacterium might be protective against the development of reflux oesophagitis. METHODS: Review of the literature. RESULTS: H. pylori is relevant to the management of oesophagitis because it increases the pH-elevating effect of proton-pump inhibitors. which increase the tendency of H. pylori gastritis to progress to atrophic gastritis, and because eradication of H. pylori increases the likelihood of oesophagitis. H. pylori increases basal gastrin levels, basal acid output, meal-stimulated maximal acid output and 24-h intragastric acidity. The effects on gastric acid production depend on the distribution of gastritis in the stomach. CONCLUSION: H. pylori eradication may induce or exacerbate gastro-oesophageal reflux by its influence on gastric acidity and the antisecretory action of proton-pump inhibitors.

Helicobacter pylori and functional dyspepsia. What to do after the Maastricht II consensus meeting?

BACKGROUND: Despite many clinical studies, there is still much discussion on the relation between Helicobacter pylori and functional dyspepsia. METHODS: Critical review of recommendations for H. pylori eradication in dyspepsia. RESULTS: The debate can be separated into three major problems. First, how to identify the dyspeptic patient suffering from H. pylori infection. Second, is H. pylori infection causative for complaints in this patient? Third, what is the clinical course of functional dyspepsia after successful H. pylori eradication? In the recent Maastricht II consensus, it is strongly recommended that H. pylori-positive patients with functional dyspepsia should be treated with anti-H. pylori therapy. In this review, the pros and cons of H. pylori eradication in patients with functional dyspepsia are discussed. The reader can decide what is the best management of an individual patient. CONCLUSIONS: This review gives the relevant background information allowing clinicians to decide what the best management is in individual H. pylori-positive patients with dyspepsia.

How do primary care physicians use long-term acid suppressant drugs? A population-based analysis of Dutch general practices.

OBJECTIVES: A considerable proportion of the medication budget of Dutch general practitioners is spent on prescribed long-term acid suppressant drugs. We investigated the magnitude of long-term prescription of acid suppressant drugs in general practice and the frequency and means of confirming the primary working diagnosis. STUDY DESIGN: We used a retrospective descriptive study of 24 general practices in the Amsterdam region. POPULATION: We identified those receiving long-term acid suppressant therapy (12 or more weeks/year) from a total of 46,813 patients by extracting data from pharmacy databases. OUTCOMES MEASURED: We measured the amount and duration of prescriptions for each medication, indications for prescription, and investigations performed by general practitioners. RESULTS: Of the 46,813 patients, 922 (2%) received long-term acid suppressant therapy. The duration of prescription varied from 12 weeks in 8% of patients to > 52 weeks in 23% of patients (mean = 33 weeks). In 25% of patients, no investigations were performed; 75% of patients underwent endoscopy or ingested a barium meal. The predominant diagnoses in investigated patients were ulcer disease (39%), gastroesophageal reflux disease (49%), and functional dyspepsia (gastritis, normal aspect; 18%). Helicobacter pylori status was available in 29% of patients with ulcer disease. Eradication therapy was reported in 44% of these patients. CONCLUSIONS: Among patients of physicians in general practice in the Amsterdam region, 2% used long-term acid suppressants. Patients with ulcer disease may stop taking acid suppressants after apparent successful H pylori eradication. Tapering strategies must be developed for patients with mild reflux disease or functional dyspepsia.

Arrest of chronic acid suppressant drug use after successful Helicobacter pylori eradication in patients with peptic ulcer disease: a six-month follow-up study.

BACKGROUND: It remains controversial whether successful H. pylori eradication leads to relief of dyspepsia and the subsequent arrest or tapering of acid-suppressant drug therapy, or to an aggravation of acid-related dyspepsia requiring more acid-suppressant drug intake. AIM: To evaluate prospectively the effect of H. pylori eradication on the requirement of acid-suppressant drug or antacids and the evolution of dyspeptic symptoms in chronic acid-suppressant drug users with peptic ulcer disease. MATERIALS AND METHODS: The use of acid-suppressant drugs, rescue antacids and predominant symptoms were recorded prospectively during 24 weeks after H. pylori eradication therapy in 75 peptic ulcer disease patients. RESULTS: In 71 patients with complete follow-up, ulcers were healed at follow-up endoscopy and H. pylori was successfully eradicated. After 6 months, 93% (66 out of 71) of chronic acid-suppressant drug users had stopped acid-suppressant drug intake. The mean daily acid-suppressant drug dosage per patient decreased from 1.72 at entry to 0.03 units acid-suppressant drug (98%; P < 0.0001) during follow-up. The mean number of antacid tablets/day/patient was 0.26 during follow-up for the relief of mild inter-current dyspeptic symptoms. Medication use was not different in peptic ulcer disease patients with or without gastro-oesophageal reflux disease at baseline. The prevalence of gastro-oesophageal reflux disease decreased from 42% before to 35% after H. pylori eradication (N.S.). CONCLUSION: Successful H. pylori eradication in peptic ulcer disease patients almost completely eliminates the need for acid-suppressant drug regardless of the presence or absence of gastro-oesophageal reflux disease at entry.

Comparison of precancerous conditions: atrophy and intestinal metaplasia in Helicobacter pylori gastritis among Chinese and Dutch patients.

AIM-Atrophy and intestinal metaplasia (IM) as precancerous conditions consistently begin in the antrum and are most severe along the lesser curvature. The aim of this study was to investigate discrepancies in the prevalence, the severity of atrophy, and IM in antral mucosa of Helicobacter pylori infected gastritis and difference in age of onset among Chinese and Dutch patients. METHODS-Two hundred and sixty five Chinese patients and 261 Dutch patients with H pylori infection were enrolled. The degrees of atrophy and IM were graded according to the updated Sydney system. RESULTS-The overall prevalences of atrophy and IM were lower in Dutch patients (42% and 26%, respectively) than in Chinese patients (52% and 32%, respectively). Only the difference in atrophy reached significance (p = 0.028). However, in both Chinese and Dutch patients, the degrees of atrophy and IM were low and severe degrees were rare. The mean ages of Chinese and Dutch patients with atrophy and IM were higher than those without atrophy and IM (with atrophy (Chinese patients): mean, 42.12; SD, 9.80; with IM (Chinese patients): mean, 42.56; SD, 9.96; with atrophy (Dutch patients): mean, 55.16; SD, 12.20; with IM (Dutch patients): mean, 57.79; SD, 11.13; without atrophy (Chinese patients): mean, 39.71; SD, 10.16; without IM (Chinese patients): mean, 40.19; SD, 9.99; without atrophy (Dutch patients): mean, 45.70; SD, 12.44; without IM (Dutch patients): mean, 46.89; SD, 12.68). Atrophy and IM occurred earlier and were more severe in Chinese patients, with both reaching a peak value in patients over 60 years. CONCLUSIONS-There are geographical differences in the prevalence and severity of H pylori infected gastritis, in particular with respect to atrophy and IM, which suggests that infection with H pylori occurs earlier in life and has a higher prevalence in CHINA:

Prevalence of Helicobacter pylori infection in stress-induced gastric mucosal injury.

OBJECTIVE: To determine the role of Helicobacter pylori infection in critically ill patients admitted to the intensive care unit in the formation of gastric and duodenal mucosal injury in these patients. DESIGN AND SETTING: Prospective cohort analysis in an 18-bed mixed medical and surgical closed format ICU in a teaching hospital. PATIENTS: Fifty consecutive patients admitted to the intensive care unit for emergency reasons and requiring mechanical ventilation were included. INTERVENTIONS: H. pylori infection was detected by the laser-assisted ratio analyzer [13C]urea breath test (UBT). Gastric and duodenal mucosal lesions were assessed by upper gastrointestinal endoscopy and classified as minor (up to five erosions or submucosal hemorrhages) or major (more than five erosions or submucosal hemorrhages) mucosal injury. MEASUREMENTS AND MAIN RESULTS: Six patients were not eligible because the UBT could not be processed. Of the 44 eligible patients 22 were H. pylori positive by UBT and 22 H. pylori negative. Either minor or major gastric mucosal injury was found on endoscopy in 66 %. Of the 29 patients with minor mucosal injury 10 (34.5 %) were infected with H. pylori as indicated by positive LARA 13C-UBT. In contrast, of the 15 patients with major mucosal injury 12 (80%) were infected with H. pylori (p = 0.004). H. pylori was the only risk factor significantly associated with major mucosal injury in a multiple regression analysis (p = 0.019). CONCLUSION: The severity of gastric and duodenal mucosal injury in critically ill patients during mechanical ventilation is significantly correlated with the presence of H. pylori infection.

Gut decontamination of critically ill patients reduces Helicobacter pylori acquisition by intensive care nurses.

The prevalence of Helicobacter pylori is increased in healthcare workers and in intensive care nurses. Exposure to H. pylori from gastric secretions and faeces are probably the main sources of transmission to healthcare workers. Routine use of selective decontamination of digestive tract (SDD) in an intensive care unit suppresses H. pylori in critically ill patients. It was questioned whether this suppression and the subsequent decreased exposure to H. pylori for intensive care nurses would lead to a lower prevalence of H. pylori infection. Helicobacter pylori infection prevalence in intensive care nurses from a unit routinely using SDD (group I) was compared to that of nurses from a unit not using SDD (group II). Heathcare workers from other departments of the hospital where no SDD was used (group III) served as a control group. Persons using proton pump inhibitors were excluded. Helicobacter pylori was detected by Laser Assisted Ratio Analyser(13)C-urea breath test (UBT) and serology. This could not be performed in three out of 64 in group I, five out of 55 in group II and five out of 55 in group III (total UBTs = 169). The prevalence of H. pylori infection was 11% (7/61) in group I and 25.5% (14/50) in group II (P= 0.027). In group III, the prevalence of H. pylori infection was 16% (8/45), which was not significantly different from both group I and II. Sero-prevalence in group I was 18.6%, 27% in group II (ns) and 24% in group III. Mean age in the three groups was 35.9, 37.8 and 36.6 years, respectively (ns). In conclusion, the prevalence of H. pylori infection among intensive care nurses is lower in nurses from a unit using SDD compared to a non SDD-using unit. Acquisition of H. pylori by transmission from critically ill patients appears to be diminished through SDD use.

Suppression of Helicobacter pylori infection during intensive care stay: related to stress ulcer bleeding incidence?

PURPOSE: To assess the prevalence of active Helicobacter pylori infection in patients admitted to the intensive care unit, to determine the effect of selective gut decontamination on the persistence of this organism, and to explore the possible relationship between H. pylori infection and stress ulcer bleeding incidence. MATERIALS AND METHODS: We determined in a prospective observational study of 300 consecutive, mechanically ventilated patients the activity of H. pylori infection and the incidence of stress ulcer-related upper gastrointestinal bleeding over time. H. pylori infection was detected by Laser-Assisted Ratio Analyzer (LARA)- (13)C-urea breath test (Alimenterics, Inc., NJ) and serology. Stress ulcer prophylaxis was not prescribed. Endoscopy was performed in cases of upper gastrointestinal bleeding. RESULTS: The prevalence of active H. pylori infection on admission was 38% as detected by urea breath test, and declined to 8% on the third day, and to 0% on the seventh day after admission as a result of antibiotic treatment. Stress ulcer-related upper gastrointestinal bleeding occurred in 1.0% (3 of 300) of the patients; none were infected with H. pylori on admission or at the time of bleeding. CONCLUSIONS: H. pylori infection monitored by LARA- (13)C-urea breath test was rapidly suppressed during intensive care treatment, which can be explained by the routine use of antibiotics for gut decontamination.The low incidence of stress ulcer-related bleeding might be related to the prevention of H. pylori-associated stress lesions by effective suppression of this microorganism, but further studies are warranted to test this hypothesis.

In vitro susceptibility of Helicobacter pylori to, and in vivo suppression by, antimicrobials used in selective decontamination of the digestive tract.

The incidence of bleeding related to stress ulcers is reduced in critically ill patients in whom gut decontamination has been performed; this may be a result of suppression of Helicobacter pylori infection. We determined the susceptibility of H. pylori to the applied antibiotics. In nine of 10 critically ill patients (using intravenous cefotaxime and topical polymyxin, tobramycin and amphotericin B (PTA) given by nasogastric tube) and all six volunteers (using PTA alone), H. pylori was suppressed as long as the topical antibiotics were ingested. The in vitro studies revealed that all strains were susceptible to cefotaxime and tobramycin. The strains were not susceptible to polymyxin or amphotericin B.

Equally high efficacy of 4, 7 and 10-day triple therapies to eradicate Helicobacter pylori infection in patients with ulcer disease.

BACKGROUND: In patients with ulcer disease the optimal dose and duration of Helicobacter pylori treatment containing omeprazole (O), metronidazole (M) and clarithromycin (C) has yet to be established. The efficacy might be influenced by metronidazole- and clarithromycin-resistance. AIM: To study the effect of duration of OMC treatment on its efficacy and influence of metronidazole-resistance and clarithromycin-resistance on the optimal duration. MATERIALS AND METHODS: Ulcer patients (n=76) were randomized to three double-blind treatments of 10 days: OMC 4 consisted of 4 days b.d. 20 mg omeprazole, 400 mg metronidazole and 250 mg clarithromycin switched over to 6 days b.d. 20 mg omeprazole and placebo antibiotics (n=27); OMC 7 consisted of 7 days b.d. omeprazole 20 mg, metronidazole 400 mg and clarithromycin 250 mg and 3 days b.d. omeprazole 20 mg and placebo antibiotics (n=25); OMC 10 consisted of 10 days b.d. omeprazole 20 mg, metronidazole 400 mg and clarithromycin 250 mg (n=24). H. pylori was assessed by biopsies for culture and histology pre- and 4-6 weeks after OMC therapy. Metronidazole-resistance and clarithromycin-resistance were assessed by the E-test. RESULTS: Intention-to-treat-eradication rates were: OMC 4, 96%; OMC 7, 92%; and OMC 10, 96% (N.S.). All of the three per protocol eradication rates were 100% (95% CI: 85.2-100). Of 75 isolates, 16 were metronidazole-resistant and one was clarithromycin-resistant. CONCLUSION: In H. pylori-positive ulcer patients, OMC 4 is highly efficacious and as effective as OMC 7 and OMC 10. No influence of metronidazole-resistance or clarithromycin-resistance was observed.

H pylori colocalises with MUC5AC in the human stomach.

BACKGROUND: The bacterium Helicobacter pylori is able to adhere to and to colonise the human gastric epithelium, yet the primary gene product responsible as a receptor for its adherence has not been identified. AIMS: To investigate the expression of the gastric mucins MUC5AC and MUC6 in the gastric epithelium in relation to H pylori colonisation in order to examine their possible roles in the binding of H pylori. PATIENTS: Seventy two consecutive patients suspected of having H pylori infection. METHODS: MUC5AC, MUC6, and H pylori were detected in single sections of antral biopsy specimens using immunohistochemical triple staining. RESULTS: MUC5AC was expressed in the superficial epithelium and the upper part of the gastric pits. MUC6 expression was detected in the lower part of the gastric pits. The expression of both mucins in the epithelium was complementary. In each patient, there was a sharply delineated transition between MUC5AC and MUC6 producing cell populations. In all H pylori positive patients there was a striking colocalization of H pylori and MUC5AC; more than 99% of the bacteria were associated with either extracellular MUC5AC or the apical domain of MUC5AC producing cells. CONCLUSIONS: H pylori is very closely associated with extracellular MUC5AC and epithelial cells that produce MUC5AC. This indicates that MUC5AC, but not MUC6, plays a role in the adhesion of H pylori to the gastric mucosa.

Quasispecies development of Helicobacter pylori observed in paired isolates obtained years apart from the same host.

Helicobacter pylori isolates show greater genetic diversity than other bacterial species studied, but the basis for this phenomenon is unknown. Whether detectable genomic mutation appears within an H. pylori population during persistent colonization was investigated. Paired H. pylori populations obtained across 7- to 10-year intervals from 13 patients were characterized by use of methods including polymerase chain reaction (PCR) genotyping for cagA, vacA, iceA, recA, and IS605; random arbitrarily primed DNA (RAPD)-PCR and amplified fragment length polymorphism (AFLP) analysis; and ELISA, to determine Lewis phenotypes. Genotyping, including recA sequence analysis, revealed that initial and follow-up populations represented the same population in 11 patients (85%). Nevertheless, distinct dissimilarities were shown within each of these 11 pairs by both RAPD-PCR and AFLP analyses. During follow-up, Lewis-y levels, but not Lewis-x levels, decreased significantly. The changes detected by RAPD-PCR and AFLP indicate that genetic drift occurs within H. pylori populations over the course of years of colonization of a single host.