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

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

Characteristics and trends of clarithromycin-resistant Helicobacter pylori isolates in Japan over a decade.

Clarithromycin has been administered to patients in Japan since 1991. Clarithromycin-resistant Helicobacter pylori strains have been on the rise in Japan. We obtained H. pylori isolates between 1989 and 2000 and examined mutations of the 23S rRNA gene, which are closely associated with clarithromycin resistance. Isolates were obtained from 356 patients with H. pylori infection treated at the Hiroshima University. Sixty-one of the patients received clarithromycin-based H. pylori eradication therapy. Mutations of the 23S rRNA gene were examined by polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) followed by sequencing analysis. Mutant strains were found in 42 of the 356 patients (11.8%). The prevalence of mutant strains increased from 0 to 20.4% during the 12-year study period. The prevalence increased to more than 10% by 1995 and then to more 20% after 1999. The H. pylori eradication rate was significantly higher in patients with wild-type strains than in patients with mutant strains (72.0 vs. 36.4%, p = 0.024). Our data indicate that clarithromycin-resistant H. pylori strains have increased rapidly since 1995 and that the effectiveness of clarithromycin-based H. pylori eradication therapies may soon be compromised. Other new therapies may be necessary as first-line treatments in Japan.     

免疫性血小板减少性紫癜的发病机制与临床研究进展

免疫性血小板减少性紫癜(Immune thrombocytopenic purpura,ITP)是自身抗体介导的血小板减少综合征,自身抗原的主要成分是血小板一种或多种糖蛋白;细胞免疫也是血小板破坏的一个重要原因.目前ITP的诊断仍是临床排除性诊断,分为原发性与继发性两种.ITP治疗的目的是使患者血小板计数提高到安全水平.肾上腺糖皮质激素仍是ITP的首选药物,静脉输注丙种球蛋白(IVIg)用于控制严重出血与重度血小板减少,脾切除仍是治疗慢性ITP的主要手段.血小板生成素(TPO)类似物可能成为新的治疗方法.对成人慢性ITP患者应常规进行幽门螺杆菌(Hp)筛查,阳性患者应根除Hp.     

Insulin-like growth factor-I in Helicobacter pylori gastritis and response to eradication using bismuth based triple therapy.

AIMS: To measure insulin-like growth factor-I (IGF-I) concentrations in the presence and absence of Helicobacter pylori infection and in response to eradication of the organism. METHODS: An enzyme linked immunosorbent assay was used to measure gastric and fasting serum concentrations of IGF-I in 17 patients with and 11 without H pylori infection. Repeat assessments were performed in the infected patients six weeks after they received a two week course of bismuth chelate, metronidazole, and amoxycillin. RESULTS: IGF-I was detected at very low concentrations in gastric juice and in mucosal incubates. The median serum IGF-I concentration was 88 micrograms/l in the patients infected with H pylori compared with 90 micrograms/l in the non-infected controls; IGF-I concentrations dropped to 77 micrograms/l following eradication therapy (p = 0.014). CONCLUSION: The similarity in baseline IGF-I concentrations in the presence and absence of H pylori suggests that their subsequent drop after treatment is more likely to be due to the treatment.     

Impact of Helicobacter pylori eradication on morphological changes in gastric mucosa

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

Ultrastructural morphology of Helicobacter pylori in post vagotomy dyspepsia

31 patients of peptic ulcer (PU) treated in the past by vagotomy with Gastrojejunostomy (GJ)/pyloroplasty, later presented with dyspesia. These postvagotomy dyspeptic patients were investigated. Antral and corpus endoscopic biopsies were taken to evaluate for Helicobacter pylori (Hp) infection by inhouse rapid urease test (RUT), histopathological examination and scanning electron microscopy (SEM). Dyspepsia score was done in both pre and post treatment phase. Hp positive patients were randomised to receive anti H. pylori therapy. Hp eradication was recorded by repeat RUT and endoscopic biopsy followed by SEM. Coccoid form of Hp were detected in 76.92% cases of vagotomy with gastrojejunostomy (GJ) and coccobacillary forms of Hp were seen in 75% cases of pyloroplasty. After treatment with anti Hp therapy coccoid forms persisted in 69.23% of GJ cases, whereas 22% of pyloroplasty cases showed coccoid transformation. Anti Hp therapy did not reveal any statistically significant improvement in 'Dyspepsia Score' in GJ group, whereas it improved significantly in pyloroplasty group (p=0.002).     

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

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

Immunoglobulin G1 antibody response to Helicobacter pylori heat shock protein 60 is closely associated with low-grade gastric mucosa-associated lymphoid tissue lymphoma.

Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is related to Helicobacter pylori infection. Specifically, it has been pointed out that pathogenesis of MALT lymphoma involves the 60-kDa heat shock protein (hsp60). To investigate humoral immune responses to the H. pylori hsp60 in patients with gastroduodenal diseases and patients with MALT lymphoma, the hsp60 of H. pylori was expressed with a glutathione S-transferase fusion protein and was purified (recombinant hsp60). Sera were obtained from H. pylori-positive patients with gastroduodenal diseases (MALT lymphoma, n = 13; gastric ulcer, n = 20; duodenal ulcer, n = 20; gastritis, n = 20) and from H. pylori-negative healthy volunteers (n = 9). Sera from patients with MALT lymphoma were also obtained at two times: before and after eradication therapy. Antibodies to hsp60 and H. pylori were assessed by enzyme-linked immunosorbent assay. The levels of immunoglobulin G (IgG) antibodies to the hsp60 of H. pylori-positive patients with gastroduodenal diseases were significantly elevated compared to those in the controls. The levels of IgG1 antibodies to hsp60 were elevated and correlated with the levels of anti-H. pylori antibodies in patients with MALT lymphoma. Humarol immunity against hsp60 may be important and relevant to gastroduodenal diseases induced by H. pylori infection.     

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

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

Cell proliferation in the post-surgical stomach, dietary salt, and the effect of H pylori eradication

AIMS: To study the epithelial kinetics of the post-surgical stomach with reference to dietary salt intake and H pylori. METHODS: Endoscopic biopsies of the antrum/anastomosis and corpus were taken for histology and MIB-1 immunostaining. The labelling index (LI%) was determined in the three zones of the gastric glands (zone 1 = surface + gastric pit; zone 2 = isthmus; zone 3 = gland base) in patients with vagotomy and pyloroplasty (n = 12), gastroenterostomy + vagotomy (n = 4), partial gastrectomy (n = 3), and Billroth I operation (n = 3). Dietary salt was determined by urinary sodium/creatinine ratio. Twelve patients were H pylori positive (10 vagotomy and pyloroplasty; 2 partial gastrectomy) and had a repeat biopsy three months after antihelicobacter treatment (10 were H pylori negative after treatment). RESULTS: There was no correlation between salt intake and antrum/anastomosis (r = -0.34; p = 0.2) or corpus (r = -0.16; p = 0.2) labelling indices. Gastric mucosal proliferation is increased in the antrum/ anastomosis compared to the corpus in H pylori positive (p = 0.014) but not H pylori negative subjects (p = 0.084). This may reflect the different types of post-surgical stomach in each group. Gastric mucosal proliferation is reduced in antrum/anastomosis (p = 0.002) and corpus (p = 0.016) following H pylori eradication. CONCLUSIONS: Dietary salt does not influence gastric mucosal proliferation in the post-surgical stomach but H pylori may have a role in gastric stump carcinogenesis.     

Absence of benefit of eradicating Helicobacter pylori in patients with nonulcer dyspepsia.

BACKGROUND: The relation between Helicobacter pylori infection and nonulcer dyspepsia is uncertain. We tested the hypothesis that curing the infection will relieve symptoms of dyspepsia. METHODS: We randomly assigned 170 H. pylori-infected patients with nonulcer dyspepsia to receive twice-daily treatment with 20 mg of omeprazole, 1000 mg of amoxicillin, and 500 mg of clarithromycin for 14 days and 167 such patients to receive identical-appearing placebos; all patients were then followed through regular visits for 12 months. Symptoms were scored on diary cards for seven days before each visit. A carbon-13 urea breath test was performed at base line and repeated at 1 and 12 months, and endoscopic biopsy was performed at 12 months to determine H. pylori status. Treatment was considered successful if the patient had only mild pain or discomfort or none at all. RESULTS: The rate of eradication of H. pylori infection was 90 percent in the active-treatment group and 2 percent in the placebo group at four to six weeks (P<0.001). At 12 months, there was no significant difference between groups in the rate of successful treatment (46 percent in the active-treatment group and 50 percent in the placebo group; relative likelihood of success with active treatment, 0.93; 95 percent confidence interval, 0.73 to 1.18; P=0.56). There was also no significant difference in the rate of successful treatment at 12 months between patients who were H. pylori-negative and those who were H. pylori-positive (48 percent vs. 49 percent). The rates of successful treatment were also similar when patients were analyzed according to the type of dyspepsia (ulcer-like, reflux-like, or dysmotility-like) and changes in the quality of life. There was no significant association between treatment success and histologic improvement in chronic gastritis at 12 months (P=0.68). CONCLUSIONS: We found no evidence that curing H. pylori infection in patients with nonulcer dyspepsia leads to relief of symptoms.     

Efficacy of levofloxacin and rifaximin based quadruple therapy in Helicobacter pylori associated gastroduodenal disease: a double-blind, randomized controlled trial

The aim of this study was to evaluate the efficacy of levofloxacin and rifaximin based quadruple regimen as first-line treatment for Helicobacter pylori infection. A prospectively randomized, double-blinded, parallel group, comparative study was performed. Three hundred consecutive H. pylori positive patients were randomized to receive: omeprazole, amoxicillin, clarithromycin (OAC); omeprazole, amoxicillin, levofloxacin (OAL); and omeprazole, amoxicillin, levofloxacin, rifaximin (OAL-R). The eradication rates in the intention to treat (ITT) and per protocol (PP) analyses were: OAC, 77.8% and 85.6%; OAL, 65.3% and 73.6%; and OAL-R, 74.5% and 80.2%. The eradication rate achieved with OAC was higher than with OAL on the ITT (P = 0.05) and PP analysis (P = 0.04). OAL-R regimen was not inferior to OAC. The frequency of moderate to severe adverse effects was significantly higher in OAC treatment group. Especially, diarrhea was most common complaint, and there was a significantly low rate of moderate to severe diarrhea with the rifaximin containing regimen. In conclusion, the levofloxacin and rifaximin based regimen comes up to the standard triple therapy, but has a limited efficacy in a Korean cohort. The rifaximin containing regimen has a very high safety profile for H. pylori eradication therapy.     

Chronic inactive gastritis and coccoid Helicobacter pylori in patients treated for gastroesophageal reflux disease or with H pylori eradication therapy

Gastric biopsy specimens from 105 consecutive adults with persistent dyspepsia who did not have changes due to esophageal reflux disease changes or gastric or duodenal ulcers at endoscopy were scored using the updated Sydney gastritis classification system. The medication history of proton pump inhibitors (PPIs) or Helicobacter pylori eradication therapy during the month before endoscopy was retrieved. Of the patients, 72 (68.6%) had chronic inactive gastritis, and 7 (6.7%) had antral-predominant, chronic mild active gastritis. H pylori infection was present in 36 patients (34.3%), of whom 29 had chronic inactive gastritis. Forty-six patients (43.8%) had a positive medication history, including 40 (56%) of 72 with chronic inactive gastritis. The most common morphologic feature associated with H pylori infection was moderate chronic inactive gastritis, which was found most often in patients who had received recent PPIs or H pylori eradication therapy. Pathologists should be aware of the extensive use of these medications, their association with chronic inactive gastritis, and rare H pylori thatfrequently are coccoid shaped. Modified Giemsa stain may not be the optimal method to detect H pylori in this group of patients.     

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

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

Use of splenic ultrasound: a new wave for immune thrombocytopenic purpura.

AIMS--To examine whether a therapeutic dose of ultrasound waves, when directed through the thoracic wall to the spleen, would significantly affect the platelet count in patients with stable immune thrombocytopenic purpura (ITP). METHODS--Continuous ultrasound at 1 W/cm2 spatial average-time average (SATA) intensity for up to one minute/5 cm2 treatment field was well tolerated in 13 patients with ITP and one with non-Hodgkin's lymphoma. Five healthy controls were also similarly treated. Peak platelet increments occurred four to eight hours after ultrasound treatment in the ITP group (n = 16 treatments). RESULTS--The mean peak platelet increment was 6.25 x 10(9)/l with a 5% confidence interval of the mean (95% CI) of 3.32 to 8.93 x 10(9)/l (p = 0.0004). The mean peak platelet increment of normal controls was 6.6 (n = 5; 95% CI = -2.3 to 15.5; p = 0.21) and for sham treated patients it was 0.66 (n = 11; 95% CI = -1.5 to 2.8; p = 0.60). There was a significant inverse correlation between patient age in the ITP group and peak platelet increment (r = -0.60; p = 0.015). CONCLUSIONS--Splenic ultrasound is a novel approach to the treatment of ITP, and may find a place in its diagnosis or management.     

Efficacy of two triple eradication regimens in children with Helicobacter pylori infection

Triple therapy with bismuth subsalicylate, amoxicillin, metronidazole (BAM) or with omeprazole, amoxicillin, clarithromycin (OAC) has been commonly used for the eradication of Helicobacter pylori infection. We compared the efficacy of these triple therapies in children with H. pylori infection. We retrospectively analyzed results in 233 children with H. pylori infection and treated with OAC (n=141) or BAM (n=92). Overall eradication rates of triple therapy with OAC and BAM were 74% and 85%, respectively, which showed no statistical difference. Our study showed that the triple therapy with BAM was more effective for the first-line eradication of H. pylori infection in Korean children, but has no statistical difference with OAC regimen.     

Efficacy of a quadruple therapy regimen for Helicobacter pylori eradication after partial gastrectomy

We aimed to evaluate the effectiveness and safety of bismuth-containing quadruple therapy plus postural change after dosing for Helicobacter pylori eradication in gastrectomized patients. We compared 76 gastric stump patients with H. pylori infection (GS group) with 50 non-gastrectomized H. pylori-positive patients who met the treatment indication (controls). The GS group was divided into GS group 1 and GS group 2. All groups were administered bismuth potassium citrate (220 mg), esomeprazole (20 mg), amoxicillin (1.0 g), and furazolidone (100 mg) twice daily for 14 days. GS group 1 maintained a left lateral horizontal position for 30 min after dosing. H. pylori was detected using rapid urease testing and histologic examination of gastric mucosa before and 3 months after therapy. Mucosal histologic manifestations were evaluated using visual analog scales of the updated Sydney System. GS group 1 had a higher prevalence of eradication than the GS group 2 (intention-to-treat [ITT]: P=0.025; per-protocol [PP]: P=0.030), and the control group had a similar prevalence. GS group 2 had a lower prevalence of eradication than controls (ITT: P=0.006; PP: P=0.626). Scores for chronic inflammation and activity declined significantly (P<0.001) 3 months after treatment, whereas those for atrophy and intestinal metaplasia showed no significant change. Prevalence of adverse reactions was similar among groups during therapy (P=0.939). A bismuth-containing quadruple therapy regimen plus postural change after dosing appears to be a relatively safe, effective, economical, and practical method for H. pylori eradication in gastrectomized patients.     

Parietal cell protrusions and fundic gland cysts during omeprazole maintenance treatment

Parietal cell protrusion (PCP), swelling and bulging of parietal cells, has been observed in the oxyntic mucosa of patients receiving omeprazole. The frequency of this event and the underlying mechanisms remain to be clarified. As such, it is unknown whether there is a relation with either serum gastrin or Helicobacter pylori infection, and whether PCP predisposes to the development of fundic gland cysts (FGC). We therefore investigated the development of PCP and FGC in gastroesophageal reflux disease (GERD) patients treated with omeprazole and correlated findings to duration of therapy, gastrin, and H pylori infection. In a randomized, double-blinded study, GERD patients were evaluated by endoscopy with biopsy sampling for histology and culture at baseline, and after 3 and 12 months' therapy with omeprazole 40 mg daily. H pylori-positive patients were randomized to additional eradication therapy or placebo antibiotics at baseline. All histological slides were scored blinded for time and outcome of culture for the presence of PCP and FGC. Fasting serum samples from all visits were used for gastrin measurements. The prevalence of PCP increased during omeprazole therapy from 18% at baseline to 79% and 86% at 3 and 12 months (P < .001, baseline v both 3 and 12 months). The prevalence of FGC increased from 8% to 17% and 35% (P < .05, baseline v 12 months). The prevalence of PCP and FGC did not differ among the H pylori-positive and H pylori-negative patients at baseline (PCP 16% v 20% and FGC 7% v 8%, respectively). Whereas H pylori eradication did not significantly affect development of PCP (P = .7), FGC developed significantly more often in the H pylori-eradicated patients when compared with persistent H pylori-positive patients (P < .05). PCP development was related to serum gastrin rise during therapy. In conclusion, PCP occurs in most patients within the first months of omeprazole treatment and is related to increased gastrin levels. FGC develops more gradually and is enhanced by H pylori eradication.     

Time course of gastric mucosal changes in the assessment of long-term results of Helicobacter pylori eradication

The impact of Helicobacter pylori (H. pylori) eradication on the gastric mucosa (GM) was studied in patients with gastroduodenal ulcers. Clinical and morphological changes in the GM were assessed in 122 patients 3-7 years (mean 4.4 +/- 1.3 years) after eradication therapy and in 12 patients who had undergone H. pylori eradication. Successful H. pylori eradication in the gastric antral and body mucosa reduced inflammation, the degree of chronic inflammation, the number of lymphoid follicles, and the magnitude of gland atrophy. There were no statistically significant changes in intestinal metaplasia. The patients who had not received eradication therapy showed no significant GM changes as compared to the baseline values. In the unsuccessful eradication group, inflammation statistically significantly diminished in the gastric antrum and body with a reduction in the density of H. pylori contamination.