摘要:

ABSTRACTBackgroundAttempts have been made to develop an accurate method for detectingHelicobacter pyloriin histological sections.Materials and Methods.Biopsy specimens were obtained from the stomachs of 167 patients with gastric ulcer (33), duodenal ulcer (52), gastroduodenal ulcer (15), chronic gastritis (45), and normal mucosa (22) before antimicrobial treatment and from 108 of these patients after treatment. Biopsy specimens were (1) cultured, (2) fixed in 10% buffered formalin, or (3) fixed in Carnoy's solution. The latter method was employed to preserve the surface mucous gel layer (SMGL) covering gastric surface mucous cells. Histological sections were stained with hematoxylin and eosin (H&E), with immunostaining using a commercially available polyclonal anti‐H. pyloriantibody.Results.Cultures were positive forH. pyloriin 61% of the cases before treatment and in 16% after treatment; by H&E staining using formalin‐fixed materials: 70% and 9%; by immunostaining using formalin‐fixed materials: 78% and 21%; and by immunostaining using Carnoy‐fixed materials: 85% and 41% of biopsy speciemens, respectively. The difference in detection rates between materials fixed in formalin and those in Carnoy's solution was due to the detection ofH. pyloriin the SMGL by the latter, especially after antimicrobial treatment.Conclusions.Immunostaining forH. pyloriusing materials fixed in Carnoy's solution revealedH. pyloriin the SMGL as well as on the surface mucous cells and in the gastric pits and permitted the optimal detection ofH. pyloriin tissue s

ISSN:1083-4389    

DOI:10.1111/j.1523-5378.1996.tb00040.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

ABSTRACTBackgroundThe colonization ofHelicobacter pyloriin the surface mucous gel layer (SMGL) was investigated.Materials and Methods.Surgically removed stomachs were obtained from patients and included gastric ulcer (4 cases), duodenal ulcer (2), and gastric cancer (24). Five of these cases were examined at 8, 19, 28, 143, and 171 days after the end of eradication therapy. For the preservation of the SMGL, these specimens were fixed in cold Carnoy's solution, cleared in xylene, and embedded in paraffin. Serial sections were obtained and were stained by dual staining with the galactose oxidasecold thionin Schiff reaction followed by paradoxical Concanavalin A staining and immunostaining forH. pylori.Results.H. pyloricharacterstically attached to surface mucous cells and colonized in the SMGL.H. pyloriin the SMGL was more abundant than that attached to the surface mucous cells. The degree ofH. pyloriinfection both on the surface of surface mucous cells and in the SMGL correlated well with the severity of gastritis. In the SMGL, this organism obviously preferred to colonize in the layer of surface mucous cell‐type mucins, and the multilaminated structure of the SMGL deteriorated markedly. Eradication ofH. pylorirestored the structure of the SMGL, and the inflammatory reaction decreased gradually.Conclusion.The SMGL is an indispensable site ofH. pyloricolonization, and this organism damaged the gastric mucosa partially by causing deterioration of the SMGL. Removal of the organism from the SMGL should be considered for eradication of this organis

ISSN:1083-4389    

DOI:10.1111/j.1523-5378.1996.tb00041.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

ABSTRACTBackgroundHelicobacter pyloriis the cause of chronic (type B) gastritis, duodenal ulceration (DU), and gastric ulceration (GU). Smoking is associated with delayed ulcer healing. Epidermal growth factor (EGF) is produced in the salivary and Brunner's glands of the upper gastrointestinal tract, inhibits gastri acid secretion, and is a powerful mitogen.Materials and Methods.We sought to determine gastric luminal EGF (GL‐EGF) in smokers and patients withHp‐associated DU and the effect ofHperadication. Our aim was to determine GL‐EGF in patients with GU and the effect of ulcer healing and to measure serum EGF in patients withHpgastritis with or without DU disease.Results.GL‐EGF was reduced in smokers compared to control (p= .008). Subjects with HP gastritis had reduced GL‐EGF compared to controls (p= .0002). There was no difference in GL‐EGF betweenHp‐positive subjects who had DU and those with chronic gastritis alone. Eradication ofHpfrom those patients with DU had no effect on the low levels of GL‐EGF. There was no difference between GL‐EGF inHpgastritis alone and inHp‐associated active GU. GL‐EGF fell after ulcer healing (p= .04), a difference confirmed by analysis of paired samples from patients before and after ulcer healing (p= .03). There was no difference in serum EGF between controls and subjects withHpinfection. There was no difference in serum EGF in subjects with DU‐associated and non‐ulcer‐associated gastritis.Conclusions.Subjects withHpgastritis, or those who smoke, had low concentrations of GL‐EGF regardless of whether DU was present. Eradication ofHpdid not return the concentrations of GL‐EGF to normal in DU subjects. Individuals withHpgastritis and inactive GU had low levels of GL‐EGF compared to non‐ulcerHpinfection. The relative increase in GL‐EGF that occurred with ulceration of the gastric mucosa may have resulted from the development of an ulcer‐associated cell lineage. Serum EGF did not play a role in the pathogenesis ofHpgast

ISSN:1083-4389    

DOI:10.1111/j.1523-5378.1996.tb00042.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

ABSTRACTBackgroundTransition mutations (A‐G) at residue 2143, cognate to position 2058 in theEscherichia coli23S rRNA gene, have been shown to confer resistance to macrolides inHelicobacter pylori.This study reports the finding that transversion mutations (A‐C) can occur at 2143 as well.Materials and Methods.Three clarithromycin‐resistantH. pyloriisolated from three different patients after treatment with clarithromycin were analyzed for point mutations by cycle sequencing of a 163‐bp amplified region surrounding residue 2143 within the conserved loop of the 23S rRNA gene.Results.Nucelotide sequence comparisons of a 163‐bp amplified product revealed that A‐C transversion mutations occurred at position 2143.H. pyloriisolated from the patients prior to treatment were susceptible to clarithromycin and displayed no polymorphism at 2143.Conclusion.This is the first report to show that A‐C transversion mutations at position 2143 can confer resistance to clarithromycin inH. pyloriand further support the role that mutations at position 2143 play in conferring macrolide resistanc

ISSN:1083-4389    

DOI:10.1111/j.1523-5378.1996.tb00043.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

ABSTRACTBackgroundAvailable data conflict regarding the possible relation between chronic gastritis, Helicohacter pylori (H p), and gastric motor disorders in nonulcer dyspepsia. The aim of this study, therefore, was (1) evaluate both gastroduodenal fasting motility and gastric emptying in subjects with functional dyspepsia, with and without gastritis, and (2) to correlate the motility pattern to H p infection.Materials and Methods.Thirty‐eight patients were studied, 20 positive for Hp infection (15 with gastritis) and 18 Hp‐negative (8 with gastritis). All the subjects underwent 240‐minute manometric recording of the interdigestive migrating motor complex, with evaluation of gastric and duodenal motility pattern and scintigraphic study of gastric emptying.Results.Whereas gastric emptying half‐times did not differ in the subgroups of dyspeptic patients, a significant reduction of gastric phase 111s of the migrating motor complex was detected between Hp‐positive and Hp negative subjects, both in overall patients (p<.01) and in patients with gastritis (p<.05).Conclusions.Hp infection seems to be related to a reduction of interdigestive gastric activity fronts, though it does not affect gastric emptying. The conflicting data regarding gastric emptying and interdigestive motility in Hp infection could be explained as probably investigating two different functiona

ISSN:1083-4389    

DOI:10.1111/j.1523-5378.1996.tb00044.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

ABSTRACTBackgroundGiven the therapeutic potential of proton pump inhibitor‐based triple therapy for successful cure ofHelicobacter pyloriinfection, we evaluated the efficacy and safety of lansoprazole with clarithromycin and amoxicillin in an open‐label, single‐center study.Materials and Methods.H. pylori‐positive patients self‐administered lansoprazole, 30 mg; clarithromycin, 500 mg; and amoxicillin, 1 gm bid for 14 days. Patients were assessed pretreatment, at which time the presence ofH.pylori was documented by rapid urease test, culture, or histology, following study drug administration (week 2) for a brief evaluation only, and at least 4 weeks posttreatment (week 6), which included endoscopy with collection of biopsy specimens for culture and histology testing.Results.Primary clarithromycin and metronidazole resistance were observed in 6% (2 of 30) and 43% (13 of 30) of study patients, respectively. One month after the end of therapy,H. pyloriinfection was cured in 23 of 25 patients (92%; 95% confidence interval, 74%‐99%). The triple‐therapy regimen was well‐tolerated; 17% of patients (5 of 30) reported mild to moderate adverse effects during the treatment period.Conclusion.A 2‐week, triple‐drug combination of lansoprazole, clarithromycin, and amoxicillin is highly effective for cure ofH. pyloriinfection. Additionally, the triple‐drug combination was well‐tolerated by patients

ISSN:1083-4389    

DOI:10.1111/j.1523-5378.1996.tb00045.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

ABSTRACTBackgroundTreatment with amoxicillin plus omeprazole results in disappointing cure rates ofHelicobacter pyloriinfection. The minimal inhibitory concentration of lansoprazole forH. pyloriin vitro is lower than that for omeprazole, prompting interest in treatment with amoxicillin plus lansoprazole.Materials and Methods.H. pylori‐infected patients with endoscopically documented duodenal ulcer either currently or within the past year were randomized to 14 days of (1) lansoprazole, 30 mg bid, plus amoxicillin, 1 gm tid; (2) lansoprazole, 30 mg tid, plus amoxicillin, 1 gm tid; (3) lansoprazole, 30 mg tid alone; or (4) amoxicillin, 1 gm tid alone. Endoscopy was done at enrollment and at 4 to 6 weeks after completion of treatment or for recurrent symptoms.H. pyloristatus was assessed by culture and histology. Ulcer prevalence was evaluated at follow‐up endoscopy.Results.Two hundred sixty‐two patients met enrollment criteria and were treated. By per‐protocol analysis,H. pyloriinfection was cured in 57% of those treated with lansoprazole twice daily plus amoxicillin and in 67% of those treated with lansoprazole three times daily plus amoxicillin, compared with 0% treated with lansoprazole alone or amoxicillin alone (p<.001 for dual therapy versus either monotherapy). Amoxicillin resistance was not observed. At follow‐up endoscopy, ulcer prevalence was 17% in patients treated with lansoprazole twice daily plus amoxicillin, 23% in those treated with lansoprazole three times daily plus amoxicillin, 33% in those treated with lansoprazole alone, and 35% in those treated with amoxicillin alone (p= .024; lansoprazole twice daily plus amoxicillin versus amoxicillin alone).Conclusions.Treatment with amoxicillin plus lansoprazole, 30 mg tid, led to cure ofH. pyloriinfection in 67% of patients with active or recently healed duode

ISSN:1083-4389    

DOI:10.1111/j.1523-5378.1996.tb00046.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

ABSTRACTBackgroundTo refine our understanding of anti‐Helicobacter pyloritreatment regimens further, we evaluated the efficacy and safety of lansoprazole given in combination with clarithromycin and metronidazole for 7 days in an open‐label, multicenter study.Materials and Methods.H. pylori‐positive patients self‐administered lansoprazole, 30 mg; clarithromycin, 500 mg; and metronidazole, 500 mg bid for 7 days. Patients were assessed at pretreatment, at which time the presence ofH. pyloriwas documented by rapid urease test or histology and culture, following study drug administration (week 1) for a brief evaluation only, and at least 4 weeks posttreatment (week 5), including endoscopy with collection of biopsy specimens for culture and histology testing.Results.Of the 60 patients enrolled in the study, 59 had confirmedH. pyloriinfection, and 51 were included in an intent‐to‐treat analysis of efficacy. Primary metronidazole and clarithromycin resistance were observed in 84% and 8% of study patients, respectively. One month after the end of therapy,H. pyloriinfection was cured in 40 of 51 patients (78%); 95% confidence interval, 65%–89%). The triple‐therapy regimen was well‐tolerated, with only 2 patients (4%) requiring premature withdrawal from the study due to treatment‐related adverse events. Taste perversion (15.0%) and diarrhea (11.7%) were the most frequently reported adverse events possibly or probably related to study medication during the treatment period.Conclusion.Despite a high prevalence of metronidazole resistance, a 1‐week, triple‐drug combination of lansoprazole, clarithromycin, and metronidazole is effective treatment for and well‐tolerated by patien

ISSN:1083-4389    

DOI:10.1111/j.1523-5378.1996.tb00047.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

ABSTRACTBackgroundRapid urease tests (RUTs) provide a simple, sensitive method of detectingHelicobacter pyloriinfection.Objectives.Our aim, therefore, was to determine whether the yield of detectingH. pyloriinfection by RUT varied depending on the site of gastric biopsy.Materials and Methods.Gastric biopsies were obtained from 50 patients for RUT by use of hpfast(GI Supply, Camp Hill, PA). Biopsies were taken from the prepyloric greater curve antrum, from the gastric angle, and from the greater curve in mid‐corpus. One biopsy specimen was placed in the RUT gel, and the biopsy from the adjacent mucosa was placed in formalin for subsequent histological evaluation by using the Genta stain. RUTs were examined and scored at intervals of 5, 10, 15, 30, and 45 minutes and after 1, 2, 4, and 24 hours.Results.Fifty patients were entered in the test (150 RUTs), 32 havingH. pyloriinfection. There were no false‐positive RUTs (specificity, 100%). The gastric angle site was positive in 100%. The prepyloric site was positive in 87%, and the corpus site was positive in 84.4% (p<.052 for angle or prepyloric antrum versus corpus). The most common pattern was for all to be positive (74%). The median time to positivity was similar with angle and prepyloric sites (37.5 and 60 minutes, respectively,p= not significant) and shorter than the corpus biopsy (180 minutes); (p<.05 for angle or prepyloric antrum versus corpus).Conclusion.The maximum probability for detectingH. pyloriinfection using a RUT is to obtain a biopsy from the gastric angle. To prevent missing a positive result when intestinal metaplasia is present, we recommend that (at a minimum) biopsies be taken from both the angle and the cor

ISSN:1083-4389    

DOI:10.1111/j.1523-5378.1996.tb00048.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

ISSN:1083-4389    

DOI:10.1111/j.1523-5378.1996.tb00049.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY