Biomedical subjects

M M Walker

Publications and source records attributed to M M Walker.

At least 37 records · Page 2Linked to original sources

PubMed1998

Changes to mucins in uninvolved mucosa and at the tumour site in gastric adenocarcinoma of intestinal type.

1. Mucin histochemistry is markedly altered in the stomach in intestinal-type adenocarcinoma. To increase understanding of these changes we have examined the content and distribution of carbohydrate in mucus glycopolypeptides isolated from non-malignant antrum, and from the uninvolved gastric mucosa and tumour site of patients with this disease. 2. The content of carbohydrate declined by 12.6% (P = 0.02) in mucus glycopolypeptides from uninvolved gastric mucosa when compared with those from non-malignant antrum, and by a further 25.4% (P < 0.001) in mucus glycopolypeptides from the tumour site. The first of these changes was accompanied by a significant decrease in the number of carbohydrate chains/1000 amino acid residues, and a significant increase in the number of monosaccharide units in each carbohydrate chain. The second of these changes was accompanied by significant decreases in both the number of carbohydrate chains/1000 amino acid residues, and in the number of monosaccharide units in each carbohydrate chain. 3. The number of sulphated monosaccharide units/100 carbohydrate chains increased from a mean of 7.2 in mucus glycopolypeptides from non-malignant antrum to a mean of 27.2 (P < 0.001) in preparations from uninvolved gastric mucosa and 22.7 (P < 0.001) in preparations from the tumour site. 4. Evidence is presented that these structural changes to mucus glycopolypeptides from the malignant stomach are due to an abnormal mucin biosynthesis by metaplastic goblet cells and/or immature gastric-type mucous cells within the uninvolved mucosa, and immature mucous cells at the tumour site.

ABO Blood-Group System↗

PubMed1998

Quantitative histopathology can aid diagnosis in painful bladder syndrome.

AIMS: To define the pathology of painful bladder syndrome using a morphometric method. METHODS: Bladder biopsy specimens from 31 patients with painful bladder syndrome and 11 controls were stained and examined at x260 magnification with the aid of a 100 square counting grid. Random counts of the different tissues and inflammatory components were made to ascertain whether constant differences occurred that could be used to define the pathology of this uncommon condition. RESULTS: In the lamina propria of painful bladder syndrome specimens, a significant increase was seen in the concentration of lymphocytes, T cells, and blood vessels; a decrease was seen in the number of fibroblasts, and no change was seen in the number of mast cells and macrophages. B cells were sporadic. The basement membrane in these specimens showed significant discontinuity and there was increased collagen deposition in the underlying muscle when compared with controls. CONCLUSION: Painful bladder syndrome exhibits constant histological features that may be used to aid diagnosis in this uncommon condition. Simple numerical cell/tissue measurement of this kind is also useful when treatment trials are considered, because objective statistical analysis (pretreatment and post-treatment) is possible without the need for expensive and complicated equipment.

Adult↗

PubMed1997

Absence of toxicity of oats in patients with dermatitis herpetiformis.

BACKGROUND: People with gluten sensitivity should avoid foods containing wheat, rye, and barley, but there has been debate about whether they should avoid oats. Although patients with celiac disease have recently been shown to tolerate oats, less is known about the effects of oats on patients with dermatitis herpetiformis. METHODS: We studied seven men and three women (mean age, 58 years) with biopsy-confirmed dermatitis herpetiformis. They had followed a strict gluten-free diet for a mean of 15.8 years, which controlled their rash and enteropathy. The patients added oats that were not contaminated with gluten to their diets for 12 weeks (mean [+/-SD] daily intake, 62.5+/-10.8 g). RESULTS: None of the patients had any adverse effects. Serologic tests for antigliadin, antireticulin, and antiendomysial antibodies were negative before oats were introduced into the diet and after they were discontinued. Villous architecture remained normal: the mean (+/-SE) ratio of the height of villi to the depth of crypts was 3.59+/-0.11 before the diet and 3.71+/-0.09 afterward (normal, 3 to 5), and the mean enterocyte heights were 31.36+/-0.58 microm and 31.75+/-44 microm, respectively (normal range, 29 to 34). Duodenal intraepithelial lymphocyte counts all remained within normal limits (mean, 13.8+/-1.03 per 100 enterocytes before the diet and 14.2+/-1.2 per 100 enterocytes afterward; normal range, 10 to 30). Dermal IgA showed no significant changes. CONCLUSIONS: Patients with dermatitis herpetiformis can include moderate amounts of oats in their gluten-free diets without deleterious effects to the skin or intestine.

Adult↗

PubMed1997

Magnetic orientation and the magnetic sense in arthropods.

The physical properties of the earth's magnetic field are summarized with the aim of emphasizing their significance as cues that can be exploited in orientational tasks. Past work has revealed magnetic orientation in vertebrates as well as invertebrates, including arthropods. The key finding to date has been that, as opposed to many vertebrates, the magnetic compass of arthropods responds to the polarity, rather than to the inclination of the earth's magnetic field. As in the case of vertebrates, the debate over how arthropods detect magnetic fields has yet to be resolved. Currently, evidence has been reported in support of a detection system based on magnetite crystals together with a variety of detection systems based on events occurring at the molecular level. Interactions between the magnetic and other compasses in orientation experiments suggest the existence of an area in the brain where spatial orientation information from magnetic and other stimuli converges. The slow advance of our knowledge on magnetic orientation in arthropods, as opposed to the much better understanding of magnetic orientation in vertebrates, arises from difficulties in identifying the appropriate behavioural contexts in which arthropods respond to magnetic fields in both laboratory and field situations. Arthropods thus present challenges not only in demonstrating magnetic orientation, but also in elucidating the sensory mechanisms involved in the perception of magnetic fields.

Animals↗

PubMed1997

A clinicopathological approach to cystitis--recommendations for simplified pathology reporting.

OBJECTIVE: To assess the accuracy of histopathology reports of bladder biopsy specimens showing chronic cystitis and to develop a standard method of reporting in the form of a template which will aid both clinician and patient in the management of this condition. MATERIALS AND METHODS: Over a 4-year period, the reports of 134 bladder biopsy specimens diagnosed as chronic inflammation of the bladder were examined for clinical details, cystoscopy findings, pathology details and conclusions. Within each of these groups, the common terms were assessed for their relevance to the final outcome. RESULTS: The analysis of each part of these reports revealed no clinical details in 33%, no cystoscopy details in 26% and no histopathology conclusion in 20%. The commonest terms used were: macroscopic haematuria (25%) for clinical details; red patch/ inflamed (40%) for cystoscopic details, morphological site involved (65%) for pathology details; and mild chronic cystitis (37%) for the conclusions. Standardized criteria were devised and after reassessing the reports, 75% were considered to be accurate and complete. CONCLUSIONS: Overall, the histopathology reports examined were more than adequate for the clinicians' use but the spectrum of details provided did not add to the usefulness of the final report. By limiting the terms available, a more standardized report can be produced, benefiting both clinician and patient.

Adult↗

PubMed1997

The effect of gastrin-releasing peptide on gastrin and somatostatin messenger RNAs in humans infected with Helicobacter pylori.

BACKGROUND & AIMS: Gastrin-releasing peptide stimulates gastrin secretion but also inhibits its release via somatostatin. Exogenous gastrin-releasing peptide stimulates a greater increase in plasma gastrin concentrations in patients infected with Helicobacter pylori than in uninfected controls. Because this infection suppressed gastric mucosal somatostatin, we studied whether the increased gastrin response was a result of an abnormal response of the somatostatin cell. METHODS: Patients without dyspeptic ulcers received an infusion of either gastrin-releasing peptide or saline on separate occasions. Acid secretion was measured, and gastric biopsy specimens were taken for gastrin and somatostatin messenger RNA (mRNA) analysis and H. pylori diagnosis. RESULTS: In response to gastrin-releasing peptide, the increase in plasma gastrin concentrations in the infected patients was significantly higher than in the uninfected. Antral gastrin mRNA also increased significantly in the infected group but decreased significantly in the uninfected group. Basal somatostatin was lower in the infected group; gastrin-releasing peptide produced a significant increase in antral somatostatin mRNA concentration in infected, but not uninfected, patients. CONCLUSIONS: The somatostatin cell responds to gastrin-releasing peptide in H. pylori infection. Gastrin-releasing peptide normally inhibits gastrin mRNA expression, but inhibition is deficient in H. pylori infection, possibly because of low stimulated somatostatin levels.

Adult↗

PubMed1997

Hunterian peptic ulcers and Helicobacter pylori.

Gastric spiral organisms were first described in man in 1939 and identified as Helicobacter pylori causing peptic ulcers in the early 1980s. Surgical specimens of gastric resections from 1939 showed H. pylori to be present. Full-thickness sections of gastric mucosa from gastric specimens from the eighteenth-century Hunterian Collection at The Royal College of Surgeons of England were examined by histology for the presence of H. pylori. Four gastric ulcers and a section from an oesophageal varix showed remarkable preservation of the overall architecture, but surface autolysis did not allow identification of the bacteria. However, the presence of lymphoid aggregates in the Hunterian specimens suggests that H. pylori may have been present before autolysis.

Female↗

PubMed1996

Gastric metaplasia: its role in duodenal ulceration.

There is good evidence to suggest that gastric metaplasia in the proximal duodenum and Helicobacter pylori gastritis are essential requirements for the development of duodenal ulceration in most cases. Gastric metaplasia is most likely to be a defence response or adaptation to excess acid reaching the duodenum. The appearance of gastric-type epithelium over the duodenal villi probably results from substitution by cells migrating from Brunner's gland ducts. These metaplastic foci provide sites for colonization by H. pylori passing through the duodenum; the organisms do not attach to native duodenal epithelial cells. Having colonized the metaplastic areas, H. pylori provokes an active chronic inflammatory response akin to that seen in the gastric mucosa. Active chronic duodenitis leads to a weakening of mucosal defence against acid-peptic attack, and erosion and ulceration may ensue. Healing of ulcers by conventional acid-reducing treatments does not influence the extent of gastric metaplasia, (although there may be some reduction with long-term proton pump inhibitors); nor do such regimens affect the background duodenitis. Only with eradication of H. pylori is there resolution of inflammation, but studies to date indicate that eradication alone has no substantial effect on the prevalence or extent of gastric metaplasia. Nevertheless the elimination of H. pylori appears to remove one of the essential co-factors for duodenal ulceration and the patient can be considered cured, despite the persistence of gastric metaplasia.

Duodenitis↗

PubMed1996

Relation between gastric acid output, Helicobacter pylori, and gastric metaplasia in the duodenal bulb.

BACKGROUND: Factors that determine gastric metaplasia in the duodenal bulb are ill defined. It is more common and extensive in the presence of high acid output and possibly in the presence of Helicobacter pylori. However, no quantitative relation between acid output and the extent of gastric metaplasia has been demonstrated and its relation to H pylori is uncertain. AIM: To determine the relation between H pylori infection and acid output and the presence and extent of gastric metaplasia in the duodenal bulb. subjects: H pylori positive and negative patients with duodenal ulcer and healthy controls were studied. METHODS: Quadrantic duodenal bulb biopsy specimens were taken and the presence and extent of gastric metaplasia determined using a computer enhanced image intensifier. Basal and stimulated acid outputs were measured. RESULTS: gastric metaplasia was significantly (p < 0.05 more common and significantly (p < 0.05) greater in extent in patients with duodenal ulcer than in controls. Neither the prevalence or extent of gastric metaplasia was affected by H pylori status. There were significant (p < 0.01) direct correlations between acid output and extent of gastric metaplasia. CONCLUSIONS: Prevalence and extent of gastric metaplasia are not related to H pylori in controls, or in patients with duodenal ulcer. Rather, high acid response to gastrin may be more important.

Adult↗

PubMed1996

Myxoid renal cell carcinoma: histological, immunocytochemical and ultrastructural study.

Renal cell carcinomas show a variety of histological features. A case of a renal tumour arising in a 44 year old African man is reported. The tumour was composed of a cobweb-like pattern of narrow anastomising tubules lined by cuboidal cells separated by a hypocellular myxoid stroma. Immunohistochemical stains were consistent with a renal cell origin. The differential diagnosis in these cases includes sarcoma.

Adult↗

PubMed1996

Parietal cells in the duodenal bulb and their relation to Helicobacter pylori infection.

AIM: To investigate the prevalence, and relation to Helicobacter pylori, of parietal cells in the duodenal bulb using a monoclonal antibody directed against H+,K(+)-ATPase (HK12.18). METHODS: Twenty six patients with duodenal ulcer disease and 16 healthy controls were studied. H pylori status was determined by gastric histology and culture and by the 13C-urea breath test. Four biopsy specimens were taken from the duodenal bulb and stained with HK12.18. The presence/absence and number of parietal cells in the duodenal bulb were assessed blindly by a histopathologist. RESULTS: The overall prevalence of parietal cells in the duodenal bulb was 31% (13/42) and was similar in patients with duodenal ulcer and in controls, and in H pylori positive and negative subjects. The median (range) number of parietal cells in the duodenal bulb was 7.5 (4-20) parietal cells/subject, and was similar in all four groups. CONCLUSIONS: The prevalence of parietal cells in the duodenal bulb (31%) is notably higher than previously reported in endoscopic studies, and is in keeping with reports from studies on necropsy/operative specimens. There was no difference in the prevalence or number of parietal cells in the duodenal bulb between patients with duodenal ulcer and controls, regardless of H pylori status. These findings suggest that parietal cells in the duodenal bulb do not contribute to the pathogenesis of duodenal ulcer.

Adult↗

PubMed1996

Lansoprazole, clarithromycin and metronidazole for seven days in Helicobacter pylori infection.

BACKGROUND: This study determines the efficacy and safety of a 1-week triple therapy regimen of lansoprazole, clarithromycin and metronidazole in an area with a high prevalence of pre-treatment metronidazole-resistant strains of Helicobacter pylori. METHODS: Seventy-five H. pylori positive patients with gastritis or duodenal ulcer were entered into an open study of lansoprazole 30 mg o.m., clarithromycin 250 mg b.d. and metronidazole 400 mg b.d. H. pylori status was determined by CLOtest, histology, culture and by 13C-urea breath test (repeated > or = 28 days after treatment). RESULTS: Seventy-one patients completed the treatment and returned for follow-up. H. pylori was eradicated in 61 of 71 (86%) patients by per-protocol analysis, and in 61 of 75 (81%) patients by intention-to-treat analysis. H. pylori was eradicated in 12 of 16 (75%) patients with metronidazole-resistant strains compared with 22 of 24 (92%) in patients with metronidazole-sensitive strains of H. pylori (P = 0.14). Fourty-five patients reported at least one adverse event, and three patients stopped treatment due to them (two with headaches and one with diarrhoea). CONCLUSIONS: A 1-week course of lansoprazole 30 mg o.m., clarithromycin 250 mg b.d. and metronidazole 400 mg b.d. eradicates H. pylori in up to 86% of patients. It is of proven benefit in patients with pre-treatment metronidazole-resistant strains of H. pylori.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1995

Lack of proliferative response by gluten-specific T cells in the blood and gut of patients with dermatitis herpetiformis.

The majority of patients with Dermatitis Herpetiformis (DH) have a gluten-sensitive enteropathy which may be triggered by a T cell-mediated immune response to gluten. Using a proliferative assay, the responses to gluten fraction III, recall antigens and mitogens of peripheral blood mononuclear cells (PBMC) and gut T cell lines (TCL) isolated from patients with Dermatitis Herpetiformis (DH) and normal controls were studied. In most cases, neither PBMC nor gut T cell lines (which were predominantly CD3+, CD4+, TCR alpha beta +) from either controls or patients proliferated in response to gluten fraction III alone. However, the addition of 10 U/ml IL-2 to PBMC cultures containing gluten fraction III resulted in a marked increase in proliferation in 9/19 DH patients and 7/11 controls compared to IL-2 alone. Furthermore, gluten-induced upregulation of IL-2 receptor (CD25) expression was demonstrated on PBMC from 4/4 patients with DH and 2/3 controls after 7 days' culture with antigen. A similar effect by exogenous IL-2, or the same concentration of IL-4, was observed in 8/11 (P = 0.02) and 5/6 respectively DH, and 3/4 normal gut T cell lines. No difference was observed in the response of DH and control PBMC to Tetanus toxin, Candida albicans and PPD; both normal and DH gut T cell lines were unresponsive to these antigens. However, the addition of IL-2 increased the response to Candida albicans by DH gut T cell lines. Moreover, the response of DH gut T cell lines to PHA (P < 0.001), Concanavalin A and anti-CD3 were markedly reduced compared to PBMC from the same patients. These findings suggest that gluten-specific T cells present in the blood and gut of normal and DH individuals are activated by but do not proliferate in response to specific antigen.

Candida albicans↗

PubMed1995

Changes in the intragastric distribution of Helicobacter pylori during treatment with omeprazole.

Omeprazole is a powerful inhibitor of gastric acid and may suppress Helicobacter pylori by effecting the pKa of H pylori urease, by altering the pattern of infection, or by promoting overgrowth of other bacteria. At routine endoscopy H pylori was detected by histology and culture before and after four weeks' treatment with omeprazole, 40 mg each morning. A 13C-urea breath test was also done at t = 0, 2, 4, and 6 weeks. Thirty nine patients with duodenal ulcer (n = 25) or reflux oesophagitis (n = 14) were studied, of whom 29 of 39 had H pylori infection. During omeprazole treatment, 13C-urea breath test values fell significantly--mean (SEM) values before treatment and at four weeks were 23.0 (2.1) and 15.5 (2.7) per mil respectively, p < 0.001. Before treatment H pylori was seen in 28 of 29 antral, 29 of 29 corpus, and 28 of 29 fundic biopsy specimens. After four weeks of omeprazole treatment, the histological density of H pylori in the antrum and corpus was reduced (p < 0.001), while that in the fundus was increased. The migration of H pylori from the antrum to the fundus was associated with a corresponding decrease in the activity of antral gastritis. H pylori was not seen in antral biopsy specimens from 12 of 29 patients whose median excess delta 13CO2 excretion fell from 23.0 to 9.9 per mil. In the body mucosa, 26 of 29 specimens were still positive for H pylori and there was no significant change in the gastritis type. Two weeks after finishing treatment, the mean (SEM) excess delta 13CO2 excretion returned to levels before treatment. Omeprazole decreases antral H pylori colonisation but increases that in the fundus. The changes in the intragastric distribution of the organism are associated with concomitant changes in the activity of gastritis and are matched by a progressive fall in the excretion of delta 13CO2.

Acute Disease↗

PubMed1995

Identification of parietal cells in gastric body mucosa with HMFG-2 monoclonal antibody.

AIMS: To identify parietal cells in the upper gastrointestinal tract by an immunoperoxidase method, using commercially available monoclonal antibodies. METHODS: Routine surgical biopsy specimens of gastric body mucosa were examined using the avidin-biotin peroxidase method with the monoclonal antibodies HMFG-1 and HMFG-2 to identify parietal cells. Double immunoperoxidase labelling with HK12.18, a well characterised monoclonal antibody directed against an epitope on the alpha (catalytic) subunit of H+ translocating, K+ stimulated adenosine triphosphatase (H,K-ATPase), was used to confirm that HMFG-1 and -2 stained parietal cells. RESULTS: HMFG-1 and HMFG-2 showed consistent parietal cell staining patterns in the gastric body mucosa. HMFG-2 gave a more intense staining pattern of the secretory canaliculi. This was confirmed by double immunolabelling with HK12.18. CONCLUSIONS: HMFG monoclonal antibodies are recommended as highly specific markers of human gastric parietal cells.

Antibodies, Monoclonal↗

PubMed1995

Aromatase activity and interleukin-6 production by normal and malignant breast tissues.

The aromatase enzyme complex, which regulates the conversion of androstenedione to estrone, may have an important role in regulating estrogen synthesis in breast tissues. In this study the effect of tumor location on aromatase activity in adjacent tissue was examined and related to interleukin-6 (IL-6) production, which has been shown to stimulate aromatase activity in breast cancer cells. Samples of normal and malignant breast tissues were obtained from 11 women undergoing mastectomy. In 7 patients, aromatase activity was highest in the quadrant in which the tumor was located or on which the tumor impinged. Aromatase activity in tumor-bearing quadrants was significantly higher than that in adjacent and opposite quadrants. Aromatase activity and IL-6 production, expressed in terms of tissue weight, were significantly higher for tumor tissue compared with normal breast adipose tissue. A significant correlation was found between aromatase activity and IL-6 production for breast tumor tissue (rs = 0.56; P < 0.05), but not for adipose tissue from the breast quadrants. Aromatase activity and IL-6 production were also measured in tissue obtained from a normal woman undergoing reduction mammoplasty who had previously had breast augmentation by silicone injection, not contained within a capsule. In tissue from this patient there was evidence of chronic inflammation and a marked macrophage response. Aromatase activity in this tissue was considerably higher than that detected in mastectomy adipose tissue samples, and a significant correlation was found between aromatase activity and IL-6 production (rs = 0.77; P < 0.05). A preliminary study to examine the potential role of cells of the immune system in regulating breast tissue aromatase activity revealed that conditioned medium collected from macrophages and lymphocytes could markedly stimulate aromatase activity in tumor-derived fibroblasts. The results of this study confirmed that breast tumor location can influence aromatase activity in adjacent tissues and showed that aromatase activity is increased in tumor-bearing quadrants. The increased production of IL-6 by tumor tissue and its correlation with aromatase activity suggest that tumors may be the major source of IL-6, which is able to influence aromatase activity in adjacent tissues.

Adipose Tissue↗

PubMed1994

One week's anti-Helicobacter pylori treatment for duodenal ulcer.

This open study tested whether eradication of Helicobacter pylori (H pylori) heals duodenal ulcers as well as decreasing recurrence. H pylori was detected in patients with endoscopic duodenal ulcers by histology, CLO-test, culture, and 13C-urea breath test (13C-UBT). Tripotassium dicitrato bismuthate (120 mg) and amoxycillin (500 mg) each four times daily, were given for seven days, with 400 mg metronidazole five times a day on days 5-7. The 13C-UBT was repeated immediately after treatment and endoscopy repeated within 21 days. After treatment unhealed ulcers were reinspected one month later and healed ulcers followed up by 13C-UBT alone for 12 months. Of 45 patients, 44 were available for follow up. Mean pretreatment excess delta 13CO2 excretion was 25.6 per mil, which fell to 2.4 per mil immediately after finishing treatment, indicating clearance of H pylori in every patient. At the second endoscopy (median interval 20 days from start of treatment) 33 of 44 (75%) duodenal ulcers had healed. Ten of the remaining 11 duodenal ulcers were smaller and those 10 healed in the next two weeks with no further treatment. Two patients' ulcers that initially healed with clearance of H pylori recurred three weeks later (both had metronidazole resistant H pylori). H pylori was eradicated in 28 of 44 (64%) patients (13C-UBT negative for median follow up 10.2 months). Overall 41 of 43 (93%, 95% confidence intervals 81%-99%) duodenal ulcers were healed at one month. This study suggests that one week of anti-H pylori triple treatment is effective in healing duodenal ulcers.

Adolescent↗

PubMed1994

Eradication of Helicobacter pylori with clarithromycin and omeprazole.

Clarithromycin, a new and well tolerated, acid stable macrolide antibiotic, has a similar antimicrobial spectrum to erythromycin but a better in vitro MIC90 (0.03 microgram/l-1) against Helicobacter pylori (H pylori). This study aimed at determining the eradication rate using clarithromycin 500 mg thrice daily and omeprazole 40 mg daily for two weeks. Patients were given an endoscopy and H pylori status assessed by antral culture (microaerobic conditions, for up to 10 days), antral and corpus histology tests (haematoxylin and eosin/Gimenez stains), and 13C-urea breath test (13C-UBT, European standard protocol, positive result = excess delta 13CO2 excretion > 5 per mil). Compliance was assessed by returned tablet counts. H pylori clearance at the end of treatment and eradication four weeks after finishing treatment were assessed by the 13C-UBT. Seventy three patients (54 men, median age 45 years) with duodenal ulcers (n = 42) or duodenitis/non-ulcer dyspepsia (n = 31) all with a positive 13C-UBT (mean (SEM) excess delta-13CO2 excretion = 26.6 (4.9) per mil) and either positive antral histology (n = 72) or positive antral culture (n = 35) were studied. Before treatment 2/27 (7%) isolates of H pylori were resistant to clarithromycin and five isolates were resistant to metronidazole. In 70/73 (96%) the 13C-UBT was negative immediately after finishing treatment. Four weeks later the 13C-UBT was negative in 57/73 (mean (SEM) excess delta 13CO2 excretion = 1.2 (0.3) per mil, eradication rate = 78%). Forty eight (66%) patients experienced a metallic taste while taking the tablets. Although four (5%) patients, however, could not complete the course of treatment, in only one of these four was H pylori not eradicated. These results show that duel therapy with clarithromycin and omeprazole is well tolerated. With an eradication rate of 78% it is an effective treatment for metronidazole resistant H pylori and may be an alternative to standard triple therapy.

Adult↗