Biomedical subjects
W L Peterson
Publications and source records attributed to W L Peterson.
The treatment of Helicobacter pylori infection in the management of peptic ulcer disease.
Antimicrobial therapy against H. pylori is indicated for all patients with documented peptic ulcer disease who have evidence of the infection. The regimen of first choice, selected on the basis of available studies, is triple therapy with bismuth, metronidazole, and tetracycline (Table 1). For patients who are known to have taken metronidazole previously, clarithromycin may be substituted for metronidazole. For patients with active, symptomatic peptic ulcers we also recommend an antisecretory drug to promote healing and relieve symptoms. Second-choice regimens consist of combinations of two antimicrobial drugs--metronidazole, amoxicillin, or clarithromycin--with an antisecretory agent, preferably an H+/K+-ATPase antagonist such as omeprazole. The combination of a single antimicrobial drug (especially amoxicillin) with omeprazole is less efficacious and cannot be recommended. Regardless of the antimicrobial regimen used, successful eradication of H. pylori infection markedly reduces the risk of recurrent peptic ulcers. If this therapeutic approach is taken with all patients with peptic ulcers, the recurrence of ulcers should become a rarity in medical practice.
Characterization of a 3.5-kbp plasmid from Helicobacter pylori.
A 3.5-kbp plasmid (pHPM180) was isolated from Helicobacter pylori (HPM180) and the DNA sequence was determined. Two open reading frames (ORF1 and ORF2) were identified which could encode polypeptides of 54,517 and 27,629 Da, respectively. Ribosome binding and promoter consensus sequences were identified, as well as two 232-bp direct repeats and four 22-bp direct repeats. DNA sequence homology was found between pHPM180 ORF1 and a 684-base pair HindIII fragment from a 5.6-kbp H. pylori plasmid. ORF1 showed amino acid homology with six replication proteins from bacterial plasmids with theta-type replicons. Additional sequence identity was found between pHPM180 noncoding DNA and a segment of H. pylori pHPK255, a plasmid that replicates via a rolling circle type mechanism. A ribonuclease protection assay determined that ORF1 was transcribed in H. pylori HPM180.
The role of acid in upper gastrointestinal haemorrhage due to ulcer and stress-related mucosal damage.
A peptic ulcer is a lesion in which acid and pepsin are essential components of pathogenesis. Regardless of the type of patient or the setting in which the ulcer presents, the basic pathogenetic scheme is the same. The primary event is disruption of mucosal integrity. In the presence of acid and pepsin, such disruption of integrity leads to an ulcer. While rarely sufficient by itself to cause ulceration, the presence of acid is a necessary cofactor. The causes of disruption of mucosal integrity include nonsteroidal anti-inflammatory drugs (NSAIDs), Helicobacter pylori and critical illness. With the latter, tissue ischaemia may be the primary event, leading to back-diffusion of H+ ions through increased membrane permeability. Impaired mucosal buffering then leads to intramural acidosis and cell death. Risk factors for bleeding peptic ulcer in the intensive care unit (ICU) include severe trauma, sepsis, respiratory failure, and coagulopathy. Potential roles for decreasing gastric acidity in the treatment of bleeding peptic ulcer include cessation of active bleeding, prevention of rebleeding in hospital and primary prevention of bleeding. Most published studies dealing with the first two situations suggest no benefit with antisecretory therapy. However, the optimal pH for clot and platelet function may be > or = 7.0. Can such pH levels be maintained with antisecretory agents such as the proton pump inhibitors? Are the published trials adequate to demonstrate any benefit from antisecretory agents? Primary prevention of bleeding ulcer in the outpatient setting includes avoidance of NSAIDs, use of antisecretory agents and eradication of H. pylori.(ABSTRACT TRUNCATED AT 250 WORDS)
Perspectives on training in gastroenterology.
Training in endoscopy has changed dramatically during the past 20 years and will probably change even more over the next 10 years. To confront these changes more effectively, the leaders of the four major digestive disease societies, collectively known as the Gastroenterology Leadership Council (GLC), encouraged the formation of a training director's committee. This article discusses several of the issues that the GLC Training Directors Committee has dealt with.
Prevention of upper gastrointestinal bleeding.
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Clarithromycin as monotherapy for eradication of Helicobacter pylori: a randomized, double-blind trial.
UNLABELLED: Current regimens to eradicate Helicobacter pylori usually consist of metronidazole plus a bismuth compound, as well as a third agent such as tetracycline. Such regimens are not ideal because organisms may be metronidazole-resistant, side-effects occur, and compliance is often poor. This randomized, double-blind study was designed to assess the ability of clarithromycin, a new macrolide antimicrobial, as monotherapy to eradicate H. pylori. Thirty-seven healthy volunteers who were H. pylori positive by 13C-urea breath test plus histology and/or culture completed 14 days of oral therapy with clarithromycin in one of three dosages. Eradication, defined as all three tests negative at 4-6 wk after the end of therapy, was achieved in 2/13 (15%) with clarithromycin 500 mg bid, 4/11 (36%) with 1000 mg bid, and 7/13 (54%) with 500 mg qid. Isolates of H. pylori were resistant to clarithromycin prior to therapy in 12% of subjects, and became resistant during therapy in 21% of subjects. Taste perversion, the most common side effect, resulted in one subject terminating therapy. CONCLUSIONS: Whereas clarithromycin is a promising antimicrobial in the eradication of H. pylori, it is not sufficient to be used as monotherapy.
Acid secretion and serum gastrin in normal subjects and patients with duodenal ulcer: the role of Helicobacter pylori.
OBJECTIVES: To compare gastric secretory function in patients with duodenal ulcer and in healthy volunteers with and without Helicobacter pylori infection. METHODS: Basal acid output, peak acid output, meal-stimulated acid output, fasting and meal-stimulated serum gastrin concentrations were measured in 136 healthy volunteers (63 H. pylori positive, 73 H. pylori negative) and 52 duodenal ulcer patients, all but one of whom were H. pylori positive. RESULTS: By multivariate linear regression analysis, H. pylori infection was a significant negative predictor of basal acid output and a positive predictor of fasting and meal-stimulated gastrin concentrations. When compared to truly normal (i.e., H. pylori-negative) control subjects, duodenal ulcer patients had elevated basal acid output, peak acid output, fasting and meal-stimulated gastrin concentrations. CONCLUSIONS: Our results show that in patients with duodenal ulcer disease, hypergastrinemia is largely related to gastric H. pylori infection, whereas acid hypersecretion is due to factors other than H. pylori.
Helicobacter pylori and peptic ulcer disease.
Medical therapy for duodenal or gastric ulcer disease has traditionally involved gastric acid antisecretory therapy for 4 to 8 weeks to promote initial healing and indefinitely to prevent recurrences of ulcer. The discovery of Helicobacter pylori in most patients with peptic ulcer disease has led to a change in this approach. Therapy designed to eradicate H pylori may facilitate ulcer healing with acid antisecretory agents and, more important, may greatly reduce the incidence of ulcer recurrence, obviating the need for maintenance antisecretory therapy. Regimens designed to eradicate H pylori are difficult to comply with, however, and are associated with adverse effects in some patients. In this article we review the diagnosis and treatment of H pylori infection in patients with peptic ulcer disease and make recommendations regarding the use of conventional ulcer therapies and therapies designed to eradicate H pylori.
Injection sclerotherapy as a cause of Klebsiella pneumoniae peritonitis.
We report a case of Klebsiella pneumoniae peritonitis after endoscopic sclerotherapy and discuss its pathogenesis and risk factors. We also review previous cases in the literature and make recommendations for prophylactic therapy. Endoscopists should be aware of peritonitis as a possible complication of endoscopic sclerotherapy.
Enteric-coated charcoal as a means of blinding studies comparing bismuth and H2-receptor antagonists.
Clinical trials comparing H2-receptor antagonists and bismuth-containing regimens in ulcer healing, ulcer relapse, or dyspepsia have not been double-blind, because bismuth darkens stools. This study was designed to determine whether enteric-coated charcoal could darken stools of subjects taking an H2-receptor antagonist without interfering with absorption of the drug. Twelve healthy volunteers participated in a randomized, double-blind, crossover trial of oral ranitidine (300 mg at bedtime) alone, ranitidine plus bismuth (30 ml Pepto-Bismol four times daily), and ranitidine plus enteric-coated charcoal (four tablets daily). Mean stool colors both with ranitidine plus charcoal and with ranitidine plus bismuth were significantly darker than with ranitidine alone, but were not significantly different from each other. Blood levels of ranitidine during the 10 h after its administration did not differ significantly among the three regimens. We conclude that enteric-coated charcoal can be used to blind clinical trials comparing an H2-receptor antagonist (e.g., ranitidine) and a bismuth regimen.
Helicobacter pylori and peptic ulcer disease.
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Controversies, dilemmas, and dialogues. Reduction of gastric acidity in the treatment of peptic ulcer disease: how low should we go?
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Helicobacter pylori gastritis: a 'normal' phenomenon.
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Pathogenesis and therapy of peptic ulcer disease.
The epithelial cells of the stomach and duodenum are normally protected from the damaging effects of acid and pepsin by a balancing mechanism of mucosal resistance. If an imbalance occurs, peptic ulcer may result. Traditional teaching has emphasized the importance of acid (and pepsin) as the cause of this imbalance; however, it is clear that acid and pepsin are not the only important factors in the pathogenesis of peptic ulcer. More recent investigative efforts have been directed at what constitutes mucosal resistance and how it can be disrupted to produce, in the presence of gastric acid, a peptic ulcer. Depletion of endogenous prostaglandins and Helicobacter pylori gastritis have emerged as prominent theories. As evidence exists both to support and refute these theories in humans, any definitive conclusions cannot be made at this time. The acute management of peptic ulcer disease is directed at relieving pain, accelerating ulcer healing, and preventing complications. Peptic ulcers can be healed with antisecretory agents (i.e., H2-receptor antagonists, omeprazole), antacids, prostaglandins, and sucralfate. Because they are effective, safe, and convenient, the H2-receptor antagonists are the most widely used agents for the management of peptic ulcer disease. Because the H2-receptor antagonist agents are equally effective in their indicated uses and are equally safe based on scientifically valid data, selection should be based primarily on cost. Omeprazole is the newest antisecretory agent: a single morning dose of 20 mg suppresses acid secretion for 24 h. The agent offers little advantage over H2-receptor antagonists for the majority of patients with peptic ulcer.(ABSTRACT TRUNCATED AT 250 WORDS)
Bleeding peptic ulcer. Epidemiology and nonsurgical management.
Bleeding peptic ulcer remains an important problem, particularly for the elderly. Recognition of the rule of nonsteroidal anti-inflammatories in bleeding ulcer and employment of endoscopic therapeutic modalities offer promise that morbidity and mortality from bleeding ulcer may be reduced.
Peptic ulcer--an infectious disease?
These discussions are selected from the weekly staff conferences in the Department of Medicine, University of California, San Francisco. Taken from transcriptions, they are prepared by Homer A. Boushey, MD, Professor of Medicine, and Nathan M. Bass, MD, PhD, Associate Professor of Medicine, under the direction of Lloyd H. Smith, Jr, MD, Professor of Medicine and Associate Dean in the School of Medicine. Requests for reprints should be sent to the Department of Medicine, University of California, San Francisco, School of Medicine, San Francisco, CA 94143.