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Peptic Ulcer Disease

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8021. Randomised study of the influence of non-steroidal anti-inflammatory drugs on the treatment of peptic ulcer in patients with rheumatic disease. (PubMed)

Randomised study of the influence of non-steroidal anti-inflammatory drugs on the treatment of peptic ulcer in patients with rheumatic disease. Sixty-seven patients with rheumatic disease, treated with non-steroidal anti-inflammatory drugs (NSAIDs), entered a controlled trial with a diagnosis of duodenal (n = 51), gastric (n = 14), or gastric and duodenal (n = 2) ulcers. The main objectives of the study were a comparison of ranitidine and sucralfate in ulcer treatment, and to observe (...) the influence of continued NSAID administration during peptic ulcer therapy. Ulcers healed within nine weeks in 52 patients. The mean healing time was similar in 27 patients given ranitidine 150 mg bd (4.9 weeks) and 25 patients given sucralfate 1 g qid (4.6 weeks). In patients with unhealed ulcers after nine weeks of treatment, healing was obtained in seven after further therapy for 3-9 weeks. Of the 30 patients who continued NSAIDs during treatment with either ranitidine or sucralfate, 23 ulcers healed

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1987 Gut

8022. Management of peptic ulcer disease not related to Helicobacter pylori or NSAIDs. (PubMed)

Management of peptic ulcer disease not related to Helicobacter pylori or NSAIDs. Helicobacter pylori (H. pylori) infection is widely accepted as the most important factor in the pathogenesis of duodenal ulcer. However, in parallel with more effective eradication of H. pylori, the prevalence of H. pylori is changing, and H. pylori-negative peptic ulcer disease appears to be increasing. When making a diagnosis of H. pylori-negative peptic ulcer disease, it is essential to avoid misclassification (...) because of inaccurate diagnosis. In addition, secondary causes may need to be excluded with appropriate investigations. In the absence of H. pylori, nonsteroidal anti-inflammatory drug usage is the most common cause of peptic ulcer; surreptitious nonsteroidal anti-inflammatory drug usage is a cause of unexplained ulcer disease in up to 60% of patients. Hypersecretory syndromes such as Zollinger-Ellison syndrome, although rare, need to be excluded. Once all known etiological factors are excluded

2002 American Journal of Gastroenterology

8023. Changing rates of Helicobacter pylori testing and treatment in patients with peptic ulcer disease. (PubMed)

Changing rates of Helicobacter pylori testing and treatment in patients with peptic ulcer disease. The aim of this study was to identify temporal trends in the rate of Helicobacter pylori (H. pylori) testing, prevalence, and treatment among patients with peptic ulcer disease in Olmsted County, MN, from 1984 through 1997.All 3317 Olmsted County residents with a clinical diagnosis of peptic ulcer disease at the Mayo Clinic from 1984 through 1997 were identified. The complete medical records (...) of an age-, sex-, and calendar year-stratified random sample were reviewed (n = 720); 298 patients (41%) had confirmed peptic ulcer disease. Changes in proportions of H. pylori testing, infection, and treatment over time were analyzed by logistic regression.Of the 298 patients with confirmed peptic ulcer disease, 32% were tested for H. pylori; 36% were positive for infection, of whom 66% received antibiotic therapy. The rate of testing for H. pylori increased from 0% in 1984 to 96% in 1997

2002 American Journal of Gastroenterology

8024. Hospitalization and mortality rates from peptic ulcer disease and GI bleeding in the 1990s: relationship to sales of nonsteroidal anti-inflammatory drugs and acid suppression medications. (PubMed)

Hospitalization and mortality rates from peptic ulcer disease and GI bleeding in the 1990s: relationship to sales of nonsteroidal anti-inflammatory drugs and acid suppression medications. Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause peptic ulcer disease and upper GI bleeding. Acid suppression medications effectively treat NSAID-induced ulcers. However, it is unknown what effect the availability of proton pump inhibitors and over-the-counter preparations of NSAIDs and histamine type 2 (...) receptor antagonists have had on population rates of hospitalization and mortality from GI toxicity. This study examines trends in hospitalization and mortality rates from GI toxicity during the 1990s.We performed an analysis of secular trends of hospitalization and mortality rates from peptic ulcer disease, upper GI bleeding, and any GI bleeding using data from the National Hospital Discharge Survey, comparing them with sales of NSAIDs, aspirin, and acid suppression medications from 1992 to 1999.From

2002 American Journal of Gastroenterology

8025. Dyspepsia, peptic ulcer disease, and esophageal reflux disease (PubMed)

Dyspepsia, peptic ulcer disease, and esophageal reflux disease 11897730 2002 04 30 2018 11 13 0093-0415 176 2 2002 Mar The Western journal of medicine West. J. Med. Dyspepsia, peptic ulcer disease, and esophageal reflux disease. 98-103 Schwartz Mark D MD Division of Primary Care, Department of Medicine, New York University School of Medicine and Veterans Affairs, New York Harbor Healthcare System Medical Service (111), 423 E 23rd St, New York, NY 10010, USA. mark.schwartz3@med.va.gov eng (...) Journal Article United States West J Med 0410504 0093-0415 AIM IM Dyspepsia diagnosis drug therapy epidemiology Gastroesophageal Reflux diagnosis drug therapy epidemiology Helicobacter Infections diagnosis drug therapy epidemiology Helicobacter pylori Humans Peptic Ulcer diagnosis drug therapy epidemiology 2002 3 19 10 0 2002 5 1 10 1 2002 3 19 10 0 ppublish 11897730 PMC1071675 CMAJ. 2000 Jun 13;162(12 Suppl):S3-23 10870511 Arch Intern Med. 1995 Sep 11;155(16):1808-12 7654116 Arch Intern Med. 1995 Nov

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2002 Western Journal of Medicine

8026. Is peptic ulcer disease an infectious disease? (PubMed)

Is peptic ulcer disease an infectious disease? 8279173 1994 02 10 2018 11 13 0093-0415 159 5 1993 Nov The Western journal of medicine West. J. Med. Is peptic ulcer disease an infectious disease? 616-8 Isenberg J I JI eng Comment Editorial United States West J Med 0410504 0093-0415 AIM IM West J Med. 1993 Nov;159(5):555-9 8279151 Gastric Mucosa microbiology Gastritis microbiology Helicobacter Infections drug therapy physiopathology Helicobacter pylori isolation & purification physiology Humans (...) Peptic Ulcer drug therapy microbiology physiopathology Risk Factors Stomach Ulcer microbiology 1993 11 1 1993 11 1 0 1 1993 11 1 0 0 ppublish 8279173 PMC1022369 BMJ. 1991 Nov 16;303(6812):1238-40 1747644 N Engl J Med. 1991 Oct 17;325(16):1127-31 1891020 N Engl J Med. 1993 Feb 4;328(5):308-12 8419816 Drugs. 1992 Dec;44(6):921-7 1282863 Gastroenterol Clin North Am. 1993 Mar;22(1):127-39 8449562 Gastroenterol Clin North Am. 1993 Mar;22(1):153-67 8449564 Gastroenterol Clin North Am. 1993 Mar;22(1):43-57

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1993 Western Journal of Medicine

8027. Serum CagA antibodies in asymptomatic subjects and patients with peptic ulcer: lack of correlation of IgG antibody in patients with peptic ulcer or asymptomatic Helicobacter pylori gastritis. (PubMed)

and to a large, well defined patient population.A validated ELISA for serum IgG to CagA was used to investigate the prevalence of CagA seropositivity in 100 patients with peptic ulcer compared with 77 with H pylori infection without ulcer disease in a North American population. The extent of antral and corpus inflammation and H pylori density in relation to CagA seropositivity in 40 subjects with H pylori infection were assessed semiquanitatively. All studies were carried out in a coded and blinded (...) revealed no differences in infiltration with acute inflammatory cells, H pylori density, or gastritis index. There was no relation evident between the degree of polymorphonuclear cell infiltration and the serum IgG antibody titre to CagA. Mononuclear cell infiltration in the antrum, but not the corpus, was greater in those with CagA IgG compared with those without (median score 5 v 3).A right association between the presence or titre of serum IgG to CagA and peptic ulcer disease, greater H pylori

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1996 Journal of Clinical Pathology

8028. Efficacy and safety of pirenzepine in peptic ulcer and in non ulcerous gastroduodenal diseases. A multicentre controlled clinical trial. (PubMed)

Efficacy and safety of pirenzepine in peptic ulcer and in non ulcerous gastroduodenal diseases. A multicentre controlled clinical trial. 6221398 1983 06 10 2015 11 19 0085-5928 81 1982 Scandinavian journal of gastroenterology. Supplement Scand. J. Gastroenterol. Suppl. Efficacy and safety of pirenzepine in peptic ulcer and in non ulcerous gastroduodenal diseases. A multicentre controlled clinical trial. 1-41 Giorgi-Conciato M M Daniotti S S Ferrari P A PA Gaetani M M Petrin G G Sala P P (...) as Topic Duodenal Ulcer drug therapy Duodenitis drug therapy Female Gastritis drug therapy Humans Male Middle Aged Morpholines therapeutic use Parasympatholytics adverse effects therapeutic use Pirenzepine Proglumide therapeutic use Pyridines therapeutic use Sialoglycoproteins therapeutic use Stomach Ulcer drug therapy 1982 1 1 1982 1 1 0 1 1982 1 1 0 0 ppublish 6221398

1983 Scandinavian journal of gastroenterology. Supplement

8029. Ulcer healing and relapse prevention by ranitidine in peptic ulcer disease. (PubMed)

Ulcer healing and relapse prevention by ranitidine in peptic ulcer disease. Ranitidine, 300 mg daily, was given to 92 patients with duodenal ulcer (DU), 38 with prepyloric ulcer (PPU), and 21 with gastric corporeal ulcer (GCU). The healing rates at 4 weeks differed for the different types of ulcers (P less than 0.01), being 91% for DU, 68% for PPU, and 81% for GCU. After established ulcer healing, maintenance treatment with either ranitidine, 100 mg twice daily or 150 mg at night, or placebo (...) was given for 1 year or until ulcer relapse in a total of 108 patients--71 with DU, 24 with PPU, and 13 with GCU. There were no significant differences in relapse rates between the two groups treated with active drug or between the three ulcer groups. However, the overall relapse rate in the active drug groups was 16%, against 72% in the placebo group (P less than 0.001).

1985 Scandinavian journal of gastroenterology

8030. Prostaglandins and peptic ulcer disease: nocturnal administration of rioprostil vs ranitidine in duodenal ulcer healing. (PubMed)

Prostaglandins and peptic ulcer disease: nocturnal administration of rioprostil vs ranitidine in duodenal ulcer healing. Hypochlorhydria induced by potent antisecretory drugs is followed by a marked elevation of serum gastrin levels which leads to changes in ECL cell density in rats. "Soft" antiulcer drugs like prostaglandins do not increase gastrin levels. Their use in peptic ulcer disease seems to be mainly limited by a relatively high incidence of diarrhea and abdominal cramps. Rioprostil (...) is a new prostaglandin E1 analogue. We compared the potency and duration of action of rioprosil 600 micrograms nocte with 300 micrograms bid on human gastric secretion in a placebo-controlled double-blind study. We further evaluated the clinical effectiveness of rioprostil 600 micrograms nocte in the acute treatment of duodenal ulcer. Nocturnal gastric acidity (24:00 to 08:00) was inhibited from 54.5 +/- 1.7 mmol H+/L (placebo experiments; n =9) to 26.7 +/- 3.5 mmol H+/L (52%) by rioprostil 300

1986 Klinische Wochenschrift

8031. Ulcer healing after treatment with sucralfate emulsion or ranitidine. Randomized controlled study in peptic ulcer disease. (PubMed)

Ulcer healing after treatment with sucralfate emulsion or ranitidine. Randomized controlled study in peptic ulcer disease. A randomized trial with a blind observer compared the efficacy of an emulsion containing micronized sucralfate (1 g four times daily) and ranitidine (150 mg twice daily) in the short-term healing of peptic ulcer. Patients with a minimum ulcer size of 5 mm located in the duodenal bulb, the pyloric canal, or in the prepyloric area within a distance of 2 cm from the pylorus (...) were included. A total of 97 patients were randomized and 85 completed the trial. The endoscopically proven healing rate at 2 weeks of 41% for both sucralfate and ranitidine improved to 76% for sucralfate and 73% for ranitidine at 4 weeks and to 95% and 96%, respectively, at 12 weeks. The difference between the two treatment groups was not statistically significant, and the 95% confidence interval for the difference in ulcer healing efficacy of sucralfate emulsion compared with ranitidine was -0.15

1988 Journal of clinical gastroenterology

8032. Rabeprazole in treatment of acid peptic diseases: results of three placebo-controlled dose-response clinical trials in duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease (GERD). The Rabeprazole Study Group. (PubMed)

Rabeprazole in treatment of acid peptic diseases: results of three placebo-controlled dose-response clinical trials in duodenal ulcer, gastric ulcer, and gastroesophageal reflux disease (GERD). The Rabeprazole Study Group. Rabeprazole, a new proton pump inhibitor, was studied in patients with acid-peptic-related diseases (duodenal ulcer, gastric ulcer, GERD) in three placebo-controlled, double-blind, randomized clinical trials. Men and women over the age of 18 were enrolled if the presence (...) the rabeprazole doses in healing active peptic lesions. The incidence of positive [13C]urea breath test for H. pylori was 53% in patients with duodenal or gastric ulcers. H. pylori status was not effected by treatment with rabeprazole.

1998 Digestive diseases and sciences

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