Publications by authors named "Pace F"

In physiological and pathological conditions, pH monitoring in the esophagus shows small variations as well as more pronounced deflections. However, only the latter are traditionally taken into account in 24-hour pH monitoring analysis. The present study was designed to establish optimal thresholds of pH fluctuations versus reflux episodes in separating physiological and pathological gastroesophageal reflux (GER) and to evaluate their significance in the diagnosis.

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Forty-four patients with esophagitis refractory to standard H2-blocker therapy, who had healed after a 4- to 16-wk course with either 20-40 mg omeprazole or ranitidine at doses of 300-600 mg daily in a randomized double-blind study, commenced a 3-month maintenance course of therapy with 40 mg bid famotidine. The aims of this investigation were to assess the effectiveness of this regimen in preventing recurrence of esophagitis lesions and symptoms in this subgroup of patients with therapy-resistant disease and to verify whether patients previously healed with omeprazole have a higher recurrence rate than those healed with ranitidine. The results of the study show that, despite the high dose of famotidine, 48% of patients relapsed within 3 months, a third of whom were asymptomatic.

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This retrospective study was undertaken to characterise the clinical course and reflux pattern of patients with gastro-oesophageal reflux without evidence of oesophagitis. We investigated 33 patients (12 women, 21 men; mean age 36 years) with typical symptoms, a negative oesophagoscopy, and a 24 hour oesophageal pH-metry indicative of pathological gastro-oesophageal reflux. All patients received antacids or prokinetic drugs or both for three to six months.

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Scarce data exist on the medical treatment of patients with peptic esophagitis who are non-responders to conventional or higher doses of H2-blocker agents, and no controlled trial on such patients has been published so far. We conducted a randomized single-blind study on the effects of 1 g sucralfate four times daily (n = 8), a mucosa-protective agent, versus 40 mg famotidine twice daily (n = 8), a new H2-blocker agent, administered for 12 weeks, in the treatment of peptic esophagitis (grades I to IV in accordance with Savary and Miller) refractory to a 6-month therapy with ranitidine at a dosage of 150 or 300 mg twice daily. Complete healing of the esophageal lesions was observed in none of eight patients receiving sucralfate, as compared with five of eight taking famotidine (p less than 0.

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In order to investigate the response of gastroesophageal reflux after medically induced healing of esophagitis and its relation to the occurrence of relapse during prophylactic treatment, 20 patients with erosive/ulcerative esophagitis underwent 24 hour esophageal pH monitoring before and after healing achieved with 12 to 24 weeks with ranitidine 150 or 300 mg bd. Compared with pretreatment values, after macroscopic healing, a significant reduction in daytime median percentage of reflux time and median number of reflux episodes lasting more than 5 min were observed, whereas during the night time reflux frequency and severity did not change. During maintenance treatment with ranitidine at half the acute dosage five of the six patients who had shown no improvement in gastroesophageal reflux after acute healing, relapsed.

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In order to investigate the response of gastro-oesophageal reflux after medically induced healing of oesophagitis and its relation to the occurrence of relapse during prophylactic treatment, 20 patients with erosive/ulcerative oesophagitis underwent 24 hour oesophageal pH monitoring before and after healing achieved with 12 to 24 week treatment with ranitidine 150 or 300 mg twice daily. Compared with pretreatment values, after macroscopic healing, a significant reduction in daytime median percentage of reflux time (10.0 v 6.

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Ambulatory 24-h esophageal pH monitoring was carried out in 54 patients with erosive/ulcerative reflux esophagitis before a 12- to 24-week treatment with either ranitidine, 150 to 300 mg twice daily, or famotidine, 20 to 40 mg twice daily. After this period, 21 patients continued to present endoscopic evidence of esophagitis. Patients who did not respond to the therapy showed a more severe pretreatment pattern of acid reflux than those who healed, with regard to both median percentage time of reflux (16.

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This review focuses on the advances made in the pathophysiology, diagnosis and treatment of gastroesophageal reflux disease. During the last five years, the factors responsible for the disease have been extensively investigated and are now relatively well understood. Little progress, however, has been made with regard to diagnostic techniques, but the roles of endoluminal pH-monitoring and esophageal manometry have greatly increased.

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Many clinical trials on the effects of H2-antagonist drugs on reflux oesophagitis have shown unsatisfactory healing rates after conventional therapy, i.e. 4 to 12-week administration of 400 or 150mg bd of cimetidine or ranitidine, respectively.

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Three different periods of intraesophageal pH-recording (24 h, 12 h, and 10 h postprandially) have been compared in 20 healthy subjects and in 20 outpatients with symptoms and endoscopic signs of peptic esophagitis, to assess their relative values of sensitivity and specificity in the diagnosis of gastroesophageal reflux. No false-positive results were obtained during any of the periods, thus yielding a 100% specificity. However, the sensitivity shown by the 24-h period of esophageal pH-recording was 81%, whereas that for the 12-h period was 50% and that for 10 h postprandially 70%.

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The aim of the present study was to assess the clinical efficacy and safety of a new H2-antagonist, nizatidine (N), administered as a single bedtime dose of 300 mg, compared with ranitidine (R) at the same dosage, in the short-term treatment of duodenal ulcer. One hundred forty one patients were included in the study: 70 were treated with N and 71 with R. During the study, three patients were withdrawn for unwanted effects not related to the treatment, and therefore, 69 patients per group were studied.

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Aspirin and other NSAIDs are drugs for which the causal association with major gastrointestinal bleeding has not been adequately or conclusively demonstrated, although a certain degree of correlation is very likely. For aspirin ingestion in particular the increased risk is confined to patients taking the drug at heavy and regular dosages (less than 1% of users), and can be reduced further by the use of enteric-coated formulations. For non-aspirin NSAIDs, the relative risk of GI bleeding after repeated and prolonged exposure (in comparison to controls) has been quantified between 1.

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Long-term esophageal pH-metry has become the preferred test to quantify acid gastroesophageal reflux, but its accuracy in separating physiologic from pathological reflux is not well defined. To establish optimal thresholds of 24-h pH-metry, we studied 45 patients with clinically proven gastroesophageal reflux disease and 42 healthy volunteers. Twenty-four-hour esophageal pH was measured while the subject was ambulatory, using a combined glass electrode connected to a portable recorder.

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The effect of cigarette smoking on gastroesophageal reflux and the effect of the pH electrode on salivary secretion and swallowing frequency were studied in 30 healthy volunteers (15 habitual smokers, 15 non-smokers) and in 10 smoking patients with proven gastroesophageal reflux disease. Twenty-four-hour pH profiles were measured while the subjects were ambulatory using a combined glass electrode connected to a portable recorder. In 8 of the smoking volunteers, swallowing frequency and salivary secretion were measured, both when smoking and when not.

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The relationship between gastric mucosal blood flow and stress lesion formation during hemorrhagic shock was studied in anesthetized dogs. Shock was induced by graded arterial bleeding. Blood flow was measured by means of the radioactive microsphere technique.

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The pathogenetic role of non-steroidal anti-inflammatory drugs (NSAIDs) in peptic ulcer disease is reviewed, on the basis of available experimental and epidemiological knowledge. In addition, original clinical data are provided concerning the prophylactic and therapeutic role of the H2-receptor antagonists ranitidine and cimetidine, and colloidal bismuth subcitrate, in the treatment of NSAID-associated peptic lesions in rheumatic patients.

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The effect of cimetidine (400 mg at night) and of low-dose antacid (400 mg of aluminum hydroxide plus 400 mg of magnesium hydroxide four times a day) given alone or in combination was assessed in a double-blind double-dummy endoscopic trial on prevention of duodenal ulcer (DU). Seventy-five outpatients with healed DU were followed up clinically for 1 year and were checked endoscopically after 6 and 12 months of therapy or in case of symptomatic relapse. After 6 and 12 months, 25% and 41%, respectively, of patients treated with cimetidine alone experienced a relapse, compared with 42% and 54% of those treated with antacid alone and 25% and 43% of patients treated with the combination therapy.

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