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Biomedical subjects

M Lazzaroni

Publications and source records attributed to M Lazzaroni.

At least 19 recordsLinked to original sources
PubMed2006

Treatment of morbid obesity by intraparietogastric administration of botulinum toxin: a randomized, double-blind, controlled study.

OBJECTIVE: The stomach is the main target organ for bariatric surgery, but no medical treatment has been developed to increase satiety and decrease food intake via gastric pathways. The aim of our study was to investigate whether or not the intraparietogastric administration of botulinum toxin A (BTX), able to modify the motility patterns of the stomach, could be useful for treatment of obesity. DESIGN: Double blind controlled study. SUBJECTS: Twenty-four morbidly obese patients (mean weight (s.e.m.) 116.1+/-4.89 kg, mean body mass index (BMI) 43.6+/-1.09 kg/m(2)) were blindly randomized to receive 200 IU BTX or placebo into the antrum and fundus of the stomach by intraparietal endoscopic administration. MEASUREMENTS: We evaluated weight loss, BMI changes, satiety score, the maximal gastric capacity for liquids and the gastric emptying time (octanoic acid breath test). RESULTS: The two groups were homogeneous for anthropometric characteristics. Eight weeks after treatment, BTX patients had significantly higher weight loss (11+/-1.09 vs 5.7+/-1.1 kg, P<0.001) and BMI reduction (4+/-0.36 vs 2+/-0.58 kg/m(2), P<0.001) and a higher satiety score on a visual analogic scale (7.63+/-0.38 vs 4.72+/-0.44, P<0.001) than controls. Furthermore, BTX patients showed a significantly greater reduction in maximal gastric capacity for liquids (266.6+/-48 vs 139+/-31, P<0.001) and a greater prolongation in gastric emptying time (+18.93+/-8 vs -2.2+/-6.9 min, P<0.05). No significant side effects or neurophysiologic changes were found. CONCLUSIONS: Topical intragastric BTX was effective in reducing food intake and body weight in morbidly obese patients.

Adult↗
PubMed2005

Preparation, premedication, and surveillance.

In the year since the last review, continuing pressure on endoscopy suites to improve efficiency and reduce costs without compromising patient care has led to growing interest in alternatives to pharmacological sedation and in the use of short-acting sedatives. Relaxation music, acupuncture, and the use of small-caliber endoscopes for unsedated peroral gastroscopy have therefore been suggested as ways of increasing tolerance and reducing discomfort. With regard to ultrathin and superthin endoscopes, the results are interesting, but further data from controlled trials and in studies including larger numbers of patients are still needed. The form of sedation for gastrointestinal endoscopy that has attracted greatest interest over the last year is the use by nonanesthetists of intravenous propofol, administered either alone at standard doses to achieve deep sedation, or at lower doses combined with benzodiazepines and opioids to achieve moderate sedation/analgesia. In comparison with benzodiazepines/opioids, the results were in favor of propofol: the mean time to sedation was shorter and the depth of sedation was greater. In addition, patients receiving propofol reached full recovery earlier and were discharged sooner. However, in the survey of patient satisfaction at discharge, it was found that the sedation methods did not have a significant impact on overall patient satisfaction. Some important issues concerning the narrow therapeutic range of propofol and the need for adequate training of endoscopists to deal with any problems related to deep sedation are still open - despite the growing amount of data suggesting that the drug is safe even when administered by registered nurses, an approach that is possibly more cost-effective than delivery by gastroenterologists or anesthetists. The morbidity and mortality associated with cardiopulmonary complications continue to be a significant concern during gastrointestinal endoscopy. Professional societies and national expert peer groups have issued practice guidelines for sedation and analgesia that call for continuous monitoring of the patient's hemodynamic and ventilatory status and consciousness. Direct observation is facilitated by electronic devices (pulse oximetry, capnography), directly indicating the patient's ventilatory status and the depth of sedation. Recently, it has been proposed that the bispectral index (BIS), an electroencephalography-based technique, can be used to monitor the depth of sedation during gastrointestinal endoscopy. However, the results of a recent study cast some doubt on the usefulness of the BIS, in its current version, for titrating boluses of propofol to an adequate level of sedation. Further data therefore appear to be needed to assess whether or not BIS values can help avoid unnecessary propofol dosage and can replace continuous assessment of the ventilatory effort.

Procedural Sedation↗
PubMed2004

Gastrointestinal side-effects of traditional non-steroidal anti-inflammatory drugs and new formulations.

Although adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs) occur in only a small proportion of users, the widespread use of these drugs has resulted in a substantial overall number of affected persons who experience serious gastrointestinal complications. Dyspeptic symptoms are estimated to occur in 10-60% of NSAID users and lead to discontinuation of treatment in 5-15% of rheumatoid arthritis patients taking NSAIDs. It is now well established that the point prevalence of peptic ulcer disease in patients receiving conventional NSAID therapy ranges between 10 and 30%, representing a 10-30-fold increase over that found in the general population. One of 175 users of conventional NSAIDs in the USA will be hospitalized each year for NSAID-induced gastrointestinal damage. The mortality of hospitalized patients remains about 5-10%, with an expected annual death rate of 0.08%. The selective COX-II inhibitors (rofecoxib, celecoxib, parecoxib, etoricoxib, valdecoxib, lumiracoxib) show consistently comparable efficacy to that of conventional non-steroidal anti-inflammatory drugs (NSAIDs) in patients with rheumatoid arthritis and osteoarthritis, but have a significantly reduced propensity to cause gastrointestinal toxicity. In many cases, the gastric effects of therapeutically active doses of COX-II inhibitors are indistinguishable from placebo. The safety benefits of COX-2 inhibitors given alone appear similar to combined therapy with conventional NSAIDs and gastroprotective agents. These findings warrant the consideration of COX-II inhibitors as first-line therapy in patients requiring long-term pain control.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2003

Preparation, premedication and surveillance.

The main end points for sedation during endoscopy are patients' satisfaction, short duration of the procedure, and safety. During the last year, attention has focused on attempting to identify the "ideal" candidate for moderate sedation/analgesia and on the importance of providing the patient with appropriate information before the procedure. The increasing pressure to perform more procedures, reduce costs, and achieve shorter patient turnaround times has affected recent approaches to sedation during endoscopy, focusing attention on alternatives to pharmacological sedation such as providing relaxing music, using small-caliber endoscopes for unsedated peroral gastroscopy, and using magnetic endoscopic imaging to increase tolerance and reduce discomfort during colonoscopy. The results, however, have not been convincing. The role of benzodiazepines was discussed in some studies, highlighting the well-known effect of midazolam on postprocedural amnesia, its pharmacological profile and tolerability after intranasal spraying in healthy volunteers, and the efficacy and safety of this route of administration as an alternative to intravenous administration in diagnostic upper gastrointestinal endoscopy. The form of sedation for gastrointestinal endoscopy that has attracted great interest over the last year is the use of intravenous propofol, either alone or with concomitant benzodiazepines or opioids. As expected in view of the drug's known pharmacological properties, the quality of sedation was better and recovery time was shorter in patients treated with propofol. However, important questions involving the narrow therapeutic range and the mode of administration of propofol (by endoscopists or nurses, or by anesthesiologists) remain open. One important aspect of sedation procedures is prevention of cardiopulmonary complications. The use of electronic monitoring techniques, with a pulse oximeter, has been recommended as a standard procedure during digestive endoscopy; however, pulse oximetry no longer reflects the normal ventilatory functions and does not detect episodes of severe CO2 retention. CO2 monitoring by transcutaneous measurement - or better, by capnography - appears to be useful, as an alternative to pulse oximetry, as a measure of hypoventilation, and for detecting potentially important abnormalities in respiratory activity in patients undergoing sedation for gastrointestinal endoscopy. With regard to preparation for endoscopic procedures, several "ideal" formulas for bowel preparation have been presented. These include the use of sodium phosphate compounds as an alternative to polyethylene glycol electrolyte lavage solutions (PEG-ELS); however, the results so far have been conflicting. The best and most cost-effective bowel cleansing procedure for colonoscopy and sigmoidoscopy has yet to be established.

Anesthesia Recovery Period↗
PubMed2002

Upper GI bleeding in healthy full-term infants: a case-control study.

OBJECTIVE: The aim of this case-control study was to evaluate the frequency and the type of mucosal lesions in newborn babies with upper GI bleeding (UGIB), the diagnostic role and safety of upper GI endoscopy, and the recognition of risk factors associated with the hemorrhagic event. METHODS: A population of 5180 infants born from June, 1988 to May, 1997 was examined. A case was defined as any patient who had UGIB within 4 days of delivery. The diagnosis was made by endoscopic examination in an endoscopy room. The following parameters were determined: amniotic fluid features, funicular blood pH, Apgar index at 5 min, neonatal weight, body length, gestational age, and the presence of other pathologies. Biochemical profiles were also evaluated. Clinical and demographic data of the mothers of the newborn babies were analyzed. Sera of cases and the respective parents were tested for gastrin and pepsinogen. As a control group, 53 full-term healthy infants matched for sex and age were randomly selected from the population of infants born in our pediatric department. RESULTS: Sixty-four of 5180 newborn babies (1.23%) suffered from UGIB within 26.5 +/- 20 h of life. In 53 of 64 cases (mean age = 24.2 +/- 25.5 h) it was possible to carry out an endoscopic examination. In one case, endoscopy was limited to the esophagus because of the presence of multiple mucosal ulcers and substenosis of the viscus. Esophageal damage was observed in 24/53 patients. The esophageal lesions were isolated in nine cases, and occurred jointly with gastric or duodenal damage in 14 cases and one, respectively. Gastric and duodenal lesions were seen in 43/52 and 1/52 patients, respectively. There were 17 cases of gastric ulcers and one case of duodenal ulcer. Blood clots were observed in 14 gastric ulcer patients; in one case there was evidence of active bleeding at the margins of a gastric ulcer. There was no significant difference with regard to the demographic and clinical characteristics of the cases and controls. Median values of serum gastrin of the cases and controls were similar. Median serum pepsinogen was significantly higher in the case group. CONCLUSIONS: UGIB in the newborn babies is often associated with clinically relevant mucosal lesions of the upper GI tract. The evolution, after treatment with antisecretory drugs, is generally rapid and favorable, with clinical recovery usually obtained within 24-48 h. The higher serum pepsinogen levels may only represent a significant risk factor of mucosal lesions and complications.

Case-Control Studies↗
PubMed2001

Nonsteroidal anti-inflammatory drug gastropathy and Helicobacter pylori: the search for an improbable consensus.

Nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori are known to share a number of pathogenic mechanisms, but there is no evidence to show a significant synergistic action between these two risk factors. Studies to assess possible interactions in the pathogenesis of dyspepsia and upper gastrointestinal mucosal lesions have differed in their endpoints, the definition of dyspepsia, and the regimens used for eradication of H. pylori. However, some conclusions may be drawn from the results of clinical trials. As far as dyspepsia is concerned, an association between NSAID dyspepsia and infection with H. pylori, seems likely, but it is difficult to make sense of the discrepant data that are currently available. On the contrary, neither short- nor long-term NSAID administration presents a definite major risk of gastric and duodenal injury or, above all, of ulcer-related complications (bleeding or perforation) in H. pylori-positive patients. Based on these considerations, what recommendations can be made with regard to H. pylori eradication in patients requiring treatment with NSAIDs? H. pylori and anti-inflammatory drugs are probably independent causes of gastric and duodenal damage. Patients taking NSAIDs who are found to have gastric or duodenal ulcers should, therefore, be tested for the bacterium and specifically treated, because H. pylori and NSAID-induced ulcers may be macroscopically indistinguishable. Whether asymptomatic patients taking NSAIDs should be tested and treated for H. pylori infection is still a matter of debate.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2001

Prophylaxis and treatment of non-steroidal anti-inflammatory drug-induced upper gastrointestinal side-effects.

The use of specific agents to heal mucosal lesions or to prevent non-steroidal anti-inflammatory drug toxicity, has focused upon two approaches: replacement of prostaglandin deficiency and inhibition of acid secretion. Acid suppression with traditional ulcer healing doses of H2-blockers is effective in healing gastric and duodenal ulcers upon discontinuation of the offending drug. In the event the non-steroidal anti-inflammatory drug must be continued, the use of H2-blockers is associated with a decrease in the healing rate. In long-term prevention studies, H2-blockers significantly reduce duodenal ulcer rates, but are ineffective in reducing gastric ulceration. More potent acid inhibition with a double-dose of H2-blockers (famotidine 80 mg daily, ranitidine 600 mg daily) may reduce the risk of gastric and duodenal ulcers. Marked acid suppression with proton pump inhibitors (omeprazole 20-40 mg, lansoprazole 30 mg daily) also appears to be very effective in healing gastric and duodenal ulcers in patients continuing the offending drug as well. An analysis of pooled data from comparative studies on omeprazole vs ranitidine, misoprostol and sucralfate shows a therapeutic advantage in favour of the proton pump inhibitor, ranging from 10 to 40%. In long-term prevention studies, omeprazole (20 mg daily) and pantoprazole (40 mg daily) have also been shown to reduce the risk of gastric and duodenal ulcers and non-steroidal anti-inflammatory drug-related dyspepsia. Current data from recent comparative studies of omeprazole (20 mg daily) vs ranitidine (150 mg daily) and misoprostol (200 microg daily) showed that, after 6 months' follow-up, the proton pump inhibitor was significantly superior to control drugs in reducing the risk both of gastric and duodenal ulcer. Misoprostol (at doses ranging from 400 microg to 800 microg/day) is an effective form of therapy for preventing non-steroidal anti-inflammatory drug-induced gastroduodenal lesions. However high-dose misoprostol only, seems adequate for the prevention of ulcer complications, mainly in high-risk non-steroidal anti-inflammatory drug users. Thus, available data are undoubtedly in favour of the proton pump inhibitors as well tolerated and effective drugs in the prophylaxis and treatment of non-steroidal anti-inflammatory drug-related mucosal lesions in the gastrointestinal tract.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2001

Review article: Helicobacter pylori and NSAID gastropathy.

Non-steroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori are known to share a number of pathogenic mechanisms, but there is no evidence to show a significant synergic action between the two risk factors. Studies assessing this subject have differed in almost every aspect of their methodology, including the definition of a NSAID user as well as the types, doses, duration and their indications for NSAID use. They also differed in their end-points, the definition of dyspepsia and the regimes used for eradication of H. pylori. However, some conclusions may be drawn from the results of clinical trials. In H. pylori-positive patients without mucosal lesions, NSAIDs may aggravate dyspeptic symptoms but, with the exception of elderly patients, they do not present a definite major risk of gastric and duodenal lesions and, above all, of ulcer-correlated complications. So what recommendations can be made with regard to H. pylori eradication in patients requiring treatment with NSAIDs? The microorganism and the anti-inflammatory drugs are undoubtedly independent causes of gastric and duodenal damage. Patients taking NSAIDs who are found to have gastric or duodenal ulcers should therefore be tested for the bacterium and specifically treated, since H. pylori and NSAID-induced ulcers may be macroscopically indistinguishable. Whether asymptomatic patients taking NSAIDs should be tested and treated for H. pylori infection is still a matter of debate.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2001

Preparation, premedication, and surveillance.

The endoscopic literature published during the past year has once again confirmed that there is significant variation from country to country regarding whether or not patients wish to receive conscious sedation during endoscopy (and particularly colonoscopy) - and there may even be variation from one endoscopic unit to another within the same country. Particular attention has been given to attempts to identify "ideal" candidates for conscious sedation, and to the importance of providing patients with information before the procedure. It has been shown that patients who receive detailed information about a medical procedure beforehand are able to benefit from this. The role of benzodiazepines, particularly midazolam, was investigated in studies emphasizing that the dosage should be kept to the minimum that is compatible with patient comfort and successful performance of the procedure. There have been few publications comparing propofol with midazolam. As expected, in view of the known pharmacological properties of the two drugs, the quality of sedation was better and the recovery time was shorter in patients who were treated with propofol. However, important questions are still open regarding the narrow therapeutic range of propofol and the methods by which it is administered (by endoscopists or by anesthesiologists). An important aspect of sedation procedures is the prevention of hypoxia and cardiopulmonary complications. Recent endoscopic reports have added little further information concerning the well-known risk of oxygen desaturation during conscious sedation. Performing endoscopy in unsedated patients reduces, but does not eliminate, the risk of hypoxia. Among the various risk factors, it has been found that chronic respiratory failure and coronary heart disease are factors predictive of severe desaturation and relevant electrocardiographic changes. The use of electronic monitoring techniques with pulse oximetry is recommended as a standard procedure during digestive endoscopy; however, it has been observed that when supplemental oxygen is administered, pulse oximetry no longer reflects normal ventilatory function and does not detect episodes of severe CO2 retention. Transcutaneous measurement of PCO2 therefore seems more reliable as a means of assessing hypoventilation. Several papers have proposed "ideal formulas" for bowel preparation for endoscopic procedures. Various regimens have been proposed as alternatives to polyethylene glycol electrolyte lavage solution (PEG-ELS) and sodium phosphate compounds, with different results. On the whole, there is still little information regarding the best and most cost-effective method of bowel cleansing for colonoscopy and flexible sigmoidoscopy.

Antiemetics↗
PubMed2001

The effects on gastroduodenal mucosa of a new nonsteroidal anti-inflammatory drug, amtolmetin-guacyl, versus piroxicam in healthy volunteers: a short-term, double-blind, endoscopically controlled study.

AIM: Amtolmetin-guacyl (AMG) (2-[2[1-methyl-5-(4-methylbenzoyl) pyrrol-2-yl] acetamido] acetic acid 2-methoxyphenyl ester) is a recent drug that, in preliminary studies, has shown effective anti-inflammatory properties with improved gastrointestinal safety. Our study was designed to investigate the effects of AMG and piroxicam on gastroduodenal mucosa in healthy volunteers. MATERIALS AND METHODS: Forty-two healthy volunteers aged 18--45 years were randomized in a double-blind manner to AMG 1200 mg for 2 days and 600 mg for 12 days, or piroxicam 40 mg for 2 days and 20 mg for 12 days. Endoscopic evaluation and laboratory tests were performed at baseline and at the end of the treatment. The mucosa was evaluated by endoscopy using a predefined scale: the score could range from 0 to 4. Only volunteers with endoscopy grade 0-1 entered the trial. RESULTS: The median post-treatment endoscopy gastric injury scores were 1 (range 0--4) in the AMG-treated volunteers and 3 (range 0--4) in the piroxicam-treated volunteers (P = 0.04). There were two cases with an endoscopic gastric score of 4 in the AMG group, and seven in the piroxicam group (P = 0.1). The corresponding values in the duodenum were 1/21 volunteers in the AMG group and 1/21 in the piroxicam group. Eight out of 11 subjects with an endoscopic score of 4 were Helicobacter pylori negative, and 3/11 were infected by the micro-organism. Different adverse reactions were reported by 15/21 volunteers (71%) in the AMG group and by 12/21 (57%) in the piroxicam group. None of these events resulted in interruption of the study. CONCLUSIONS: AMG is a new anti-inflammatory drug with limited gastric toxicity. If these findings are confirmed on a wider scale in long-term trials, then the drug might become a valid alternative to current treatments, especially for patients such as those with rheumatoid arthritis who need steroids and second-line drugs simultaneously.

Adult↗
PubMed2000

Efficacy of pantoprazole in the prevention of peptic ulcers, induced by non-steroidal anti-inflammatory drugs: a prospective, placebo-controlled, double-blind, parallel-group study.

AIM: To evaluate the efficacy of pantoprazole in preventing gastrointestinal lesions in patients with rheumatic diseases receiving continuous, long-term treatment with non-steroidal anti-inflammatory drugs. MATERIAL: This was a prospective, randomised, double-blind, unbalanced, placebo-controlled, parallel group study. Outpatients (n= 104, age range 22-80 years, mean age 59.5) with rheumatoid arthritis or osteoarthritis, requiring chronic intake of NSAIDs (at least 8 weeks prior to the start of the study), were randomised and enrolled to receive either 40 mg pantoprazole (n=70) or placebo (n=34) once daily, for 12 weeks. Patients had endoscopically confirmed gastric and duodenal lesions grade 0, 1 or 2 (Lanza classification grade 0: normal to hyperaemic mucosa; grade 1: 1 to 3 erosions, submucosal haemorrhage or petechiae, grade 2: 4 to 10 erosions, submucosal haemorrhages or petechiae). Clinical and endoscopic evaluations were performed at baseline, after 4, and 12 weeks. The primary end-point of the study was the incidence of gastric or duodenal ulcers after 4 and 12 weeks of treatment. RESULTS: Patients (n=95) were evaluated: 65 in the pantoprazole group and 30 in the placebo group. When considering all patients (those with Lanza score grade 0, 1, 2 at baseline), the overall proportion of patients in remission was 82% and 77% after 4 weeks, and 72% and 59% after 12 weeks in pantoprazole and placebo groups, respectively (cumulative survival analysis according to Kaplan-Meier). The difference between the treatment groups was even more marked when only those patients with normal mucosa at baseline (grade 0) were considered. After 12 weeks, the proportion of patients in remission was 82% (95% confidence limits 70% - 94% in the pantoprazole and 55% (95% confidence limits 33% - 77%) in the placebo treatment group, p=O.036. Adverse events were reported in 4% and 6% of patients in pantoprazole and placebo treatment groups, respectively CONCLUSIONS: Pantoprazole 40 mg once daily was well tolerated and is more effective than placebo in the prevention of peptic ulcers in patients with rheumatic diseases who require continuous, long-term, treatment with NSAIDs.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1999

Premedication, preparation, and surveillance.

During the last two years, the well-known positive role of benzodiazepines (midazolam and diazepam) in conscious sedation, both in adults and pediatric patients, has been confirmed by several studies. However, problems concerning the role of sedation and analgesia in nonoperative endoscopy are still a matter of debate. Particular attention has focused on attempts to identify the "ideal candidate" for conscious sedation, and on the importance of providing patients with information before the procedure, which should be matched to each patient's style of coping. Before detailed information about a medical procedure is given blindly, the clinician should investigate whether such information will benefit or adversely affect the patient receiving it. An important aspect of the sedation procedure is the prevention of hypoxia and cardiopulmonary complications. Recent endoscopic experience has provided little additional information concerning the well-known risk of oxygen desaturation during conscious sedation. Performing endoscopy in sedated patients reduces, but does not eliminate, the risk of hypoxia. Some independent variables capable of predicting severe desaturation have been recognized, such as basal SaO2 < 95%, respiratory disease, more than one attempt needed for intubation, emergency procedure, and an American Society of Anesthesiologists score of III or IV. As far as preparation is concerned, some light has been cast by a meta-analysis of available studies concerning the role of sodium phosphate and polyethylene glycol electrolyte lavage solution (PEG-ELS). The former preparation has been found to be as effective and less costly compared with the latter. In particular, sodium phosphate may be preferable in patients without cardiovascular or renal co-morbidity, and in those with a tendency to develop nausea or bloating.

Adult↗
PubMed1999

Non-steroidal anti-inflammatory drug gastropathy: clinical results with antacids and sucralfate.

The efficacy of antacids in the short- and long-term treatment of peptic ulcers, has suggested a possible use in the prevention and in the treatment of non-steroidal anti-inflammatory drug related gastroduodenal lesions. In short-term prevention studies, significant protection against ASA-related lesions was observed when antacids at high-dose were given before the administration of the offending drug. To the contrary, antacids at low dose did not prevent ASA-induced lesions of gastric and duodenal mucosa. As for long-term prophylaxis, no clinical effect was observed. In the treatment of non-steroidal anti-inflammatory drug-related mucosal lesions in patients who were able to discontinue the offending drugs, antacids proved of some use, when compared with placebo, but were significantly less effective than H2 blockers, as cimetidine. Sucralfate is an effective antiulcer drug thought to provide cytoprotective action. Although initial studies utilizing sucralfate for protection against short-term aspirin administration were encouraging, longer term studies (more than 7 days) were generally disappointing. A comparative study with misoprostol demonstrated that the PGE1 analogue was far superior for the prevention of non-steroidal anti-inflammatory drugs ulcers, and that ulceration rates in the sucralfate group were equivalent to rates in the placebo group. As far as the treatment of non-steroidal anti-inflammatory drug-related mucosal lesions is concerned, sucralfate proved superior to placebo, similar to ranitidine, but significantly less effective than omeprazole.

Antacids↗
PubMed1999

Non-steroidal anti-inflammatory drug gastropathy: clinical results with H2 antagonists and proton pump inhibitors.

While the most effective strategy to prevent non-steroidal anti-inflammatory drug-related gastrointestinal toxicity is not to prescribe the medication, this option is often impractical. The use of specific agents to heal mucosal lesions or to prevent non-steroidal anti-inflammatory drug toxicity, has focused upon two approaches: replacement of prostaglandin deficiency and inhibition of acid secretion. Acid suppression with traditional ulcer healing doses of H2-blockers is effective in the cure of gastric and duodenal ulcers upon discontinuation of the offending drug. In the event the non-steroidal anti-inflammatory drug must be continued, the use of H2-RAs is associated with a slight decrease in the healing rate. In long-term prevention studies, H2-blockers significantly reduce duodenal ulcer rates, but are ineffective in reducing gastric ulceration. More potent acid inhibition with double-doses of H2-blockers may also reduce the risk of gastric (famotidine 80 mg) and duodenal ulcers (famotidine 80 mg or ranitidine 600 mg daily). Proton pump inhibitors (omeprazole 20-40 mg, lansoprazole 30 mg daily) appear more effective in healing gastric and duodenal ulcers in patients continuing the offending drug. Comparative studies of omeprazole vs ranitidine, misoprostol and sucralfate show a therapeutic gain in favour of the proton pump inhibition, ranging from 10 to 40%. In long-term prevention studies, omeprazole (20 mg daily) and pantoprazole (40 mg daily) have also been shown to reduce the risk of gastric and duodenal ulcers. Comparative studies of omeprazole (20 mg daily) vs ranitidine (150 mg daily) and misoprostol (200 micrograms daily) showed that after 6 months' follow-up the proton pump inhibition was significantly superior to control drugs in reducing the risk of both gastric and duodenal ulcer.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1998

Omeprazole and sucralfate in the treatment of NSAID-induced gastric and duodenal ulcer.

AIM: To establish the healing efficacy of two drugs, omeprazole and sucralfate, when given to patients who had developed gastric or duodenal ulcer while undergoing chronic treatment with non-steroidal anti-inflammatory drugs (NSAIDs). METHODS: Ninety-eight patients with arthritis or arthrosis and NSAID-related gastric or duodenal ulcer were admitted to the endoscopic, single-blind study. They were randomized to receive either omeprazole 20 mg o.m. or sucralfate 2 g b.d. for 4-8 weeks. The patients continued to receive the same NSAID during the trial. Upper gastrointestinal endoscopy was performed at entry and after 4 or 8 weeks. RESULTS: Eighty-eight patients completed the 4-week study, but only 81 were available for final analysis at 8 weeks. Omeprazole was significantly superior to sucralfate in inducing gastric ulcer healing after both 4 (87 vs. 52%, P = 0.007) and 8 weeks (100 vs. 82%, P = 0.04). No statistically significant difference in duodenal ulcer healing rates emerged between the two groups either at 4 (79 vs. 55%) or 8 weeks (95 vs. 73%). The healing rates in patients with combined gastric and duodenal ulcer were 67 vs. 33% after 4 weeks and 6 7 vs. 6 7% after 8 weeks of treatment. The percentages of asymptomatic patients were similar in the two treatment groups both at 4 (70 vs. 73%) and 8 weeks (70 vs. 75%). H. pylori infection did not influence healing rates, but significantly more H. pylori-positive patients healed with omeprazole. CONCLUSIONS: The results of this study show that omeprazole is superior to sucralfate in healing NSAID-induced gastroduodenal ulcer in patients who continue to take anti-inflammatory drugs. The good results observed were unrelated to H. pylori status.

Administration, Oral↗
PubMed1998

Peptic ulcer therapy with cimetidine versus tripotassium dicitrato bismuthate in rheumatoid arthritis patients undergoing chronic NSAID treatment.

AIM: To compare the efficacy of cimetidine and tripotassium dicitrato bismuthate (TDB) in arthritic patients who had developed gastric (GU) or duodenal (DU) ulceration while taking non-steroidal anti-inflammatory drugs (NSAIDs). METHODS: Eighty-six rheumatoid arthritis (RA) patients affected by endoscopically proven DU (n = 44) or GU (n = 42), and on chronic NSAID therapy which was not suspended during anti-ulcer therapy, were randomized to cimetidine (400 mg t.d.s.) or TDB (120 mg q.d.s.). A repeat endoscopy was planned after 4 weeks (and 8 weeks, in case of failed healing). The patients who were unhealed after 8 weeks of therapy were allocated to the alternative anti-ulcer drug for a further 8 weeks without interrupting the anti-inflammatory therapy. RESULTS: At week 4 of therapy. 14/24 (58%) DU and 9/20 (45%) GU patients treated with cimetidine were healed, compared with 12/20 (60%) and 10/22 (45%) TDB-treated patients (N.S.). At week 8 of therapy, the DU healing rates were 15/24 (63%) with cimetidine and 14/20 (70%) for TDB. The corresponding GU healing rates were 12/20 (60%) with cimetidine and 13/22 (60%) for TDB (N.S.). At week 16, complete healing with cimetidine was observed in 67% of DU and 57% of GU patients unhealed with TDB; the corresponding figures in the patients crossed to TDB were 83% for DU and 63% for GU patients (N.S. vs. cimetidine). CONCLUSIONS: No statistically significant difference was found between the healing activities of cimetidine and TDB in rheumatoid arthritis patients with peptic ulcer who did not interrupt their NSAID treatment for arthritis. This trial showed that the continued consumption of NSAIDs appears to slow the ulcer healing process, especially in GU patients.

Administration, Oral↗