misoprostol and Gastritis

The conflicting data about the influence of Helicobacter pylori infection on the ulcer risk in patients receiving NSAIDs can be accounted for by the heterogeneity of study designs and the diversified host response to H. pylori. Factors that will affect the outcome include the choice of H. pylori diagnostic tests, previous ulcer complications, concurrent use of acid suppressants, NSAID-naive versus long-term users, low-dose aspirin (acetylsalicylic acid) versus non-aspirin NSAIDs and whether the result was derived from a pre-specified endpoint or post hoc subgroup analysis. Current evidence suggests that H. pylori eradication reduces the ulcer risk for patients who are about to start receiving NSAIDs but not for those who are already on long-term NSAID therapy. Since treatment with a proton pump inhibitor (PPI) worsens H. pylori-associated corpus gastritis, H. pylori should be tested for, and eradicated if present, before starting long-term prophylaxis with PPIs. Patients with H. pylori infection and a history of ulcer complications who require NSAIDs should receive concomitant PPIs or misoprostol after curing the infection. Among patients receiving low-dose aspirin, who have H. pylori infection and previous ulcer complications, long-term treatment with a PPI further reduces the risk of complicated ulcers if H. pylori eradication fails or if patients use concomitant non-aspirin NSAIDs. Current data on the gastric safety of COX-2 selective NSAIDs in H. pylori-infected patients are conflicting. Limited data suggest that the gastroduodenal sparing effect of rofecoxib is negated by H. pylori infection in patients who have had prior upper gastrointestinal events. In light of potential cardiovascular risk with COX-2 selective NSAIDs, it is important to weigh the potential adverse effects against the benefits for an individual patient.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Apoptosis; Aspirin; Gastric Acid; Gastritis; Helicobacter pylori; Humans; Misoprostol; Peptic Ulcer; Prostaglandins

Topics: Anti-Inflammatory Agents, Non-Steroidal; Arthritis; Butanones; Gastritis; Humans; Ibuprofen; Misoprostol; Nabumetone; Naproxen; Randomized Controlled Trials as Topic; Risk Factors; Stomach Ulcer

Whether misoprostol, a synthetic prostaglandin E1 analogue, should be routinely prescribed along with nonsteroidal anti-inflammatory drugs (NSAIDS) to prevent gastric damage is of great clinical importance and has profound cost implications. No consensus exists on whether misoprostol cotherapy results in a cost-saving, is cost-effective, or is costly. The different conclusions reached by five economic evaluations of misoprostol can be explained solely by the assumed absolute risk reduction of symptomatic ulcer, which was more than seven times greater in the studies that concluded that misoprostol was cost-effective than in a study that concluded misoprostol to be costly. Since no study has directly shown the effectiveness of misoprostol cotherapy in preventing clinically significant ulcer disease (ie, hemorrhage and perforation), it is impossible to judge which assumptions are most appropriate. The absence of firm data on the rate of NSAID-induced gastric ulcers reduced by misoprostol makes it impossible to conclude whether it is cost-effective in patients with chronic arthritis who use NSAIDS.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Arthritis; Cost-Benefit Analysis; Gastritis; Humans; Misoprostol

An endoscopic screening was carried out during the period between July 1989 and December 1991 in the Municipality of Roccagorga (LT) in order to: a) evaluate the presence of various forms of gastritis and pre-cancerous lesions; 2) verify the effect of the administration of prostaglandins (Misoprostol) on the evolution of superficial chronic gastritis (CG). A total of 468 endoscopy were performed (17% of the population aged between 20 and 75 years old). 22% of the subjects examined were found to be endoscopically normal; 34% presented symptoms of mild esophagitis and 4% of moderate esophagitis. The prevalence of duodenal ulcer was 10.6% and gastric ulcer 3.4%. Gastric carcinoma was diagnosed in 6 patients (1.2%). 8.5% of patients were found to have atrophic CG and 15.3% superficial CG. Thirty-six patients with superficial CG were randomly divided into two groups: A) treated with Misoprostol 600 mg/day for 6 months; B) controls (placebo). The administration of Misoprostol did not influence the evolution of CG, whereas it caused a reduction in the incidence of type 1 intestinal metaplasia. Misoprostol also led to an improvement in dyspeptic symptoms. The results of the present study do not suggest a role of prostaglandins in the natural evolution of CG.

Topics: Adult; Aged; Chronic Disease; Diagnosis, Differential; Duodenal Ulcer; Female; Gastritis; Gastroscopy; Humans; Male; Middle Aged; Misoprostol; Stomach Neoplasms; Stomach Ulcer

To assess the efficacy of misoprostol for the treatment of chronic erosive gastritis and associated symptoms.. We performed a double-blind controlled trial, administering 200-micrograms misoprostol tablets or placebo twice daily for 2 months to 48 patients with symptomatic chronic erosive gastritis. Symptomatology was assessed by means of a standard questionnaire at the beginning and at the end of the study, as well as endoscopic and histologic changes of the gastric mucosa.. At the end of the treatment period, a significant reduction in symptom score was observed in misoprostol-treated (from 86.6 +/- 66.2 to 17.6 +/- 18.2, p < 0.001) but not in placebo-treated patients. Endoscopic score was significantly reduced at the end of the treatment period in the misoprostol group, compared with that of the placebo group (p < 0.05). A significant reduction in the activity of histologic gastritis was observed only in patients on misoprostol. The prevalence of gastric colonization by Helicobacter pylori was rather low (30%), and no effect of treatment was observed.. Patients with symptomatic chronic erosive gastritis seem to profit from treatment with misoprostol: the treatment with misoprostol, but not with placebo, was effective in significantly reducing the extent of symptoms. Such an improvement was associated with a substantial improvement in the endoscopic and histologic appearance of the gastric mucosa.

Topics: Chronic Disease; Double-Blind Method; Female; Gastric Mucosa; Gastritis; Gastroscopy; Helicobacter pylori; Humans; Male; Middle Aged; Misoprostol

Our aim was to investigate the effect of misoprostol on NSAID-induced gastroduodenal mucosal damage in patients with rheumatoid arthritis. The study included 40 patients, and it was designed as a double-blind, placebo-controlled trial. Misoprostol significantly reduced the gastroduodenal mucosal lesions found at endoscopy (P < 0.05) and prevented the development of ulcers. The cumulative incidence of ulcers at four weeks was 5% in the placebo group and 0% in the misoprostol group. The basal and pentagastrin-stimulated acid output as evaluated after 23 days of treatment with misoprostol was not significantly affected. Forty-one percent of the patients had signs of current Helicobacter pylori infection, 33% had positive serology only, and 26% had no evidence of infection. Most of the patients with current infection belonged to blood group O (P < 0.05). Misoprostol treatment did not affect the occurrence of Helicobacter pylori or the rheumatic disease activity. It is concluded that the protective actions of misoprostol on the gastroduodenal mucosa of NSAID-treated patients are largely mediated by mechanisms other than inhibition of acid secretion. The relationship among active Helicobacter pylori infection, blood group O, and peptic ulcer may be helpful to identify a subpopulation of patients taking NSAIDs at risk of developing peptic ulcers.

Topics: ABO Blood-Group System; Aged; Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Rheumatoid; Double-Blind Method; Duodenum; Female; Gastric Acid; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Mucosa; Male; Middle Aged; Misoprostol; Peptic Ulcer

Ibuprofen, a commonly proscribed nonsteroidal anti-inflammatory drug that is also available in many countries, including the United States, without a prescription, is known to cause hemorrhage and erosion of the gastroduodenal mucosa. This study was conducted to compare the efficacy of 200, 100, and 50 micrograms of misoprostol and placebo administered qid for 6 days, with a final dose on the morning of the 7th day, in the prevention of gastric and duodenal lesions induced by the concurrent administration of 800 mg of ibuprofen qid. A total of 120 healthy subjects with endoscopically normal gastric and duodenal mucosae were enrolled in the study. The endoscopic examination was repeated 2 h after the final dose on day 7, and the mucosae were graded on a 0 to 4+ scale. In the stomach, all three misoprostol groups were significantly more protective than placebo and did not differ significantly from each other. In the duodenum, the endoscopic scores of the 200- and 100-micrograms misoprostol groups, but not the 50-micrograms group differed significantly from placebo. The 200- and 100-microgram groups did not differ significantly from each other, but both differed from the 50-micrograms group for duodenal mucosal injury. Subjective symptoms thought to be primarily attributable to the NSAID (e.g., pain, indigestion/heartburn and nausea) were recorded by each subject in a diary. Subjects in the 200-micrograms misoprostol group attained the greatest degree of mucosal protection and had a significantly higher incidence of indigestion/heartburn and abdominal pain than the placebo group. One can conclude that misoprostol in both antisecretory (200- and 100-micrograms) and non-antisecretory (50-micrograms) doses protects the gastric mucosa from injury from high anti-inflammatory doses of ibuprofen (3200 mg/day). Only the antisecretory doses (100 and 200 micrograms qid) were effective in the duodenum, suggesting that acid suppression is necessary for mucosal protection to occur in the duodenum.

Topics: Adult; Alprostadil; Anti-Ulcer Agents; Dose-Response Relationship, Drug; Double-Blind Method; Drug Evaluation; Duodenitis; Female; Gastritis; Humans; Ibuprofen; Male; Middle Aged; Misoprostol; Random Allocation

The natural history of chronic antral gastritis in relation to the healing of duodenal ulcer and its response to treatment, if any, are unknown. We performed a double-blind controlled trial using an oral prostaglandin E1, misoprostol, in 229 patients with active duodenal ulcer randomized to receive placebo (n = 76), misoprostol 200 micrograms (n = 77), or misoprostol 300 micrograms (n = 76), q.i.d. orally. Healing of duodenal ulcer was assessed biweekly up to 12 wk by endoscopy, during which procedures at least two antral and two fundal biopsy specimens were taken. The activity and the degree of chronic inflammation of gastritis, as assessed histologically by the infiltration of polymorphs and chronic inflammatory cells, respectively, was graded blindly by two pathologists as nil, mild, moderate, or severe. Before treatment, 99% of patients had chronic antral gastritis and 1.5% had chronic fundal gastritis. In the placebo group, healed duodenal ulcer was associated with significantly (p less than 0.01, life table analysis) higher incidence of improvement of the activity of the antral gastritis (nil or mild as endpoint) than unhealed ulcer (30% vs. 4% at week 8). Irrespective of whether duodenal ulcer was healed or unhealed, significantly (p less than 0.01) more patients on misoprostol (50% at week 8) showed improvement (nil or mild as endpoint) than the placebo group. The degree of chronic inflammation of the antral gastritis showed similar significant changes in favor of misoprostol. Smoking and alcohol intake had no significant effect on the improvement of chronic antral gastritis. In conclusion, healing of duodenal ulcer was associated with improvement of the activity of chronic antral gastritis, which, as shown for the first time, could be further enhanced by a therapeutic agent--prostaglandin E1.

Topics: Adult; Alprostadil; Chronic Disease; Double-Blind Method; Duodenal Ulcer; Female; Gastritis; Humans; Male; Misoprostol; Placebos; Prostaglandins E; Random Allocation

Topics: Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Duodenitis; Gastritis; Humans; Misoprostol; Proton Pump Inhibitors; Ranitidine

Prostaglandins are widely used in the prevention and healing of non-steroidal anti-inflammatory drug (NSAID) induced gastric and duodenal ulcers, but their longterm effect on the human gastric mucosa is unknown. This study assessed the effect of coadministration of prostaglandins with NSAIDs on the histology of the gastroduodenal mucosa. Histological appearances (using the Sydney system) of gastric biopsy specimens from 180 patients receiving longterm NSAID treatment of whom 90 had been receiving misoprostol (400-800 micrograms/day) for one to two years were studied. Both groups of patients were comparable with regard to clinical and demographic details. There was no significant difference (p > 0.1) in the prevalence of chronic gastritis (total, corpus or antrum only) between patients receiving (36 of 90 (40%)) or not receiving misoprostol (35 of 90 (39%)). Chronic gastritis was equally associated with the presence of Helicobacter pylori, 86% and 73% (p > 0.1), respectively, in the two groups. Significantly fewer patients receiving misoprostol had reactive gastritis than those receiving only NSAIDs (8 (9%) versus 27 (30%), p < 0.01). Reactive gastritis was not associated with H pylori. Thirty nine (43%) of the misoprostol treated patients had normal histology compared with 16 (18%) receiving only NSAIDs (p < 0.01). These results show two different patterns of gastric damage in patients receiving NSAIDs, namely chronic and reactive gastritis. Misoprostol treatment was associated with a significantly reduced prevalence of reactive gastritis and it is suggested that this, along with its antisecretory action, may explain the reduced prevalence of gastroduodenal lesions when coadministered with NSAIDs.

Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Arthritis; Drug Therapy, Combination; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Misoprostol; Time Factors

In the present study, the protective effect of omeprazole on gastric mucosa injury induced by ethanol.HCl in rats and the putative mechanisms involved in this action were investigated. Misoprostol and ranitidine were used as reference drugs. The morphometric analysis of histological sections showed that omeprazole caused a significant reduction of mucosal necrotic damage, this effect being associated with a marked increase in Alcian blue recovery from gastric bound mucus. In addition, omeprazole elicited a significant inhibition of gastric acid secretion from pylorus-ligated rats. Misoprostol exerted similar effects to those obtained with omeprazole, even if the Alcian blue recovery and the acid output were affected to a lesser extent. By contrast, ranitidine failed to influence both the mucosal damage and the Alcian blue recovery, while it exerted a marked inhibition on acid secretion. The present results indicate that omeprazole is effective in protecting gastric mucosa from necrotic damage induced by ethanol.HCl and suggest that an enhancement of gastric mucus barrier may account for this protective action.

Topics: Animals; Ethanol; Gastric Acid; Gastric Mucosa; Gastritis; Hydrochloric Acid; Male; Misoprostol; Mucus; Necrosis; Omeprazole; Ranitidine; Rats; Rats, Wistar

To explore the role of prostaglandins in protecting against chilli-induced early gastric vascular damage.. Early gastric vascular damage was induced in rats by oral administration of 8 mg/Kg chilli extract. The damage was assessed by estimating spectrophotometrically the amount of Evan's blue leaking into gastric tissue and luminal contents 10 min after exposure to chilli. Further groups of rats were pretreated with misoprostol (10, 25 or 50 micrograms/Kg) or dazmegrel (1, 5 or 25 mg) to evaluate their protective effects.. Both misoprostol and dazmegrel were able to reduce gastric vascular damage induced by chilli in a dose-dependent fashion.. Prostaglandins may play a role in protecting against chilli-induced early gastric vascular damage.

Topics: Animals; Capsaicin; Female; Gastric Mucosa; Gastritis; Imidazoles; Male; Misoprostol; Premedication; Prostaglandins; Rats; Rats, Wistar; Thromboxane-A Synthase

In a cohort of children with juvenile rheumatoid arthritis treated with nonsteroidal antiinflammatory drugs and referred for gastrointestinal complaints, more than 75% had gastritis, antral erosions, or ulcers. Epigastric pain strongly correlated with documented gastroduodenal injury. Therapy with ranitidine or misoprostol led to clinical improvement. Nonsteroidal antiinflammatory drugs are associated with significant gastrointestinal abnormalities in children.

Topics: Abdominal Pain; Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Juvenile; Child; Cohort Studies; Duodenitis; Gastritis; Humans; Misoprostol; Peptic Ulcer; Pilot Projects; Ranitidine

Topics: Anti-Inflammatory Agents, Non-Steroidal; Cost-Benefit Analysis; Drug Therapy, Combination; Gastritis; Humans; Misoprostol; Ulcer

NSAID induced gastropathy is linked to the inhibition of endogenous synthesis of prostaglandins. Gastropathies are made of erythematous, erosive or ulcerative lesions. Their localization is mainly antral or prepyloric. Their incidence is quite large and very severe in the elderly patient treated for long time with NSAID. The author presents several strategies either to prevent (with administration of misoprostol) or to treat (with prescription of omeprazole) this iatrogenic gastropathy.

Topics: Adult; Aged; Anti-Inflammatory Agents, Non-Steroidal; Gastritis; Humans; Intestinal Mucosa; Misoprostol; Peptic Ulcer

Topics: Alprostadil; Animals; Cats; Diarrhea; Dinoprostone; Dogs; Enprostil; Ethanol; Female; Gastric Acid; Gastric Mucosa; Gastritis; Guinea Pigs; Histamine; Indomethacin; Misoprostol; Muscle, Smooth; Myometrium; Prostaglandins E, Synthetic; Rats; Receptors, Prostaglandin; Uterine Contraction

Biopsy specimens from the stomach and duodenum of 45 duodenal ulcer patients treated with ranitidine, misoprostol, or an antacid were examined. During 4 weeks of treatment the duodenal ulcer healed in 31 patients. The treatment regimens showed no significant effect on the amount of Helicobacter-like structures (HLS) or the presence of active inflammation, either in the stomach or in the duodenum. All patients had chronic active antral gastritis before and after treatment. HLS were found histologically in 91.7% of all antral specimens, in 94.2% of the gastric corpus specimens, in 15.9% of the duodenal bulb specimens, and in 0.9% from the lower duodenal knee. The frequency of chronic active gastritis was clearly lower in the gastric corpus than in the antrum, whereas the occurrence of HLS was about the same. This may indicate a higher resistance of the gastric corpus mucosa to H. pylori.

Topics: Adult; Aged; Alprostadil; Antacids; Anti-Ulcer Agents; Biopsy; Duodenal Ulcer; Duodenitis; Female; Gastritis; Helicobacter pylori; Humans; Male; Middle Aged; Misoprostol; Ranitidine

Topics: Alprostadil; Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Gastritis; Humans; Misoprostol; Rheumatic Diseases

The administration of oral S-adenosylmethionine (SAMe) (100 mg/kg body weight) was well tolerated by the rat gastroduodenal tract. Moreover, rats given SAMe exhibited a significant increase in non-protein sulfhydryl groups of gastroduodenal mucosa as compared with control animals. The abilities of SAMe and misoprostol, a prostaglandin E1 analogue, to protect the gastric mucosa against necrosis induced by various noxious stimuli (ethanol, aspirin, stress) were also compared in standardized, experimental rat models. Pretreatment with SAMe or misoprostol significantly and to the same extent reduced gastric mucosal injury. The experiments described herein indicate that SAMe, a molecule used for the treatment of osteoarthritis, can exert a gastric cytoprotective effect in animals. As preliminary data have shown that this effect may also be reproduced in humans, SAMe seems to provide a therapeutic advantage, in contrast to currently available nonsteroidal anti-inflammatory agents.

Topics: Alprostadil; Animals; Anti-Ulcer Agents; Aspirin; Ethanol; Gastric Mucosa; Gastritis; Intestinal Mucosa; Male; Misoprostol; Rats; Rats, Inbred Strains; S-Adenosylmethionine; Stress, Physiological; Sulfhydryl Compounds

The effects of misoprostol on human gastric antral mucosa were investigated in patients with established diagnoses of either gastric or duodenal ulcer. All patients had pretreatment biopsy. After starting treatment with misoprostol, antral biopsies were taken at four and eight weeks and were fixed in formaldehyde. Following fixation and routine tissue processing, the slides were stained with hematoxylin and eosin. A pathologist from the laboratory preparing the slides reviewed the slides and prepared surgical pathology reports. An identical slide of each biopsy was sent to pathologists at G.D. Searle and Company who were unaware of the diagnoses and who issued an independent descriptive report. Representative cases are presented for discussion. Misoprostol was administered at doses of 100 or 200 micrograms for four or eight weeks. No cellular or mucosal changes were observed. Both groups of pathologists were unable to recognize any dose-related or structural alterations. No special studies were performed on these tissues due to their fixation and sample size. Infiltration of the mucosa by chronic inflammatory cells with a variable number of granulocytes was the most common finding. There were a few cases of goblet cell metaplasia and mild hyperplasia both before and after treatment. By the application of histochemical and immunohistochemical staining methods it is hoped that the constituents in mucus and specialized cells can be identified.

Topics: Alprostadil; Anti-Ulcer Agents; Duodenal Ulcer; Gastric Mucosa; Gastritis; Humans; Hyperplasia; Misoprostol; Peptic Ulcer; Pyloric Antrum; Random Allocation; Stomach Ulcer