Misoprostol Heals Gastroduodenal Injury in Patients With Rheumatoid Arthritis Receiving Aspirin

The Japanese Society of Gastroenterology (JSGE) revised the evidence-based clinical practice guidelines for peptic ulcer disease in 2014 and has created an English version. The revised guidelines consist of seven items: bleeding gastric and duodenal ulcers, Helicobacter pylori (H. pylori) eradication therapy, non-eradication therapy, drug-induced ulcer, non-H. pylori, non-nonsteroidal anti-inflammatory drug (NSAID) ulcer, surgical treatment, and conservative therapy for perforation and stenosis. Ninety clinical questions (CQs) were developed, and a literature search was performed for the CQs using the Medline, Cochrane, and Igaku Chuo Zasshi databases between 1983 and June 2012. The guideline was developed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system. Therapy is initially provided for ulcer complications. Perforation or stenosis is treated with surgery or conservatively. Ulcer bleeding is first treated by endoscopic hemostasis. If it fails, surgery or interventional radiology is chosen. Second, medical therapy is provided. In cases of NSAID-related ulcers, use of NSAIDs is stopped, and anti-ulcer therapy is provided. If NSAID use must continue, the ulcer is treated with a proton pump inhibitor (PPI) or prostaglandin analog. In cases with no NSAID use, H. pylori-positive patients receive eradication and anti-ulcer therapy. If first-line eradication therapy fails, second-line therapy is given. In cases of non-H. pylori, non-NSAID ulcers or H. pyloripositive patients with no indication for eradication therapy, non-eradication therapy is provided. The first choice is PPI therapy, and the second choice is histamine 2-receptor antagonist therapy. After initial therapy, maintenance therapy is provided to prevent ulcer relapse.

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“…The healing rate of gastric and duodenal ulcers with misoprostol 800 lg/day was significantly higher than with placebo [100].…”

Section: Drug-induced Ulcermentioning

confidence: 80%

Evidence-based clinical practice guidelines for peptic ulcer disease 2015

et al. 2016

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“…Therefore, it is assumed that PGs should be effective on NSAID-induced gastric mucosal impairment. Actually, many clinical studies have demonstrated the defensive effects of PGs on gastric mucosa (3) as well as effects of accelerating repair, especially on NSAID-induced injury (4,5). However, side effects, including diarrhea and uterine contraction, make many physicians reluctant to prescribe them (6).…”

Section: Introductionmentioning

confidence: 99%

Hepatocyte growth factor as a key to modulate anti-ulcer action of prostaglandins in stomach.

Takahashi¹,

Ota²,

Hata³

et al. 1996

J. Clin. Invest.

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Although the clinical efficacy of prostaglandins (PGs), especially on gastric mucosal injuries induced by nonsteroidal antiinflammatory drugs, is widely appreciated, their mechanism of action, apart from acid suppression, is quite unclear. In this study, we have established a primary culture system of human gastric fibroblasts and clearly demonstrated that PGs strongly induce the expression of hepatocyte growth factor (HGF) in the fibroblasts, which is mediated by PGE specific receptor, EP2 or EP4. Since HGF facilitates repair and protection of gastric epithelial cells in a paracrine manner, it is assumed that some of the beneficial effects of PGs may be mediated by HGF. To confirm this assumption, we established a simplified in vitro culture gastric mucosal model which consists of gastric epithelial cells and gastric fibroblasts. Using the model, we performed a round wound restitution assay. PGE1 remarkably accelerated restitution which was completely inhibited by anti-HGF antibody, indicating that the action was mediated by HGF. To confirm these in vitro data, we further demonstrated that HGF mRNA expression is downregulated at the edges of nonsteroidal antiinflammatory drug-induced gastric ulcers where PGs should be depleted. In summary, we proposed that gastric fibroblasts are newly recognized targets of PGs, and HGF produced by human gastric fibroblasts may be a key factor for anti-ulcer action of PGs in the stomach. ( J. Clin. Invest. 1996. 98:2604-2611.)

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“…Misoprostol, a synthetic analog of prostaglan din Ei, has comparable efficacy to FT antago nists in the healing of ordinary peptic ulcers (unrelated to NSAID ingestion) [68], The one trial which studied the effects of misoprostol on ulcer healing with continued use of NSAID (in this case aspirin) found healing rates supe rior to placebo (67 vs. 26%) [69], This benefi cial effect on ulcer healing is believed to result primarily from misoprostol's weak antisecretory properties [38], It is in a prophylactic role that misoprostol has been found most useful. Graham et al [70] prospectively studied the efficacy of mi soprostol in preventing NSAID-induced gas tric ulcers.…”

Section: Prostaglandin Analogsmentioning

confidence: 99%

Nonsteroidal Anti-Inflammatory Drugs: Gastroduodenal Injury and Beyond

Bernsdorff¹,

Agrawal²,

Brodmerkel³

1995

Dig Dis

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The use of nonsteroidal anti-inflammatory drugs (NSAIDs) is extensive, and the upper gastrointestinal (GI) side effects of these drugs have been well recognized. Although much attention has been focused on gastroduodenal ulceration and attendant complications, it is becoming more apparent that NSAIDs exert potentially important effects on the small bowel and colon. The widespread effects of NSAIDs on the GI system, including theories of pathogenesis, will be presented here.

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Misoprostol Heals Gastroduodenal Injury in Patients With Rheumatoid Arthritis Receiving Aspirin

Cited by 117 publications

References 31 publications

Evidence-based clinical practice guidelines for peptic ulcer disease 2015

Evidence-based clinical practice guidelines for peptic ulcer disease 2015

Hepatocyte growth factor as a key to modulate anti-ulcer action of prostaglandins in stomach.

Nonsteroidal Anti-Inflammatory Drugs: Gastroduodenal Injury and Beyond

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