A report of three multiclinic trials evaluating arbaprostil in arthritic patients with ASA/NSAID gastric mucosal damage

Euler, Arthur R.; Safdi, Michael; Rao, Jaideepraj; Jaszewski, Richard; Welsh, James W.; Le, Vu; Raskin, Jeffrey B.; Fleischmann, R.; Razzaque, Muhammad Raheel Abdul; Champion, Christopher; Gottlieb, Gilbert; Nashel, David J.; Veer, Lindsley Van der; Levine, Joel S.; Barreiro, Manuel; Cheatum, Don E.; Mena, Hector R.; Budiman‐Mak, Elly; Roth, Sanford H.; Gaskill, Harold V.; Levine, Barton S.; Swinehart, James M.; McClain, Charles; Riff, Dennis; Graham, Daniela; Phan, Tuan; Burns, M.; Lookabaugh, Janice L.; Wood, Douglas E.

doi:10.1016/0016-5085(90)91089-o

Cited by 14 publications

(3 citation statements)

References 35 publications

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“…This would suggest that the large number of short term studies which provide evidence of a protective action with misoprostol are clinically relevant for patients on longer term NSAID therapy. Drug Safety 7 (2) 1992 Other prostaglandin analogues have been used in the prevention and treatment ofNSAID damage with similar results (Euler et at. Bardhan et at.…”

Section: Preventionmentioning

confidence: 88%

Gastroprotection and Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

Hayllar

Bjarnason

1992

Drug Safety

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There is no doubt that nonsteroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal injury. The most serious consequences are gastric and duodenal ulcers which can cause bleeding and perforation, and which may lead to the premature death of 3000 to 4000 patients in the UK annually. The immediate actions of NSAIDs operate at a subcellular level; in particular altering of mitochondrial function which causes depletion of ATP and renders the cell vulnerable to oxidant stress. Secondary consequences follow, such as the inhibition of prostaglandin synthesis which delays cellular repair. While adaptation can be shown in volunteers despite continued NSAID ingestion, studies in patients suggest mucosal damage develops continuously and cumulatively even with low doses of aspirin. Histamine H2-receptor antagonists and proton pump inhibitors heal NSAID-related ulcers, though healing rates with H2-antagonists are slower in patients who continue NSAID treatment. They have little role in preventing damage. In addition to acid suppression, prostaglandin analogues cause bicarbonate secretion and enhance mucosal blood flow. They have a specific role in both prevention and treatment of NSAID-related damage. The use of misoprostol offers a rational approach to reduce the high prevalence of unwanted gastroduodenal damage from NSAIDs. On a purely financial basis more information is needed before routine coprescribing can be recommended. However, for any patient on NSAIDs with a previous ulcer or for patients aged over 60 years (where the risks and seriousness of complications are markedly increased), the use of misoprostol should be considered. Further developments in prostaglandin analogues may reduce their adverse effects and perhaps thereby improve their efficacy at symptom control.

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Section: Preventionmentioning

confidence: 88%

Gastroprotection and Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

Hayllar

Bjarnason

1992

Drug Safety

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“…The results of a similar analysis of four placebo-controlled, double-blind trials with prostaglandins [32][33][34][35] are shown in figure 4. The prostaglandins investigated were miso prostol.…”

Section: Prostaglandinsmentioning

confidence: 95%

The Role of Acid Regulation in the Treatment of NSAID-induced Mucosal Damage

Yeomans¹,

Skeljo²,

Giraud³

1992

Digestion

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Gastric acid probably exacerbates mucosal injury caused by non-steroidal anti-inflammatory drugs (NSAIDs) in two ways: first, by increasing absorption of NSAIDs, which are weak acids and predominantly in their undissociated form at low pH – this is probably mainly relevant for salicylates; then, by a ‘second wave’ of injury that leads to deeper erosions, as gastric acid accesses the partially denuded mucosa. Regulation of gastric acid secretion by acid-inhibitory drugs has been shown to decrease acute NSAID-induced injury to varying extents, depending on the drug used and the method of assessing mucosal damage. Healing of chronic NSAID-induced ulcers is slow if NSAID therapy is continued, but is facilitated by treatment with H₂-receptor antagonists or prostaglandins. One study of the acid pump inhibitor omeprazole has shown a high rate of healing, even though NSAID therapy was continued.

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“…Significant improvement in NSAID-associated gastric and duodenal lesion scores and in gastrointestinal symptoms has been re ported after misoprostol 400 pg bd for 4 weeks in patients with rheumatoid arthritis who continued NSAID treatment [9], Miso prostol 200 pg bd for 4 weeks also signifi cantly reduced gastric lesion score, but not duodenal lesion score, in arthritic patients continuing NSAIDs [ 10], Other prostaglandin analogues that have been reported to heal NSAID-associated gas tric damage include enprostil 70-105 pg/day [11] rioprostil 400-450 pg/day [12], and arbaprostil 10-50 pg/day [ 13].…”

Section: Prostaglandin Analoguesmentioning

confidence: 99%

Treatment of Nonsteroidal Anti-Inflammatory Drug-Associated Gastric and Duodenal Damage

Pipkin¹,

Mills²

1995

Dig Dis

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Nonsteroidal anti-inflammatory drugs (NSAIDs) are the mainstay of treatment for rheumatic diseases. However, a significant number of patients receiving these drugs experience upper gastrointestinal side effects, including physical injury to the gastroduodenal mucosa. This may range from clinically insignificant bleeding and minor erosive changes to deeper ulceration, with attendant risk of haemorrhage or perforation. The majority of the published literature concerning healing of NSAID-associated peptic ulcer with antisecretory drugs involves studies of the use of the H₂-receptor antagonists, ranitidine and cimetidine. Peptic ulcers associated with NSAID use can be healed with these H₂-receptor antagonists using the same doses as those used for healing of idiopathic gastric or duodenal ulceration. Most ulcers heal within 4-8 weeks in those patients who are able to discontinue their anti-inflammatory therapy. If the NSAID is continued, healing may be slightly delayed. At present, limited data only are available with respect to the use of the proton pump inhibitor, omeprazole, and no firm conclusions can be drawn regarding the use of the prostaglandin analogue, misoprostol, for the healing of NSAID-associated peptic ulceration.

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A report of three multiclinic trials evaluating arbaprostil in arthritic patients with ASA/NSAID gastric mucosal damage

Cited by 14 publications

References 35 publications

Gastroprotection and Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

Gastroprotection and Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

The Role of Acid Regulation in the Treatment of NSAID-induced Mucosal Damage

Treatment of Nonsteroidal Anti-Inflammatory Drug-Associated Gastric and Duodenal Damage

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