What is an NSAID? Nonsteroidal Anti-inflammatory drug. In this paper, the mechanism of action of NSAIDs and their critical gastrointestinal complications have been reviewed. This paper also provides. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most highly prescribed drugs to decrease NSAID-induced GI damage including use of.

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These problems can be overcome by the use of more potent acid suppression. It is suggested that NSAIDs cause membrane permeabilization leading to disruption of epithelial barrier [ 46 ]. The neutrophil infiltration is essential in the development of macroscopic lesion.

Though COX-2 inhibitors decrease the GI toxicity to a considerable amount, there is an associated risk of cardiovascular complications due to myocardial infarction and thrombosis associated with their use [ 99 — ]. View at Google Scholar S. Leukotrienes cause inflammation and tissue ischaemia leading to gastric mucosal injury [ 5152 ]. These strategies are based on multiple risk factors associated with NSAID-induced GI complications including age of the patient, simultaneous medications, prior medical history, and Helicobacter pylori infection.

When refering to evidence in academic writing, you should always try to reference the primary original source.

The main drawback of PPIs is that they are less effective against mucosal injury in more distal parts of the intestine gastropsti NSAID-induced colonopathy [ 81 ]. Though PPIs can help with gastric irritation, it is also found that they can induce risk of osteoporosis which often cause hip fractures in elderly patients as well as increase cardiovascular risk due to low serum magnesium levels in the blood.

See Tamblyn et al study on high gastropathy diagnostic rates by physicians [6]. Patients gastropagi aspirin represent a real challenge for treatment, since interaction with frequently prescribed NSAIDs e.

Current Perspectives in NSAID-Induced Gastropathy

Please review our privacy policy. Opening of MPTP also leads to cytochrome c realase into the cytosol, resulting in cellular apoptosis. For high-risk patients requiring continuing NSAID use co-prescription of omeprazole or misoprostol should be considered. H2 receptor antagonists are effective in preventing duodenal ulcer but not gastric ulcer. Free Radic Biol Med. However, these methods also have limited potency because of their additional cardiovascular effects [ 16 — 19 ].


The uncoupling of mitochondrial oxidative phosphoryaltion In these pathophysiological processes, the NSAID-induced inhibition of oxidative phosphorylation in mitochondria is considered as the main underlying mechanism. Hydrogen sulfide H2S also exerts its gastroprotective effects and reverses preexisting ulcers. View at Google Scholar L.

Prevention and Treatment of NSAID Gastropathy.

Some of the adverse effects of NSAIDs may be asymptotic, but in many cases there are reports of life-threatening incidents [ 10 ]. On the other hand, in small intestine, NSAID-induced mucosal injury cannot be explained, although controversy exists, by the PG deficiency alone. By far, celecoxib and rofecoxib stand out as the most effective COX-2 inhibitors and show efficacy over nonselective NSAIDs in regard to GI complications including mucosal lesions and other adverse GI symptoms [ 8687 ].

The increased intestinal permeability The mechanisms that the inhibition of oxidative phophorylation increases intestinal permeability are not well understood, but are explained as follows: Further clinical trials are in progress in osteoarthritis patients [ ]. Secondly, the inhibition of oxidative phosphorylation causes dysfunction of the tight intracellular junctions and increases the intestinal permeability.

Safe NSAID prescription should be straightforward since the most relevant aspects are clinical in nature. Cimetidine tablets or suspension for the prevention of gastrointestinal mucosal lesions caused by non-steroidal, anti-inflammatory drugs.

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Since PGs play a critical role in maintaining gastric mucosal defense system, the inhibition of COX leading to decreased mucosal PGs is considered as the most important in the pathogenesis of NSAID-induced gastric damage.

However, the fluorescence intensities of cells pretreated with rebamipide were significantly reduced than those in cells treated with indomethacin alone: Indexed in Science Citation Index Expanded. Presently, the most common protective strategies adopted are 1 combination therapy of NSAIDs with gastroprotective agents and 2 use of selective COX-2 inhibitors Table 2. Nonsteroidal anti-inflammatory drug enteropathy in rats: Licofelone [2,2-dimethyl 4-chlorophenyphenyl-2,3-dihydro-1H-pyrrazolineyl]acetic acid has been identified as one of the most convincing compounds in this group [ ].


This further leads to occlusion of gastric microvessels leading to reduced gastric blood flow and release of oxygen-derived-free radicals [ 54 ]. In general, they contain an acidic group mostly carboxylic acids or enols.

T39.395 Non-steroidal anti-inflammatory drug-associated gastropathy (disorder)

The pathophysiology of NSAID-induced small intestinal injuries was less well understood than that of gastric injuries. PG-dependent mechanism and non-PG-dependent mechanism.

NSAIDs also have a direct cytotoxic effect on gastric mucosal cell causing lesions and injury [ 4243 ]. The relative physiological importance of PGs in maintaining mucosal defense system between stomach and small intestine may contribute to the experimental and clinical results of NSAID-induced mucosal injuries. More recently, experimental data in animal demonstrated that for gastric ulceration to occur, both COX-1 and COX-2 must be inhibited. Healing of NSAID ulcers by conventional doses of H2 antagonists is slow and H2 antagonists are poor at preventing gastric ulcer development or recurrence.

The role of bacteria as an aggravating factor of NSAID-induced small intestinal injury is suggested by the experimental results that NSAIDs induced very few intestinal lesions in germ-free animals and that pretreatment with antimicrobials reduced NSAID-induced small intestinal damages.

Gastrointest Endosc Clin N Am. Peptic ulcers are typically caused by H. Therefore, the treatment for NSAID-induced small intestinal mucosal injuries should include medications other than conventional acid-reducing agents such as histamine 2 receptor antagonists H 2 RAs and proton pump inhibitors PPIs.

For correctness, completeness and topicality or designations no liability is assumed. National Center for Biotechnology InformationU. Salicylate- and aspirin-induced uncoupling of oxidative phosphorylation in mitochondria isolated from the mucosal membrane of the stomach.

It has been found to preferentially inhibit COX-2 but exhibited the anti-inflammatory, antipyretic, and analgesic activities of NSAIDs [ 869394 ].

Scand J Rheumatol Suppl. Gastric mucosal injury occurs when the causative agents such as gastric acid and NSAIDs overwhelm the mucosal defense. Mostly they are organic acids with pKa in the range of 3—5 [ 5 ].