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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Resistance of germfree rats to indomethacin-induced intestinal lesions. Several studies have shown that the antipyretic action of NSAIDs is via inhibition of PGE2 synthesis in and near the preoptic hypothalamic area in circumventricular organs [ 31 — 33 ].

Non-steroidal anti-inflammatory drug gastropathy: causes and treatment.

The uncoupling of mitochondrial oxidative phosphoryaltion Nsaud these pathophysiological processes, the NSAID-induced inhibition of oxidative phosphorylation in mitochondria is considered as the main underlying mechanism. Derivatives of naproxen, diclofenac, nsajd indomethacin which can release H2S have been reported [ — ]. As a result, the pH at the surface of gastric mucosal epithelial cells normally is maintained in the neutral range when the pH at the gastric luminal surface reaches 1 to 2.

Dual antiplatelet therapy with thienopyridine like clopidogrel and NSAID like aspirin is prescribed to decrease adverse cardiac events in patients suffering from acute coronary syndromes or placement of an intracoronary stent [ 7273 ], but they are associated gqstropati high risks of GI bleeding [ 21 ]. It also removes acid and other toxic metabolic by-products. Retrieved from ” https: Bjarnason I, Hayllar J. Non-steroidal anti-inflammatory drug-associated gastropathy disorder.


It seems that the framework of pathophysiology of NSAID-induced mucosal injury may differ in stomach and in small intestine. This is an open access article distributed under the Creative Commons Attribution Licensewhich permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Other treatment options include misoprostol which is a synthetic prostaglandin designed to replace those loss by NSAIDs.

Prevention and Treatment of NSAID Gastropathy.

Results for Non-steroidal anti-inflammatory drug-associated gastropathy disorder and additional nsaif. However, the fluorescence intensities of cells pretreated with rebamipide were significantly reduced than those in cells treated with indomethacin alone: There are, however, prospects for selective cyclooxygenase 2 inhibitors.

For high-risk patients requiring continuing NSAID use co-prescription of omeprazole or misoprostol should be considered. Blood flow provides an adequate supply of micronutrients and oxygen in order for epithelial cells to secrete mucous and bicarbonate. NSAIDs were also able to induce both necrosis and gastroopati in gastric mucosal cells [ 47 ]. NSAID induced gastropathy can result in stomach or duodenal ulcers which may even lead to death. Bellarmine Student Project Medical Pharmacology. It is notable that the difference of aggravating factors between small intestine and stomach may explain the different biological responses and therefore the gastropat lesions.

It is suggested that NSAIDs cause membrane permeabilization leading to disruption of epithelial barrier [ 46 ].


PPIs are found to be effective in reducing the risk of GI bleeding in such patients [ 23 ]. View at Google Scholar F. Robert A, Asano T. Calcium potentiates the peroxidation of erythrocyte membrane lipids. Misoprostol reduces indomethacin-induced changes in human small intestinal permeability.

Mediators of Inflammation

In addition to energy metabolism, the regulation of cell death has recently considered as a second major function of mitochondria. Use case Healthcare Patents Pharma Others.

Though several approaches for limiting these side effects have been adopted, like the use of Gasteopati specific drugs, comedication of acid suppressants like proton pump inhibitors and prostaglandin analogs, these alternatives have limitations in terms of efficacy and side gastro;ati.

Table of Contents Alerts. NSAID prodrugs are potential agents for enhancing the antioxidant activity, water solubility and dissolution, release of nitric oxide and hydrogen sulfide, gaxtropati targeting and delivery, and inhibiting anticholinergic and acetylcholinesterase activity [ — ].

Recently it has been reported that the single-tablet formulations of diclofenac and misoprostol which have been found to be effective in arthritis and in reducing the NSAID-induced gastropathy [ 57 ]. Secondly, the inhibition of oxidative phosphorylation causes dysfunction of the tight intracellular junctions and increases the intestinal permeability.