Mediators of Inflammation / 2013 / Article / Tab 2

Review Article

Current Perspectives in NSAID-Induced Gastropathy

Table 2

. Strategies to prevent NSAID-induced gastrointestinal injury.

Treatment procedure MechanismAction

Gastroprotective drugs
(i) PG analoguesReplacement of PGReduces ulceration and other GI damages
Cannot prevent dyspepsia
(ii) Acid suppressants like
proton pump inhibitors
Increase of intragastric pHDecreases dyspepsia, ulceration, and associated damages
Not suitable for patients with H. pylori infections

Selective COX-2 inhibitorsDoes not inhibit COX-1, and hence synthesis of gastroprotective PG is maintainedReduces dyspepsia, reverses gastroduodenal ulcers, and prevents other GI damages
Associated with prothrombotic events and enhances cardiovascular risks

NSAID prodrugs like NO-NSAIDs Release of NO maintains microvascular integrity Reduces GI damage, has antithrombotic effects

Inhibitors of COX and 5-LOXBlocks formation of leukotrienes and other proinflammatory mediatorsMaintains gastroprotection and reduces GI damage

Role of lactoferrin Structural studies suggest binding of C-terminal lobe of lactoferrin with NSAIDs and sequestration of unwanted NSAIDsAnimal studies indicate reversal of gastric bleeding and inhibition of myeloperoxidase formation

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