Current Perspectives in NSAID-Induced Gastropathy

Table 2

. Strategies to prevent NSAID-induced gastrointestinal injury.

Treatment procedure	Mechanism	Action
Gastroprotective drugs
(i) PG analogues	Replacement of PG	Reduces ulceration and other GI damages; Cannot prevent dyspepsia
(ii) Acid suppressants like; proton pump inhibitors	Increase of intragastric pH	Decreases dyspepsia, ulceration, and associated damages; Not suitable for patients with H. pylori infections
Selective COX-2 inhibitors	Does not inhibit COX-1, and hence synthesis of gastroprotective PG is maintained	Reduces 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-LOX	Blocks formation of leukotrienes and other proinflammatory mediators	Maintains gastroprotection and reduces GI damage
Role of lactoferrin	Structural studies suggest binding of C-terminal lobe of lactoferrin with NSAIDs and sequestration of unwanted NSAIDs	Animal studies indicate reversal of gastric bleeding and inhibition of myeloperoxidase formation