Sunday, August 11, 2013

MedicalConspiracies- Pain medications work by causing injury to the stomach (New Research)

It looks like both mechanisms work by stomach injury, I thought the stomach injury from (OTC)  over the counter pain medication was well established years ago?  G.

The pathophysiology of non-steroidal anti-inflammatory drug (NSAID)-induced mucosal injuries in stomach and small intestine

Proposed Mechanisms of NSAID-Induced Stomach Injury

The defense mechanisms of stomach against NSAID can be divided into 2 categories: PG-dependent mechanism and non-PG-dependent mechanism.

The pathophysiology of PG-dependent NSAID-induced stomach injury

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. Aspirin inhibits COX irreversibly, while other NSAIDs inhibit COX in a reversible, concentration-dependent manner.() Two COX isoforms were identified in early 1990s in mammalian cells, COX-1 and COX-2. COX-1 is constitutively expressed in most of tissues including stomach and responsible for maintaining gastric mucosal integrity at base line, whereas COX-2 participates in inflammation. Gastric injury was thus considered to be ascribed to gastric mucosal PG deficiency by COX-1 inhibition. In human stomach, little or no COX-2 protein and activity was demonstrated, while abundant COX-1 protein and activity was demonstrated.() Therefore, NSAIDs that selectively inhibit COX-2 were developed and applied in a clinical setting.

More recently, experimental data in animal demonstrated that for gastric ulceration to occur, both COX-1 and COX-2 must be inhibited.() The result challenges the concept that only COX-1 plays a housekeeping role in the stomach. Recent researches suggested that both COX-1 and COX-2 may play a role in PG synthesis and maintenance of gastric mucosal integrity, and that COX-2 plays a “back-up” role by alleviating PG deficiency which is induced by COX-1 inhibition.()

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