This is different because in the stomach there is a local inhibition of prostaglandin synthesis but in the small intestine and the colon the mechanism is unknown at the moment

Dear Sir

Thanks for joining the discussion. My point is since prostaglandins show efficacy against both gastric as well as intestinal ulcers, mucosal protective agents are also effective against both type of ulcers, then can we think of a common mechanism? Can we point out or move towards a common solution. 

The pathophysiology of Nsaids inducing gastropathy is different with -enteropathy.

In the latter, NSAIDs suppress COX isoenzymes and directly damage intestinal epithelium. Intercellular junctions weaken and then intraluminal aggressors including neutrophils, inflammatory mediators, bile acid, bacteria, enzymes attack the intestinal epithelial cells. While the secondary damage with intestinal ulceration, and/or stricture is augmented by the enterohepatic circulation of NSAID.

PPI can't protect NSAIDs induced intestinal injuries; Selective coxibs improved upper and lower GI safety according to results of clinical trials.

Few studies had demonstrated misoprostol co-therapy can reduce the incidence of small intestinal lesions induced by Nsaids --> suggested to read Prevention of nonsteroidal anti-inflammatory drug-induced small-intestinal injury by prostaglandin: a pilot randomized controlled trial evaluated by capsule endoscopy by Fujimori et al. Gastrointest Endosc. 2009;69:1339–1346. 

I think more studies are required to work up for that.

I still believe that the pathophysiology of NSAID induced gastropathy and enteropathy are similar. In my view one need to search for the proper target and therapeutic agents. We need to study these two problems in a single model. What is your opinion on this. I am open for discusssions, This issue needs to be addressed.