The pro-drug sulindac may reduce the risk of intestinal damage associated with the use of conventional non-steroidal anti-inflammatory drugs

2007 ◽  
Vol 5 (6) ◽  
pp. 593-598 ◽  
Author(s):  
G. R. DAVIES ◽  
D. S. RAMPTON
2012 ◽  
Vol 181 (1) ◽  
pp. 98-110 ◽  
Author(s):  
Yuji Nadatani ◽  
Toshio Watanabe ◽  
Tetsuya Tanigawa ◽  
Hirohisa Machida ◽  
Hirotoshi Okazaki ◽  
...  

2013 ◽  
Vol 144 (5) ◽  
pp. S-718-S-719
Author(s):  
Ken Narabayashi ◽  
Yuko Ito ◽  
Taisuke Sakanaka ◽  
Kaori Fujiwara ◽  
Satoshi Harada ◽  
...  

2014 ◽  
Vol 146 (5) ◽  
pp. S-787
Author(s):  
Ken Narabayashi ◽  
Naoki Yorifuji ◽  
Kaori Fujiwara ◽  
Taisuke Sakanaka ◽  
Munetaka Iguchi ◽  
...  

2018 ◽  
Vol 6 (12) ◽  
Author(s):  
Aracely Evangelina Chávez-Piña ◽  
Reyes Roderico Abril-Urías ◽  
Doris Cerecedo

Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used type of drugs, as they are very effective as antiinflammatory, anti-pyretic and analgesic. Their use has increased dramatically over the years even without a medicalprescription¸however the use of NSAIDs is limited due to the adverse effect in the gastrointestinal tract, heart and kidney. Thisresearch work is focused on the adverse effect in the gastrointestinal tract. The mechanisms involved in gastric damage caused byNSAIDs are well known compared to those in the intestinal area. Research on NSAID-induced intestinal damage is very limited,despite its higher mortality rate, partially due to the difficulty of reaching this area. Therefore, this review mentions some of themechanisms involved in small intestinal damage to help as a reference to continue doing research about new strategies to come upwith an effective clinical therapy.


2010 ◽  
Vol 138 (5) ◽  
pp. S-431-S-432
Author(s):  
Yuji Nadatani ◽  
Toshio Watanabe ◽  
Tetsuya Tanigawa ◽  
Fumikazu Ohkawa ◽  
Koji Otani ◽  
...  

2019 ◽  
Vol 47 (6) ◽  
pp. 559-567 ◽  
Author(s):  
A. E. Karateev ◽  
E. V. Moroz ◽  
E. V. Kryukov

The use of nonsteroidal anti-inflammatory drugs (NSAID), even if short-term, may be associated to small intestinal complications, such as erosions, ulcers and chronic mucosal inflammation. Video capsule endoscopy allows for identification of such lesions in 20 to 55% of the patients who have taken nonselective NSAID for 2 to 4  weeks. The pathophysiology of NSAID-induced enteropathy is related to a reduced reparative potential of the mucosa and abnormalities of the microbial balance in the small intestine. In real world practice, NSAID enteropathy is commonly asymptomatic, and its manifestations, such as bleeding, perforation and ileus, are quite rare (about 0.3 episodes per 100  patient-years). The main manifestation of NSAID enteropathy is chronic iron deficient anemia. The use of rebamipide, sulfasalazine, mesalazine, and rifaximin has been discussed in the treatment of NSAID enteropathy, whereas its prevention implies preferential administration of coxibs, the use of rebamipide and probiotics.


2017 ◽  
Vol 95 (3) ◽  
pp. 222-227
Author(s):  
O. N. Sulaieva ◽  
J. L. Wallace

Despite the introduction of anti-inflammatory drugs that selectively inhibit cyclo-oxygenase-2 (COX-2), and potent inhibitors of gastric acid secretion, the gastrointestinal adverse effects of non-steroidal anti-inflammatory drugs (NSAIDs) remain a significant clinical problem. Combined use of antisecretory drugs and COX-2 inhibitors is helpful to limit the damage in the proximal gastrointestinal tract (stomach and duodenum), but it increases the risk of injury of small intestine and colon. It was proven that proton pump inhibitors and H2 receptor antagonists significantly worsen NSAID-induced small intestinal damage and microbiota balance. Nowadays, there is no proven effective preventative or curative treatment for NSAID-induced enteropathy. The new strategy of gastrointestinal protection is based on the discovery of endogenous cytoprotective molecules such as hydrogen sulfide (H2S). H2S is a gaseous mediator that produces strong cytoprotective and antioxidant effect on the gastrointestinal tract. The role of H2S in promoting mucosal integrity, healing of tissue injury and resolution of inflammation has been well documented. In addition, H2S stimulates productions of other cytoprotective molecules including prostaglandins, carbon monoxide and nitric oxide. Nowadays, the new generation of H2S-releasing non-steroidal anti-inflammatory drugs is developed and tested in clinical trials. H2S-NSAIDs possess enhanced anti-inflammatory activity and high gastrointestinal safety.


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