Non Steroidal Anti-inflammatory Drug Induced
Damage on Lower Gastro-intestinal Tract:
Is There an Involvement of Microbiota?

FROM:   Curr Drug Saf. 2014;   9 (3):   196–204

Lucia Montenegro, Giuseppe Losurdo, Raffaele Licinio, Maria Zamparella,
Floriana Giorgio, Enzo Ierardi, Alfredo Di Leo
and Mariabeatrice Principi

Gastroenterology,
Department of Emergency and Organ Transplantation,
70124 Bari, Italy.
enzo.ierardi@fastwebnet.it

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The most commonly used agents for preventing or treating nonsteroidal anti-inflammatory drugs (NSAIDs)-induced damage are proton pump inhibitors (PPIs). However, these medications do not offer protection to the lower small intestine and actually exacerbate NSAID-induced small intestinal lesions. A critical role of bacteria composing gut microbiota was recently reinforced by a study demonstrating that NSAID enteropathy in rats is exacerbated by concomitant treatment with a PPI through a dysbiotic mechanism. Specifically, the investigators identified a marked loss of Bifidobacterium and Lactobacilli following PPI treatment. [39] NSAID-related gastroenteropathy is due to a decrease of Lactobacilli, with an impairment of the maintenance of luminal pH, mucosal permeability, enterocyte adhesion, mucus production, and immune system modulation.   The concomitant decrease of Bifidobacterium exacerbates both intestinal motility and local immunity. [40] FROM: Combining Pain Therapy with Lifestyle: The Role of Personalized Nutrition and Nutritional Supplements According to the SIMPAR Feed Your Destiny Approach J Pain Res. 2016 (Dec 8);   9:   1179–1189

Intestinal microbiota is composed by a community of microorganisms, which regulate intestinal functions and affect the global health. It is presumable that the well-known intestinal damages induced by Non Steroidal Antiinflammatory Drugs (NSAIDs) mirror on the homeostasis of microbiota, as confirmed by studies investigating this aspect. This review reports the evolving knowledge in this field taking into account both intestinal damage and microbiota involvement. In addition, we analyze a recent study reporting how NSAIDs change intestinal bacterial composition and, on this basis, hypothesize further possible interactions. Indeed, NSAIDs are responsible for a marked reduction of Lactobacilli, which act in the maintenance of luminal pH, mucosal permeability, enterocyte adhesion, mucus production, and immune system modulation. Moreover, Bifidobacteria are involved in the modulation of intestinal motility and local immunity and the demonstrated dangerous effect of NSAIDs could operate through an interference with these functions. A participation of microbiota in mesalazine and salycilate prevention of intestinal cancer may be supposed through their ability to stimulate bacterial production of molecules interfering with cell cycle on the basis of scanty available data. Finally, a supplementation with probiotics in chronic users of NSAIDs may help microbiota remodeling in a damaged intestine, but the poor current knowledge does not allow setting a clear indication for their use despite few evidences of a beneficial effect. In conclusion, it is presumable that the multiple effects of NSAIDs on the lower gastro-intestinal tract may involve microbiota alterations and this consideration suggests further investigations.

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