Mechanism of action and therapeutic benefit of rifaximin in patients with irritable bowel syndrome: a narrative review.
William D CheyEric D ShahHerbert L DuPontPublished in: Therapeutic advances in gastroenterology (2020)
Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder with a multifactorial pathophysiology. The gut microbiota differs between patients with IBS and healthy individuals. After a bout of acute gastroenteritis, postinfection IBS may result in up to approximately 10% of those affected. Small intestinal bacterial overgrowth (SIBO) is more common in patients with IBS than in healthy individuals, and eradication of SIBO with systemic antibiotics has decreased symptoms of IBS in some patients with IBS and SIBO. The nonsystemic (i.e. low oral bioavailability) antibiotic rifaximin is indicated in the United States and Canada for the treatment of adults with IBS with diarrhea (IBS-D). The efficacy and safety of 2-week single and repeat courses of rifaximin have been demonstrated in randomized, placebo-controlled studies of adults with IBS. Rifaximin is widely thought to exert its beneficial clinical effects in IBS-D through manipulation of the gut microbiota. However, current studies indicate that rifaximin induces only modest effects on the gut microbiota of patients with IBS-D, suggesting that the efficacy of rifaximin may involve other mechanisms. Indeed, preclinical data reveal a potential role for rifaximin in the modulation of inflammatory cytokines and intestinal permeability, but these two findings have not yet been examined in the context of clinical studies. The mechanism of action of rifaximin in IBS is likely multifactorial, and further study is needed.
Keyphrases
- irritable bowel syndrome
- placebo controlled
- double blind
- stem cells
- liver failure
- genome wide
- endothelial cells
- open label
- mesenchymal stem cells
- bone marrow
- artificial intelligence
- physical activity
- helicobacter pylori
- machine learning
- deep learning
- helicobacter pylori infection
- replacement therapy
- phase ii
- drug induced