Antibiotics and Probiotics in Inflammatory Bowel Disease: Why, When, and How

Cosimo Prantera; Maria Lia Scribano


Curr Opin Gastroenterol. 2009;25(4):329-333. 

In This Article

Antimycobacterial Therapy and Crohn's Disease

The pathological aspects of IBD lesions are similar to those of an infectious disease, and many studies have been directed towards the identification of a specific causative agent.

During the 1980s and 1990s some investigators reported the presence of atypical Mycobacteria in Crohn's disease intestine, with limited supporting immunological evidence.[4,5] With the hope of curing Crohn's disease, antibiotics active against atypical Mycobacteria have been tested with conflicting outcomes.[6] The most important study, published at the end of 2007, employed the antibiotic clofazimine together with clarithromycin and rifabutin, against placebo, for up to 2 years, in addition to a 16-week tapering course of prednisolone.[7] This antibiotic combination was chosen because of its activity against Mycobacterium paratuberculosis (MAP), the agent of Johne's disease in animals, considered a potential cause of Crohn's disease. Two hundred and thirteen Australian patients were enrolled and randomized. The only significant benefit was observed at 16 weeks, when antibiotics were combined with steroid. A modest nonsignificant advantage of antibiotics over placebo in reducing Crohn's disease relapse was registered at every observation time point during the 2-year period. In conclusion (and in line with a previous meta-analysis), this trial has shown that antimycobacterial treatment is not effective in inducing remission without a course of corticosteroids, and that the advantage of adding antimycobacterials to steroids is minimal.

Some comments supported the conclusions of this trial, whereas others disputed it, affirming that the causality of MAP in Crohn's disease cannot still be completely refuted.[8,9–12] The main objections were: the well known antibiotic resistance of MAP, the relatively low doses of antimycobacterials employed, and the use in the placebo arm of mesalamine and/or azathioprine which have a potential anti-MAP effect. Such arguments, however, are unconvincing in view of the fact that current antitumour necrosis factor (TNF) treatments induce remission of active Crohn's disease and heal colonic and ileal lesions. TNF plays a key role in the host reaction against mycobacteria, namely granuloma formation and control of inflammatory disease. Over 70 cases of tuberculosis in close temporal association with the initiation of treatment with anti-TNF agents have been reported in Crohn's disease. However, anti-TNF therapy has never been associated with disseminated MAP in Crohn's disease, a strong argument against the role of MAP as infectious agent of Crohn's disease.

Consequently, it would seem that the small clinical advantage observed with antimycobacterials, as shown in some studies, is ascribable to a generic effect directed towards those commensal enteric bacteria which may have a pathogenic potential without being typical infectious agents.[13]


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