Written by Angeline A. De Leon, Staff Writer. Oral intake of Bifidobacterium breve Bif195 is safe and significantly reduces the risk of small-intestinal enteropathy caused by acetylsalicylic acid in humans.

health hazards - pharmaceuticalsAcetylsalicylic acid (ASA), known as Aspirin, is one of the most commonly prescribed nonsteroidal anti-inflammatory drugs (NSAIDs), with over 30% of middle-aged Americans estimated to be taking low-dose ASA on a daily, long-term basis 1. From fever and headache to inflammation and heart disease prevention, ASA offers great medical utility, but is also accompanied by a host of adverse effects, including small-intestinal lesions and ulcers 2,3. ASA is known for compromising the mucosal phospholipid layer, which subsequently alters intestinal permeability and increases inflammation levels 4,5. Experimental studies indicate a protective, anti-inflammatory effect of bifidobacteria 6 against NSAID-induced enteropathy (small-intestine disease) and ulcer formation 7-9, the strain Bifidobacterium breve specifically known to improve epithelial proliferation 10. A 2019 study 11from Denmark examined whether oral administration of Bifidobacterium breve Bif195 would effectively reduce small-intestinal injury induced by ASA.

A total of 75 healthy subjects (aged 18 to 50 years) with and without gastrointestinal (GI) symptoms were enrolled in a single-site, randomized, double-blind, placebo-controlled parallel-group trial. Participants were randomized to receive oral capsules of either Bif195 (≥5 x 1010 colony-forming units) or matching placebo daily for 8 weeks. To induce small-intestine damage, all subjects were also co-treated with 300 mg of ASA daily for the first 6 weeks. Participants completed 6 laboratory visits, and at each visit, fecal and blood samples were taken and the GI Symptoms Rating Scale (GSRS) administered. Video capsule endoscopy (VCE) was used to monitor bowel pathology, and a mean Lewis score categorizing small intestinal mucosal damage was calculated (time course of effects of ASA and Bif195 expressed as area under the curve, AUC of Lewis score).

At the end of 8 weeks, AUC Lewis score, as captured by VCE, was found to be significantly lower in the Bif195 group vs. placebo (3040 +/- 1340 arbitrary units vs. 4351 +/- 3195 au, p = 0.0376). AUC ulcer number was also statistically lower in Bif195 participants vs. the placebo group (50.4 +/- 53.1 au vs. 75.2 +/- 85.3 au, p = 0.0258). No significant differences were observed for secondary measures, except for fecal calprotectin (marker of GI inflammation) AUC, which was found to be lower in the Bif195 group vs. placebo (p = 0.0347). An exploratory tertile stratification of ulceration revealed that in the first tertile, where ASA damage was greatest, a significant protective effect of Bif195 was observed, relative to placebo (31.0 +/- 16.8 au vs. 41.6 +/- 25.2 au, p = 0.03).

Current findings confirm a protective effect of Bif195 against small-intestinal damage induced by ASA. Co-treatment with Bifidobacterium breve Bif195 led to reduced enteropathy, lower incidence of ulceration, and diminished GI inflammation. Bif195 may be considered an effective preventative tool against gastric damage caused by chronic low-dose ASA use, but further work is needed to identify the therapeutic actions of Bif195 (i.e., whether clinical outcomes are achieved through its proliferative effect on small-intestine epithelium). A primary strength of the study relates to its use of VCE, a sensitive and dynamic assessment tool for observing the digestive tract. Limitations to consider involve the relatively short follow-up period in the study and the use of an ASA dose that is somewhat higher compared to the typical prescription dose advised by doctors for chronic, long-term use.

Source: Mortensen B, Murphy C, O’Grady J, et al. Bifidobacterium breve Bif195 protects against small-intestinal damage caused by acetylsalicylic acid in healthy volunteers. Gastroenterology. 2019; 157: 637-646. DOI: 10.1053/j.gastro.2019.05.008.

© 2019 by the AGA Institute. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.(http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Posted January 22, 2020.

Angeline A. De Leon, MA, graduated from the University of Illinois at Urbana-Champaign in 2010, completing a bachelor’s degree in psychology, with a concentration in neuroscience. She received her master’s degree from The Ohio State University in 2013, where she studied clinical neuroscience within an integrative health program. Her specialized area of research involves the complementary use of neuroimaging and neuropsychology-based methodologies to examine how lifestyle factors, such as physical activity and meditation, can influence brain plasticity and enhance overall connectivity.

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