4.1 Review

Prophylactic probiotics for cancer therapy-induced diarrhoea: a meta-analysis

Journal

CURRENT OPINION IN SUPPORTIVE AND PALLIATIVE CARE
Volume 12, Issue 2, Pages 187-197

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/SPC.0000000000000338

Keywords

cancer therapy; chemo/radiotherapy; diarrhoea; meta-analysis; probiotics

Funding

  1. National Health and Medical Research Committee CJ Martin Biomedical Research Fellowship [APP1140992]
  2. NIH
  3. National Cancer Institute [CA206039]
  4. NATIONAL CANCER INSTITUTE [R21CA206039] Funding Source: NIH RePORTER
  5. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK052574] Funding Source: NIH RePORTER

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Purpose of review Strong preclinical data support prophylactic probiotics as an effective preventive strategy for diarrhoea secondary to anticancer therapies. To determine the composite evidence that this approach translates to the clinic, we performed a meta-analysis of randomized controlled trials (RCTs) of prophylactic probiotics for the prevention of cancer therapy-induced diarrhoea. Recent findings A three-step search strategy was used to identify relevant studies (1 June 2000-1 June 2017) investigating probiotic intervention for diarrhoea secondary to any cancer therapy (cytotoxic, targeted and immunotherapies). RCTs across PubMed, Embase, CINAHL and CENTRAL were assessed for eligibility and assessed using RevMan 5.3 (The Cochrane Collaboration). Seven trials with a total of 1091 patients were included in this meta-analysis. Compared with placebo, prophylactic probiotics did not prevent or reduce the overall incidence of diarrhoea or severe CTCAE Grade at least 3 diarrhoea [relative risk (RR) = 0.81, 95% confidence interval (95% CI) = 0.60-1.09, Z = 1.41, P = 0.16; RR = 0.54, 95% CI = 0.25-1.16, Z = 1.58, P = 0.11], nor did it influence the use of rescue medication (RR = 0.93, 95% CI = 0.53-1.65, Z = 0.24, P = 0.81). Summary Current evidence does not support widespread implementation of probiotics for diarrhoea secondary to cytotoxic therapy and the tyrosine kinase inhibitor, dacomitinib. Research efforts should be diverted to pair specific forms of gastrointestinal toxicity and their unique microbial phenotype to develop the ideal microbial protectant.

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