Irinotecan (CPT-11), an inhibitor of DNA topoisomerase I, plays an important role in the treatment of colon and small cell lung cancer in two- or multi-drug combination regimens based on irinotecan. However, delayed diarrhea is the limiting toxicity of irinotecan, and it has been reported abroad that 20%-40% of patients treated with irinotecan may develop 3rd to 4th degree diarrhea and discontinue chemotherapy regimen early [Limonti A, et al. This is significantly lower than the incidence of diarrhea reported in the West. The author believes that differences in the genetic background of the population are the main reason for the different incidence of diarrhea. Intestinal carboxylesterase can convert irinotecan directly into the active metabolite SN-38 in the intestinal lumen. human intestinal tissue biopsies suggest the presence of carboxylesterase and in vitro tests have found that it can convert irinotecan into SN-38. active SN-38 can be converted to inactive glucuronidated SN-38 (SN-38G) by hepatic uridine diphosphate glucosyltransferase. Therefore, inhibition of carboxylesterase and inhibition of bacterial β-glucuronidase may provide an effective measure to combat the enterotoxicity of irinotecan. Irinotecan remains a symptomatic agent for the treatment of delayed diarrhea, but the possibility of adverse effects paralytic intestinal obstruction increases with increasing doses of irinotecan. From the present findings, it appears that inhibition of bacterial β-glucuronidase activity with antibiotics, altering the metabolic pathway or reducing the concentration of active metabolites in the intestine may prevent and reduce the incidence of delayed diarrhea.