irinotecan/diarrhea

The dose-limiting toxicity of the highly effective anticancer agent 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxy-camptothecin (irinotecan; CPT-11) is delayed diarrhea. This is thought to be caused by either bacteria-mediated hydrolysis of the glucuronide conjugate of the active metabolite

OBJECTIVE One of the significant dose-limiting toxicities of irinotecan hydrochloride (CPT-11) is severe diarrhea due to impairment of the intestinal membrane induced by the excreted CPT-11 and its metabolites. AST-120 (Kremezin) is a prominent oral adsorbent that consists of porous spherical

The therapeutic efficacy of irinotecan (CPT-11), a DNA topoisomerase inhibitor, is often limited by the induction of severe late-onset diarrhea. This prodrug and its active metabolite, 7-ethyl-10-hydroxy-camptothecin (SN-38), have a labile alpha-hydroxy-lactone ring that undergoes pH-dependent

For characterization of the mechanism(s) of severe diarrhea due to the anticancer agent, irinotecan hydrochloride (CPT-11), examination was made of the relation of CPT-11-related diarrhea to colonic prostaglandin E2 (PGE2) and water absorption in rats. Acute diarrheal symptoms were observed within 1

OBJECTIVE Kampo medicine Hangeshashin-to (TJ-14) which contains baicalin, a beta-glucuronidase inhibitor, alleviates diarrhea induced by irinotecan (CPT-11). We conducted a randomized comparative trial to investigate whether support with TJ-14 would prevent and control CPT-11-induced

Irinotecan hydrochloride is an inhibitor of DNA topoisomerase I enzyme by its main active metabolite SN-38. However, irinotecan-induced severe diarrhea has often limited its more widespread use. We assessed the effect of oral administration of Lactobacillus casei strain Shirota (LcS) on

BACKGROUND We performed a prospective study to evaluate the efficacy of activated charcoal (AC) to prevent irinotecan-induced diarrhea (IID). METHODS We designed a prospective trial including all patients receiving irinotecan as part of their chemotherapy treatment. Patients were divided into two

A combination of irinotecan hydrochloride (CPT-11; 160 mg/m2, intravenous infusion, day 1) and cisplatin (5-day continuous intravenous infusion; 20 mg/m2/day) was administrated to advanced non-small cell lung cancer patients. They were given Hangeshashin-to (TJ-14), a Kampo medicine, to prevent the

OBJECTIVE UGT1A1*28/*6 as predictors of severe irinotecan-related diarrhea (SIRD) were duplicated by many studies. However, some patients of lower risk genotype (UGT1A1*1/*1) still suffered SIRD and the extremely low frequency of UGT1A1*6/*6 limited its clinical usage. Previous studies proved that

OBJECTIVE Calcium aluminosilicate clay (CASAD) is a naturally occurring clay that serves as a cation exchange absorbent. We hypothesized that oral administration of CASAD would reduce the rate of grade 3/4 diarrhea associated with irinotecan use for metastatic colorectal cancer (CRC) by adsorbing

We assessed the involvement of UDP-glucuronosyltransferase (UGT) activity in episodes of irinotecan hydrochloride (CPT-11)-induced delayed-onset diarrhea using a mutant rat strain with an inherited deficiency of UGT1A (Gunn rats). Gunn rats exhibited severe diarrhea after the intravenous

Two phase I trials of irinotecan (CPT-11) in combination with cisplatin were conducted. In both cases, the dose-limiting toxicities were leukopenia and/or diarrhea. During these trials the pharmacokinetics of CPT-11 and its active metabolite, 7-ethyl-10-hydroxycamptothecin (SN-38), were investigated

Irinotecan is increasingly being used in pediatric oncology. Amelioration of diarrhea associated with protracted irinotecan administration may reduce morbidity and improve dose intensity. In this review, we discuss what is known about the pathogenesis of this toxicity as well as potential

Irinotecan and its active metabolite, SN-38, were reported to have the absorption characteristics of weakly basic drugs. Moreover, stasis of these compounds is thought to induce damage to the intestinal mucous membrane. The purpose of this report was to examine whether oral alkalization (OA)