PATHOPHYSIOLOGY, SEVERITY, PATTERN, AND RISK-FACTORS FOR CARBOPLATIN-INDUCED EMESIS

Carboplatin has proven efficacy in the treatment of ovarian cancer and has been proven to be less toxic compared to the parent compound cisp latin. Nevertheless, emesis is still a major problem associated with c arboplatin-containing chemotherapy. Several investigators have focusse d on the understanding of the pathophysiology and pattern of cisplatin -induced emesis. Data describing both the pathomechanisms and pattern of carboplatin-induced emesis are still lacking. This paper combines d ata from the literature with our own experience with the pattern and c ontrol of carboplatin-induced emesis, and presents data contributing t o the understanding of the underlying pathomechanisms. Carboplatin ind uces a significant increase in urinary 5-HIAA excretion, the main meta bolite of serotonin. 5-HIAA excretion levels remain elevated over 3 da ys following chemotherapy. Carboplatin-induced emesis is observed in a bout 40% of patients despite anti-emetic prophylaxis with 5-HT3 antago nists. Vomiting after carboplatin extends over days 1-3 with an equal distribution regarding the severity on each day. Analysis of the patte rn of emesis revealed that delayed emesis (>24 h after chemotherapy) i s a major problem associated with carboplatin therapy. Description of the pattern of emesis as 'prolonged emesis' seems to be appropriate. 5 -HT3 receptor antagonists such as ondansetron seem to be efficacious b oth in the control of acute and prolonged emesis following carboplatin chemotherapy, but randomly controlled data comparing ondansetron with other anti-emetic regimens have not yet been published. Univariate an alysis reveals gender and combination therapy containing carboplatin a nd cyclophosphamide and/or anthracyclines as risk factors for emesis.