Clinical governance benchmarking issues in oncology: aggressiveness of cancer care and consumption of strong opioids. A single-center experience on measurement of quality of care.

AIMS AND BACKGROUND: The aggressiveness of cancer care near the end of life and the consumption of opioids are potential indicators of quality of care in palliative and end-of-life settings. The purpose of this article is to present a retrospective analysis regarding these themes and the adopted procedures to improve quality of care. METHODS: We evaluated all cancer patients treated and deceased during 2008 and considered those who died and received any antiblastic therapy within 14 and 30 days prior to death. Moreover, we evaluated the annual consumption of pure opioids during 2007 and 2008 in our inpatient clinic. We found that 5% and 9% of all treated patients were still receiving antiblastic treatment near the end of life within respectively 14 and 30 days prior to death (respectively 29.6% and 51.5% of deceased patients). All but 2 patients died from progressive disease, one patient died from acute myocardial infarction during chemotherapy, and one of severe sepsis after chemotherapy for non-Hodgkin lymphoma. As regards the annual consumption of strong opioids, there was a 179% increase in the use of morphine-equivalent doses of oral long-acting opioids (+228% for oxycodone) after the introduction of daily pain measurement through a numerical rating scale. CONCLUSIONS: To reduce the administration of chemotherapy near the end of life, we introduced the palliative prognostic score, to be administered to all advanced cancer patients with performance status of at least 2. To evaluate the effectiveness of analgesics and to reduce the cases of undertreatment of cancer pain, we adopted, in addition to the numerical rating scale, Cleeland's Pain Management Index. We are convinced that attempts to improve the quality of care can be achieved by the collaboration of all health professionals, patients and care givers.

Ifosfamide encephalopathy and use of methylene blue. A case report of different sequential neurotoxicity.

Neurotoxicity is a clinically relevant adverse event observed with the use of ifosfamide. It is usually mild, occasionally severe and seldom fatal. Ifosfamide-induced encephalopathy requires interruption of chemotherapy, intravenous hydration and administration of methylene blue. Less is known about the efficacy of methylene blue in avoiding a second episode of ifosfamide-induced encephalopathy while maintaining chemotherapy with ifosfamide. We report a case of a different clinical manifestation of ifosfamide-induced encephalopathy after continued ifosfamide use and despite methylene blue in a patient with retroperitoneal sarcoma.

The role of UGT1A1*28 polymorphism in the pharmacodynamics and pharmacokinetics of irinotecan in patients with metastatic colorectal cancer.

PURPOSE: UGT1A1*28 polymorphism has been associated with decreased glucuronidation of SN38, the active metabolite of irinotecan. This could increase toxicity with this agent. PATIENTS AND METHODS: In a prospective study, 250 metastatic colorectal cancer patients were treated with irinotecan, fluorouracil, and leucovorin as first-line treatment. UGT1A1*28 polymorphism was investigated with respect to the distribution of hematologic and nonhematologic toxicity, objective response rate, and survival. Pharmacokinetics was investigated in a subgroup of patients (71 of 250) who had been analyzed with respect to toxicity and efficacy. RESULTS: UGT1A1*28 polymorphism was associated with a higher risk of grade 3 to 4 hematologic toxicity (odds ratio [OR], 8.63; 95% CI, 1.31 to 56.55), which was only relevant for the first cycle, and was not seen throughout the whole treatment period for patients with both variant alleles TA7/TA7 compared with wild-type TA6/TA6. The response rate was also higher in TA7/TA7 patients (OR, 0.32; 95% CI, 0.12 to 0.86) compared with TA6/TA6. A nonsignificant survival advantage was observed for TA7/TA7 when compared with TA6/TA6 patients (hazard ratio, 0.81; 95% CI, 0.45 to 1.44). Higher response rates were explained by a different pharmacokinetics with higher biliary index [irinotecan area under the curve (AUC)x(SN38 AUC/SN38G AUC)] and lower glucuronidation ratio (SN38G AUC/SN38 AUC) associated with the TA7/TA7 genotype and a higher response rate, indicating that the polymorphism is functionally relevant. CONCLUSION: The results indicate that UGT1A1*28 polymorphism is of some relevance to toxicity; however, it is less important than discussed in previous smaller trials. In particular, the possibility of a dose reduction for irinotecan in patients with a UGT1A1*28 polymorphism is not supported by the result of this analysis.