Summary:Carboplatin hypersensitivity has rarely been reported in patients receiving repeated cycles of therapy, but has not been reported in transplant settings. We report a case of carboplatin hypersensitivity during conditioning for autologous PBSC transplantation. The patient suddenly developed chest tightness, hemoptysis, hypoxia and hypotension, resulting in a transient myocardial ischemia. The pathophysiologic mechanism for the event seemed to be non-immune-mediated direct histamine release given the lack of prior exposure to platinum. Contrary to advice not to continue further treatment with carboplatin by some authors, we successfully desensitized the patient and subsequently gave more carboplatin as a part of conditioning. Awareness of carboplatin as one of the causes of hypersensitivity may help avoid further problems either by substitution or desensitization, along with premedications. Keywords: carboplatin; hypersensitivity; conditioning; PBSC transplantation; desensitization Carboplatin, a second-generation, platinum-containing chemotherapeutic agent, is increasingly used in transplant conditioning regimens for a variety of solid tumors. Although type I hypersensitivity has been reported in 1% to 20% of patients who receive cisplatin, there are few reports of similar reactions in patients receiving repeated cycles of carboplatin therapy.1,2 To our knowledge, there have been no reported cases of life-threatening carboplatin hypersensitivity in the transplant setting.We report a case of carboplatin hypersensitivity who presented with hemoptysis and hypoxia resulting in transient myocardial ischemia during conditioning for autologous PBSC transplantation. Most of the patients reported who have had allergic reactions to carboplatin were unable to tolerate further treatment with it despite heavy premedication with steroids and antihistaminics. however, carboplatin was re-introduced successfully as a conditioning regimen after a course of desensitization. Case reportAn 8-year-old girl was admitted for autologous PBSC transplantation. One year earlier she had developed fever and jaundice, and was diagnosed to have a sarcoma botryoides arising in the bile duct. The tumor was stage III and only a partial resection was possible at that time. Chemotherapy consisting of vincristine, actinomycin-D and ifosfamide (VAI) along with radiotherapy had effected a good response on the second-look operation. A total of six leukaphereses were performed by CS3000+ after two mobilization cycles employing VAI plus G-CSF. The planned conditioning regimen was: carboplatin 800 mg/m 2 once daily i.v. on days Ϫ6 and Ϫ5, etoposide 200 mg/m 2 twice daily i.v. on days Ϫ6 to Ϫ4 (total six doses), and melphalan 180 mg/m 2 i.v. on day Ϫ2. The first morning dose of etoposide was administered uneventfully. Carboplatin was dissolved in 500 ml of D 5 . saline solution. Five minutes after starting the infusion when a total of about 10 mg of carboplatin had been administered, she suddenly developed tachypnea, chest tightness, cyanosis, vomit...

Phase lag entropy, an electro-encephalography-based hypnotic depth indicator, calculates diversity in temporal patterns of phase relationship. We compared the performance of phase lag entropy with the bispectral index TM in 30 patients scheduled for elective surgery. We initiated a target-controlled infusion of propofol using the Schnider model, and assessed sedation levels using the Modified Observer's Assessment of Alertness/Sedation scale every 30 s with each stepwise increase in the effect-site propofol concentration. Phase lag entropy and bispectral index values were recorded. The correlation coefficient and prediction probability between phase lag entropy or bispectral index and the sedation level or effect-site propofol concentration were analysed. We calculated baseline variabilities of phase lag entropy and bispectral index. In addition, we applied a non-linear mixed-effects model to obtain the pharmacodynamic relationships among the effect-site propofol concentration, phase lag entropy or bispectral index and sedation level. As sedation increased, phase lag entropy and bispectral index both decreased. The prediction probability values of phase lag entropy and bispectral index for sedation levels were 0.697 and 0.700 (p = 0.261) and for the effect-site concentration of propofol were 0.646 and 0.630 (p = 0.091), respectively. Baseline variability in phase lag entropy and bispectral index was 3.3 and 5.7, respectively. The predicted propofol concentrations, using the Schnider pharmacokinetic model, producing a 50% probability of moderate and deep sedation were 1.96 and 3.01 lg.ml À1 , respectively. Phase lag entropy was found to be useful as a hypnotic depth indicator in patients receiving propofol sedation.

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