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The aim of our study was to determine phenazone pharmacokinetics as an index of hepatic microsomal enzymes activity and acetylation phenotype in women with breast cancer. Phenazone test was made in 41 women with breast cancer and in 25 healthy women as a control group. Acetylation phenotype was measured in 40 women with breast cancer and in 25 healthy women as a control group. The plasma concentration of phenazone was estimated by the spectrophotometric method of Brodie and associates. Acetylation phenotype was determined by the Bratton-Marshall method in Varley's modification. The mean phenazone half-life time (t0,5), shortened significantly and the mean elimination rate constant (K) increased in women compared with a group of healthy persons. Mean clearance rate was increased in women with breast cancer too, compared with a group of healthy women. Acceleration of phenazone elimination may suggest that in patients with breast cancer elimination of the other drugs metabolized by the pathway similar to phenazone also may be changed. This should be considered in selection of their dosage. We have observed the predominance of rapid acetylators in women with breast cancer comparing with healthy persons. This difference was not statistically significant. Our results of acetylation phenotype in women with breast cancer suggests that rapid acetylation may be a factor of susceptibility to breast cancer.

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The one of the most unpleasant undesirable symptoms of chemotherapy are nausea and vomiting. Authors evaluated and efficacy of ondansetron in anti-emetic therapy in 217 patients. In they opinion is very effective and improves a quality of life.

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From January 1991 to August 1993, 237 women with metastatic breast cancer were recruited into a multicentric phase II clinical trial designed to assess the cardioprotective activity of Cardioxane (ICRF-187). All patients were treated with 5-fluorouracil 500 mg/m2, doxorubicin 50 mg/m2, cyclophosphamide 500 mg/m2 (FDC) and Cardioxane 1000 mg/m2, in cycles repeated every 3-4 weeks. Cardiac functions were assessed at baseline by physical examination, ECG, and resting ultrasound left ventricle ejection fraction (LVEF). The same tests were repeated regularly after the 3rd, 6th, 8th cycle and every additional 100 mg/m2 of doxorubicin. At the end of the study there were 212 evaluable patients. Prior to analysis, patients were stratified according to the presence of cardiac risks at study entry. One hundred thirty-three patients (63%) bore one or more cardiac risks. The average total cumulative dose of doxorubicin administered to the group was 311 mg/m2 (range: 200-900 mg/m2). Overall response (CR + PR) was 49.5% (105/212), with 12% of patients entering complete remission. General toxicity (WHO grading) was mild and tolerable; no excessive myelosuppression or related symptoms were observed. Three patients from the risk group experienced cardiotoxicity, with an LVEF fall below 45%, and had to be removed from the study. Another 3 patients (1 from the risk group) were removed from the study due to clinically documented congestive heart failure after 200, 300 and 400 mg/m2 of doxorubicin. In our study, Cardioxane (ICRF-187) did not influence the antitumor efficacy of FDC chemotherapy, nor did concomitant administration of Cardioxane and chemotherapy result in any other or severer toxicity than that already known for this regimen. Finally, the observation that 51% of patients with preexisting cardiac risks received doxorubicin at dose range of 450-900 mg/m2 without significant clinical or laboratory signs of cardiotoxicity supports the evidence that Cardioxane provided cardiac protection offering the possibility of longer doxorubicin chemotherapy.

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A case of the idiopathic form of facial midline granuloma is described in a man aged 35 years. Good result was obtained after radiotherapy, cobalt radiotherapy and chemotherapy. After 4 years no relapse or generalization of changes were noted.

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Phenazone pharmacokinetics was determined in 24 healthy women and in 39 women with breast cancer; in the latter before and after antineoplastic treatment. The mean phenazone half-life time (t0.5) was significantly shorter in patients with breast cancer (8.880 +/- 2.5585 h) than in healthy persons (12.024 +/- 3.8486 h, P less than 0.001). Mean elimination rate constant (K, 0.063 +/- 0.0197 h-1) and mean metabolic clearance rate (MCR, 54.968 +/- 20.3476 ml/min) differed statistically (P less than 0.01) from the same parameters in control group, where K was 0.063 +/- 0.0197 h-1, MCR was 41.832 +/- 14.7153 ml/min. In patients receiving antineoplastic drugs, pharmacokinetic parameters of phenazone did not differ significantly in comparison with the initial values. Our results obtained with phenazone as a model substance suggest that in breast cancer elimination of other drugs metabolized by the pathway similar to phenazone also may be changed. This should be considered in selection of their dosage.

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