Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0854467 (myelosuppression)
 5,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-two courses of carboplatin (Paraplatin; Bristol-Meyers, Evansville, IN) (CBDCA) were administered to 15 patients with advanced cancer on a continuous 24-hour per day infusion schedule for either 5 days or 14 days. The objective of the trial was to establish the optimal dose rate and cumulative dose for this treatment schedule. The dose-limiting toxicity was myelosuppression, with leukopenia and thrombocytopenia observed. The optimal dose rate for the 5-day infusion was 75 mg/m2/d or a total cumulative dose of 375 mg/m2/d. The optimal dose rate for the 14-day infusion was 25 mg/m2/d or a total cumulative dose of 350 mg/m2/d. The times to nadir levels of leukocyte and platelet counts were 34 days and 25 days, respectively, with a median time to recovery of 14 days and 7 days, respectively, in patients with Grade 3 or greater marrow suppression. The pattern of hematologic toxicity with infusional CBDCA is comparable to that seen with bolus schedules. There is, therefore, no clinical advantage of the infusional schedule for CBDCA in terms of toxicity and the dose delivered per cycle, and the dose intensity is slightly less than with a bolus schedule. If there is a therapeutic advantage for the infusional schedule, a prospective comparative trial against the standard bolus schedule will be required to establish it. Bolus and infusional schedules for CBDCA are associated with a delayed pattern of thrombocytopenia and prolonged leukopenia, necessitating 5 or more weeks between treatment cycles.
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PMID:Infusional carboplatin. Phase I studies of 5-day and 14-day infusions. 204 55

Carboplatin (CBDCA; commercial name: Paraplatin) is a platinum complex having 1-cyclobutanedicarboxylic acid group at the two chlorine positions of cisplatin (CDDP). In the preclinical studies, CBDCA was proved to be almost equally effective to various murine tumors compared to cisplatin. Compared to cisplatin, of which free platinum was not detected from 2 hr after administration, the free type of more than 85% of total platinum concentration remained in the blood even 8 hrs after administration. Total urine excretion at 2-4 hrs after administration of CBDCA was about 57-82%, indicating CBDCA's relative rapid urine excretion compared to CDDP. In the clinical trials in Japan, appreciable clinical responses were observed in head and neck, small cell lung, ovarian, uterine cervical cancers, testicular tumor and malignant lymphoma. The renal toxicity was considerably slight, resulting in almost no hydration during treatment. Nausea and vomiting were also slight and there were no hearing-loss and neurotoxicities. The dose-limiting factor (DLF) in the phase I study was myelosuppression. From these results, it was found that carboplatin's antitumor efficacies were almost identical with cisplatin and much less toxic than cisplatin. Carboplatin will serve as a useful antitumor drug in current cancer chemotherapy.
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PMID:[Development of carboplatin]. 220 18

Cisplatin has modest activity in squamous cancer of the oesophagus but substantial toxicity limits its usefulness. Carboplatin (Paraplatin; BM Group), a second-generation platinum analogue, was developed to maintain the antitumour activity of cisplatin and reduce toxicity. Eleven patients with advanced oesophageal cancer were treated with carboplatin. A partial response was seen in 1 patient (9%) and minor responses in 2 cases. The median survival was 12 months in responding patients and 3 months in non-responders. One patient suffered reversible myelosuppression but nephrotoxicity and vomiting were not observed. Carboplatin is well tolerated and may have a role as a less toxic substitute for cisplatin in combination chemotherapy regimens for oesophageal cancer.
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PMID:Carboplatin in the treatment of oesophageal cancer. 267 77

Lung cancer is the leading cause of death due to cancer in the United States, and approximately 178,100 new cases were estimated to occur last year. Small-cell lung cancer (SCLC) accounts for approximately 17% to 25% of all lung cancers. Due to its aggressive nature and rapid proliferation rate, small-cell lung cancer is usually widespread at diagnosis. Therefore, chemotherapy is the cornerstone of therapy for this disease. Cisplatin (Platinol) is an active chemotherapeutic agent used to treat small-cell lung cancer, but its toxicity, including nausea and vomiting, nephrotoxicity, neurotoxicity, and ototoxicity, has led to the investigation of combination regimens with different toxicity profiles. Carboplatin (Paraplatin), a derivative of cisplatin, has far less nonhematologic toxicity, although myelosuppression may be slightly greater than that observed with cisplatin. The reduced toxicity and equivalent efficacy of carboplatin have resulted in the increased use of carboplatin-based regimens to treat small-cell lung cancer. Phase I and II trials of carboplatin as single-agent treatment for small-cell lung cancer resulted in overall response rates of approximately 60% for previously untreated patients and 17% for those who had received prior therapy. New combination chemotherapy regimens that include carboplatin may improve survival in patients with small-cell lung cancer and potentially cure those patients with limited disease. Further investigation of carboplatin and other new agents is warranted.
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PMID:The role of carboplatin in the treatment of small-cell lung cancer. 951 10