Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.
Evidence of activity of vinorelbine (VNR) in patients (pts) with previously treated epidemic Kaposi's sarcoma (KS) (Meeting abstract).
Proc Annu Meet Am Soc Clin Oncol; 16:A146 1997. Unique Identifier : AIDSLINE MED/97622137 Errante D; Spina M; Tavio M; Vaccher E; Landonio G; Pagani L; Bottura P; Fasan M; Tirelli U; For the Italian Cooperative Group on AIDS and Tumors (GICAT), C.R.O.; Aviano, Italy
Abstract:
VNR is a new semisynthetic vinca alkaloid that seems to disorganize microtubules of the mitotic figure at a lower concentration than other vinca alkaloids. Moreover it does not affect the axonal microtubules. Vinca alkaloids are active agents in the treatment of KS and form the basis for combination regimens, but there is no experience on the use of VNR. From December 1994 and October 1996, within the GICAT we treated 28 pts with advanced KS with 30 mg/m2 VNR given intravenously every two weeks. Eligible pts must have relapsed after previous chemotherapy or progressed during their previous cytotoxic regimen for KS, including anthracyclines or vinca alkaloids. Granulocyte colony-stimulating factor (G-CSF) was given subcutaneously at a dose of 5 mcg/kg/day beginning on day 2 at the discretion of the treating physicians to pts experiencing severe granulocytopenia in the previous cycle. Assessments of toxicity and response were performed according to the World Health Organization and AIDS Clinical Trial Group criteria, respectively. All pts were males with a median age of 36 years 27-55). Nineteen were homosexuals, 5 were intravenous drug users, and 4 heterosexuals. The median entry CD4+ lymphocyte count was 16/mm3 (1-356). Twenty pts had prior ABV; 7 had VCR + BLM; and 1 had liposomal doxorubicin. One pt was not evaluable for response because he was lost to follow-up after receiving the second cycle of VNR. The toxic effects of VNR consisted predominantly of myelosuppression. In particular, grade 3 and 4 leukopenia was observed in 8 and 5 pts respectively. Eighteen pts actually received G-CSF for secondary prophylaxis. Grade 3 thrombocytopenia occurred in one pt and grade 3 anaemia in 2 pts. We did not observe neurotoxicity. In no pt treatment was discontinued due to toxicity. The median number of cycles actually administered was 4 (range, 1 to 11 cycles). Complete remission occurred in 3 of 27 evaluable pts (11%; exact 95% confidence interval; 2-29% ) with a duration of 5, 8 and 15 months, respectively. We observed 9 partial remissions (33%) with a median duration of 3 months (range, 1 to 6 ). All other pts had stable (9 pts) or progressive (6 pts) disease. All the 12 responding pts previously failed vinca alkaloids. In conclusion, our results suggest that VNR is active, non-cross resistant with other vinca alkaloids, and well tolerated also in previously treated pts with KS. VNR can be (C) American Society of Clinical Oncology 1997
Keywords: *Antineoplastic Agents, Phytogenic/THERAPEUTIC USE *Sarcoma, Kaposi/DRUG THERAPY *Vinblastine/ANALOGS & DERIVATIVES 971230
M97C1597
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