Philadelphia-chromosome metaphases in 57% of the patients (7% became Phnegative). The corresponding ngureS after two intensive cytotherapies were 70% (40% Ph-negative). Eighteen patients were autotrausplanted. Seven have relapsed with Ph-positivity 3-22 months after ABMT, while nine are Ph-negative at 1-32+ months after ABMT (two not yet analyzed). Seventeen patients are alive and well, while one died one month rreatmen~ Ph-analysis was performed. Patients with Press 1066-5099/93/$5.00/0 after ABMT due to interstitial pneumonia. Of the remaining 79 patients, 32 are in continuous chronic phase, 34 were allotramplanted and 13 have died (three during Daunorubicin Ara-C [DA]) treatment, one refusing transfusions, nine in blastic transformation). We conclude that intensive treatment effectively reduces the Ph-positive clone in CML. Bone marrow can remain Ph-negative for 32+ months after ABMT. A long follow-up is needed to see whether this treatment prolongs time to metamorphosis.
Free fatty acids (FFA), triglycerides (TG), total and free cholesterol, total phospholipids and the individual phospholipids lysolecithin, sphingomyelin, lecithin and cephalin were determined in four groups of women, each consisting of nine or ten subjects. The determinations were performed before treatment and about every third month during one year of medication. Two combined drugs, Anconcene® (Chlormadinone acetate = CMA, 3 mg + mestranol 0.1 mg) and Conluten® (Norethindrone = NET, 2 mg + mestranol 0.1 mg) and two low-dose gestagen drugs, CMA 0.5 mg and NET 0.4 mg were used.
FFA decreased in the Anconcene group. TG increased among those taking Anconcene, Conluten and NET. Slight increases of cholesterol were noted in the two groups taking combined drugs. Total phospholipids were increased in the Anconcene group and the Conluten group. Among the individual phospholipids, changes appeared similar to those found during pregnancy. They were most pronounced in the Anconcene group.
It seems that it is the oestrogenic component of the combined drugs that is responsible for many of the alterations. It is suggested that the testosterone derivative NET but not the progesterone derivative CMA may have anti-oestrogenic effect in this connection.
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