A case-control interview study of 125 adult patients with acute leukemia and 125 controls matched with respect to age (-+ four years), sex, and residence was carried out in central Sweden during the period from September 1980 to May 1983. Their history of organic solvent exposure is described. A significant overrisk of developing acute leukemia was found when comparison between patients and controls revealed a difference in the solvent exposure rate, which was significantly higher in patients than in controls, with an estimated odds ratio (OR) of 4.9,95% CI (2.2 to 12.1). The most frequently exposed profession, painters, exhibit a relative risk of 13 (2.0 to 554). These results suggest that an etiologic relationship exists between organic solvent exposure and the development of acute leukemia in man.
In the light of previous findings that treatment of leukemia patients with DNA-linked doxorubicin gave higher doxorubicin concentrations in leukemic cells than treatment with doxorubicin alone, the Leukemia Group of Middle Sweden performed a randomized clinical trial to compare the effects of doxorubicin and doxorubicin-DNA in patients with acute non-lymphoblastic leukemia. One hundred and twenty consecutive patients within the age range 15 to 60 years were randomized to one of three treatment groups. In two of these, remission induction treatment was performed with prednisolone, vincristine, ara-C and thioguanine combined with either doxorubicin or doxorubicin-DNA. Patients entering a complete remission received intensive consolidation during 16 months with 4 courses each of doxorubicin (+/ - DNA)/ara-C, doxorubicin (+/ - DNA)/azacytidine, ara-C and amsacrine. The third treatment group followed a protocol from a previous study with daunorubicin and ara-C for induction therapy and a less intensive maintenance therapy. No further patients were assigned to this "control" group after 3 years or to the two other groups after 6 years. This report is based on a follow-up 31 months thereafter. The overall rate of complete remission was 67% and the mean time to complete remission was 71 days, with no differences between the treatment groups. Patients treated with the doxorubicin-DNA conjugate had a significantly longer survival [median for all patients 27.2 months (p < 0.01) and for patients in CR 47.0 months (p < 0.025)] and longer duration of first remission (median 23.6 months, p < 0.025) than the other groups. There were significantly fewer reports of cardiotoxicity (p < 0.05) and severe intestinal toxicity (p < 0.02) in patients treated with the doxorubicin-DNA conjugate and there was a tendency towards less hepatic (p < 0.08) and renal toxicity (p < 0.08). The frequency of myelosuppression, fever and infectious complications was similar in all three groups. Complex binding to DNA appears to increase the therapeutic effects and reduce some toxic effects of doxorubicin in patients with ANLL.
ABSTRACT. Three patients with multiple myeloma received bone marrow grafts from HLA‐identical sibling donors. One of the patients, with IgA kappa myeloma, refractory to alkeran‐prednisone therapy, is well and still without sign of disease 26 months post transplantation. A second patient with Bence‐Jones kappa myeloma is well, and sceletal pain and Bence‐Jones proteinuria has disappeared 2 months after transplantation. A third patient with IgG‐lambda myeloma died of effusive pericarditis shortly after transplantation. Bone marrow transplantation may be indicated in a selective group of patients with multiple myeloma.
Thirteen patients with acute myelocytic leukemia (AML) and with clonal aberrations involving chromosome 3 were studied. Three patients had monosomy 3, four had trisomy 3, and six had structural aberrations of chromosome 3. In the majority of cases chromosome 3 aberrations were parts of complex karyotypes, but in two patients, the abnormalities appeared as single aberrations, one as an interstitial deletion del(3)(p13p21) and the other as monosomy 3. All breakpoints of chromosome 3 were found in the fragile site regions 3p14.2, 3q21 and 3q26-27. All patients with monosomy 3 or structural aberrations of chromosome 3 and one of the four patients with trisomy 3 had been exposed to mutagens, such as occupational exposures to organic solvents and/or petroleum products or treatments with irradiation or antineoplastic agents. The association among mutagen exposure, structural chromosome 3 aberrations and fragile sites in AML may indicate that targeting of the mutagens to these sites is of importance for the etiology of the disease. Leukemia (2000) 14, 112-118.
Lindquist R, Nilsson B, Eklund G, Gahrton G. Acute leukemia in professional drivers exposed to gasoline and diesel. Eur J Haematol 1991: 47: 98–103. Abstract: The environmental exposure to the petroleum products gasoline, diesel, and their motor exhausts was studied in a case‐control interview of 125 patients with acute leukemia and 1 matched control per patient. Odds ratios were calculated by comparing discordant matched patient‐control pairs. An excess risk for developing acute leukemia was found for the professional drivers, and odds ratio was determined to be 3.0 (95% CI: 1.1–9.2/p<0.02). For those who were exposed for more than 5 years in their life‐time, or more than 1 yr during the 5–20 yr period prior to diagnosis, the odds ratio was 5.0 (p?<0.05). This finding remains after consideration is given to exposures to organic solvents, smoking and therapeutic x‐ray treatment. No excess risk was observed for persons professionally exposed to motor oil and machine oil without exposure to fuels and exhausts. No preferential type of acute leukemia was found to be associated with exposure to fuels and their exhausts. The results indicate an etiological relationship between the development of acute leukemia and exposure to petroleum products as fuels and exhaust.
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