PubMed · 5944985
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
J Krácmar. 1966. [Busulphanum].. https://pubmed.ncbi.nlm.nih.gov/5944985/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
A liquid chromatographic-mass spectrometric method has been developed to determine busulfan concentrations in the cerebrospinal fluid and serum of some children undergoing bone marrow autotransplantation. After two liquid-liquid extraction steps with dichloromethane on a biological matrix, the separation of busulfan was carried out by isocratic reversed-phase chromatography. The mass spectrometric system was operated in electron-impact mode. Principal ions at m/z 175, 111 and 79 were observed for busulfan, but only m/z 175 was chosen for the quantification of the analyte. The retention time of busulfan was 2.5 min. The detection limit of 100 ng/ml allowed the determination of cerebrospinal fluid and serum busulfan concentrations during the four days of high-dose (1 mg/kg) treatment prior to autotransplantation in five child patients.
Philadelphia chromosome-positive chronic myeloid leukaemia (CML) developed three years after the diagnosis of Waldenström macroglobulinemia (WM) in a patient who had received chlorambucil and prednisone during this time. Treatment with busulphan was started and two and a half years later the died in blastic crisis. Six months before the blastic transformation of the leukaemia the amount of IgM, which remains stable (above normal values) along the chronic phase, initiates a decrease, reaching normal values in the phase of acute transformation. CML is a very rare second neoplasia in patients receiving anticancer drugs. The correlation between the decrease of IgM and the blastic crisis is very interesting. We do not find an explanation for this finding although similar observations have been described heralding the appearance of second neoplasias in WM, and one might speculate with a possible role of IgM in the control of chronic phase of the myeloid leukaemia or if the overgrowth of blastic cells could overwhelm the development of lymphoplasmacytoid cells.
A 47-year-old woman with chronic myelogenous leukemia was treated with daily busulfan (total dose approximately 500 mg) from December 1988 to January 1990. The disease thereafter remained stable with no evidence of blastic transformation. In February 1990 she developed productive cough and abnormal acinar lung shadows appeared transiently on her chest X-ray. In October 1990, productive cough and linear and abnormal acinar lung shadows reappeared. Expectorated sputa contained acid-fast bacilli (Gaffky 6, 10). Antituberculous therapy was started, which caused severe liver dysfunction. She was admitted to our hospital for evaluation of abnormal lung shadows. Transbronchial lung biopsy revealed pulmonary alveolar proteinosis with thickening of alveolar septa. The alveolar septal thickening was suspected to be a pathological change following pulmonary alveolar proteinosis. Cultures from sputum, cerebrospinal fluid, and bone marrow aspiration specimens revealed atypical mycobacterium (M. avium complex), and the diagnosis of disseminated atypical mycobacteriosis was established. The pathogenesis of the disseminated atypical mycobacteriosis was considered to be superinfection by mycobacteria.