Four patients with acute nonlymphocytic leukemia and leukocyte counts of more than 200,000/mm3 developed respiratory distress due to pulmonary leukostasis within 10–48 hours after initiation of chemotherapy. Clinically, the patients manifested fever, dyspnea, tachypnea, diffuse pulmonary rales, pleural effusions, and severe hypoxemia. Chest roentgenograms displayed diffuse pulmonary infiltrates, vascular engorgement, cardiomegaly, and pleural effusions. Three patients died from progressive respiratory failure despite ventilatory support. Pulmonary histology revealed thrombi composed of leukemic blast cells which obstructed and distended the lumens of pulmonary arterioles, capillaries, and venules. Electron microscopy studies of lung tissue showed pulmonary alveolar endothelium and basement membrane damage and interstitial edema. The pathophysiologic basis of pulmonary leukostasis and potential treatment modalities are discussed.
We employed four crossmatch techniques to select platelet donors for refractory patients. Forty-four donor-recipient pairs were studied in 32 patients. Analysis of effectiveness of platelet transfusions revealed that only 18 percent of transfusions gave a borderline response; the remainder were either effective or not effective at all. The corrected predictive values of three crossmatch tests were as follows: enzyme-linked immuno-specific assay, 81 percent; platelet immunofluorescence test, 73 percent; and lymphocytotoxicity, 70 percent (p greater than 0.05). The predictive value of these tests did not differ in HLA-matched versus unmatched platelet transfusions. Donor selection by lymphocytotoxicity compatibility did not appear to be useful if donors were selected by either of the other two methods. The fourth test, antiglobulin-modified lymphocytotoxicity, offered no advantage over lymphocytotoxicity. Our data suggest that platelet crossmatching assays are a useful adjunct to the selection process for the platelet donor in addition to ABO, Rh, and HLA matching.
A 73-year-old female developed pulmonary disease during treatment with chlorambucil for polycythemia vera. Cough and dyspnea were prominent symptoms. A chest roentgenogram revealed interstitial fibrosis. The diffusing capacity was markedly reduced. Pathologic findings included alveolar lining cell dysplasia, interstitial round cell infiltrates and interstitial fibrosis. Resolution of the pulmonary symptoms and partial clearing of the fibrosis on chest roentgenogram followed discontinuation of the chlorambucil and institution of steroid treatment. Chlorambucil may cause pulmonary fibrosis similar to busulfan and cyclophosphamide and this may be a potential complication of all alkylating agents.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.