Multifocal osseous blast crisis preceding marrow blastic phase in chronic myeloid leukemia.
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Biomedical subjects
Publications and source records attributed to B S Parikh.
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Childhood leukemic hyperleukocytosis poses a serious threat to life because of its associated metabolic complications. The present prospective trial utilized conservative management of childhood acute lymphoblastic leukemia with hyperleukocytosis (total white cell count equal or > 100 x 10(9)/L) by intravenous hydration, urinary alkalinization, and allopurinol presenting without severe life-threatening complications. The median reduction in WBC count was 81.51% (range: 66-98.8%) within a median period of 36 hours (range: 12-60 hours) following hospitalization. There were no failures or treatment related complications. Thus we conclude that in childhood acute lymphoblastic leukemia, hyperleukocytosis can be managed safely and effectively with intravenous hydration, urinary alkalinization, and allopurinol before starting any specific anti-leukemic chemotherapy avoiding risk-associated cranial irradiation, leukapheresis, and exchange transfusion.
Several derivatives of erythro-beta-hydroxy-DL-aspartic acid (1) were prepared as a potential inhibitors of L-asparagine synthetase (ASase) from rat Novikoff hepatoma. Benzylation of 1 gave the dibenzyl ester 2 which upon coupling with carbobenzoxyglycine afforded the blocked dipeptide 3. Deblocking of 3 gave glycl-erythro-beta-hydroxyl-DL-aspartic acid (4) which could not be diazotized. The dimethyl ester of 1 was coupled with carbobenzoxyglycine to give the blocked dipeptide 7a which was deblocked to give dimethyl glycel-erythro-beta-hydroxy-DL-aspartate hydrochloride (8). Diazotization of 8 gave impure diazo compound 9 which on reaction with HCl gave the chloro compound 10. The methods of isolation, assay, and inhibition of ASase are discribed. At 10 mM concentrations 10, 1, and its D and L enantiomers inhibit ASase by 45, 47, 36 and 66 percent, respectively.
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