913 PREVENTION OF CYCLOPHOSPHAMIDE (CY) INDUCED HEMORRHAGIC CYSTITIS: UPDATE ON THE USE OF ASCORBIC ACID (AA) TO REDUCE URINARY

Abstract

HC occurs in up to 50% of patients(pts.) receiving CY which results from bladder mucosal damage caused by acrolein, a degradation product of CY metabolism. Attempts to decrease HC which leads to severe morbidity have included urinary acidification with AA to diminish the formation of acrolein. In an earlier report (Proc. ASCO: 23, 1983), we evaluated 47 pts. receiving high-dose CY prior to bone marrow transplant(BMT) and found a low incidence of HC(10.6%) in pts. receiving AA. Subsequently, an additional 100 pts. undergoing BMT between 1982 and 1984 have been evaluated. Disease categories included: acute lymphocytic leukemia, 33; chronic myelogenous leukemia, 22; acute myelogenous leukemia, 14; aplastic anemia, 8; immunodeficiency, 8; neuroblastoma, 6; Ewing's sarcoma, 2; lymphoma, 2; myelodysplastic syndrome, 2; osteopetrosis, 2; and Hurler's syndrome, 1. The incidence of HC was 23%. The development of HC dependent upon various preparative regimens differed as follows: CY and fractionated total body irradiation(TBI), 17 of 6* (26.5%); CY, vinsristine, melphelan and TBI, 5 of 8(62.5%); CY and single dose TBI, 1 of 11 (9%); CY, procarbazine, antithymocyte globulin and TBI, 0 of 4 (0%); and in all other regimens not including TBI, 0 of 13 (0%). The pts. at highest risk were those with malignancy who had frequently been previously treated with CY. We conclude that AA alone is not sufficient to prevent HC, particularly in pts. at high risk. Further studies are needed to evaluate the efficacy of sulfhydryls such as 2-mercaptoethanol sodium or N-acetylcysteine with or without AA for the prevention of HC.

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