Correspondence DOUGLAS W. HUESTIS,Editor Tucson, Arizona
Leukapheresis for Hyperviscosity
To the Editor: Treatment of chronic granulocytic leukemia (CGL) by leukapheresis is We report the successful use of leukapheresis to treat a patient with hyperviscosity and leukostasis secondary to CGL in the interval before chemotherapy became effective. A 61-year-old Caucasian man was admitted to our hospital for evaluation of an elevated white blood cell count discovered during routine check-up. The leukocyte count was 225,OOOfpl with 45% segmented neutrophils, 13% bands, 20% metamyelocytes, 5% myelocytes, 4% promyelocytes, 4% myoblasts, 6% lymphocytes, 3% monocytes, and there were 3 nucleated red blood cells per 100 WBCs. Cytogenetic studies demonstrated the presence of phl chromosome. On the fourth hospital day, he was started on 300 mg/day of Allopurinol and 6 mg/day of Busulfan. One week after chemotherapy, he suddenly developed severe headache, vomiting and blumng of vision. Bilateral retinal hemonphages and dilatation of the retinal veins were observed. The white blood cell count at this point was 40O,OOO/pl and the whole blood viscosity, measured by the method of Williams3 using whole blood instead of serum, was 10.5; the viscosity of normal whole blood at a hematocrit of 45% being 4 to 5. A regimen of six-cycle leukapheresis on two consecutive days using a Haemonetics Model 30 blood cell separator with 6% hydroxyethyl starch as a sedimenting agent was initiated. A total of 51.3 x 10'O white blood cells were removed and the white blood cell count decreased to 193,OOO/pl after leukapheresis. There was prompt relief of the patient's symptoms after this procedure and his whole blood viscosity declined to 6.2. By the third week after chemotherapy there was gradual resolution of the retinal hemorrhages, his leukocyte count started to decrease and within six weeks it was down to 36,OOO/pl.
Transfusion November-December 1979
787
In the past decade, a number of investigators have controlled the clinical and hematologic manifestations of CGL by leukapheresis alone.'^^ This method of therapy is attractive because it involves no exposure to possibly mutagenic drugs, but, unfortunately, is inconvenient, expensive and time consuming. There is no evidence at the present time that such treatment is superior to chemotherapy in prolonging survival and decreasing morbidity. Our patient however, does indicate that leukapheresis has a place in treating those patients with CGL who are at risk of developing leukostasis in the interval before chemotherapy becomes effective. --Samir K . Ballas, M.D. and Judith K . Kiesel, R.N., The Cardeta Foundation for Hematologic Research, Thomas Jefferson University Hospital Blood Bank, Philadelphia, PA 19107. References 1. Lowenthal, R. M.: Chronic leukaemias:Treatment by leukapheresis. Exp. Hematol. 5: (Suppl.): 73, 1977. 2. Spiers, A. S. D.: The treatment of chronic granuocytic leukemia. Br. J. Hematol. 32: 291, 1976. 3. Williams, W. J.: Serum viscosity. I n : Hematology, 2nd ed. W. J. Williams, E. Beutler, A. J. Erslev, and R. W. Rundles, Eds. New York, McGraw-Hill, 1977, p. 1640. 4. Vallejos, C. S., K. B. McCredie, G . M. Brittin and E. J. Freireich: Biological effects of repeated leukapheresis of patients with chronic myelogenous leukemia. Blood 42925, 1973. 5. Hadlock, D. C., I. E. Fortuny, J. J. McCuUough, and B. J. Kennedy: Continuous flow centrifuge leukapheresis in the management of chronic myelogenous leukemia. Br. J. Haematol. 2 9 443, 1975.
Anti-K12 in a Black? To the Editor: In the early 1970s, Mr. Sp., a donor of a commercial blood and plasma facility in South
Volume 19 Numkr 6
Leukapheresis for Hyperviscosity
To the Editor: Treatment of chronic granulocytic leukemia (CGL) by leukapheresis is We report the successful use of leukapheresis to treat a patient with hyperviscosity and leukostasis secondary to CGL in the interval before chemotherapy became effective. A 61-year-old Caucasian man was admitted to our hospital for evaluation of an elevated white blood cell count discovered during routine check-up. The leukocyte count was 225,OOOfpl with 45% segmented neutrophils, 13% bands, 20% metamyelocytes, 5% myelocytes, 4% promyelocytes, 4% myoblasts, 6% lymphocytes, 3% monocytes, and there were 3 nucleated red blood cells per 100 WBCs. Cytogenetic studies demonstrated the presence of phl chromosome. On the fourth hospital day, he was started on 300 mg/day of Allopurinol and 6 mg/day of Busulfan. One week after chemotherapy, he suddenly developed severe headache, vomiting and blumng of vision. Bilateral retinal hemonphages and dilatation of the retinal veins were observed. The white blood cell count at this point was 40O,OOO/pl and the whole blood viscosity, measured by the method of Williams3 using whole blood instead of serum, was 10.5; the viscosity of normal whole blood at a hematocrit of 45% being 4 to 5. A regimen of six-cycle leukapheresis on two consecutive days using a Haemonetics Model 30 blood cell separator with 6% hydroxyethyl starch as a sedimenting agent was initiated. A total of 51.3 x 10'O white blood cells were removed and the white blood cell count decreased to 193,OOO/pl after leukapheresis. There was prompt relief of the patient's symptoms after this procedure and his whole blood viscosity declined to 6.2. By the third week after chemotherapy there was gradual resolution of the retinal hemorrhages, his leukocyte count started to decrease and within six weeks it was down to 36,OOO/pl.
Transfusion November-December 1979
787
In the past decade, a number of investigators have controlled the clinical and hematologic manifestations of CGL by leukapheresis alone.'^^ This method of therapy is attractive because it involves no exposure to possibly mutagenic drugs, but, unfortunately, is inconvenient, expensive and time consuming. There is no evidence at the present time that such treatment is superior to chemotherapy in prolonging survival and decreasing morbidity. Our patient however, does indicate that leukapheresis has a place in treating those patients with CGL who are at risk of developing leukostasis in the interval before chemotherapy becomes effective. --Samir K . Ballas, M.D. and Judith K . Kiesel, R.N., The Cardeta Foundation for Hematologic Research, Thomas Jefferson University Hospital Blood Bank, Philadelphia, PA 19107. References 1. Lowenthal, R. M.: Chronic leukaemias:Treatment by leukapheresis. Exp. Hematol. 5: (Suppl.): 73, 1977. 2. Spiers, A. S. D.: The treatment of chronic granuocytic leukemia. Br. J. Hematol. 32: 291, 1976. 3. Williams, W. J.: Serum viscosity. I n : Hematology, 2nd ed. W. J. Williams, E. Beutler, A. J. Erslev, and R. W. Rundles, Eds. New York, McGraw-Hill, 1977, p. 1640. 4. Vallejos, C. S., K. B. McCredie, G . M. Brittin and E. J. Freireich: Biological effects of repeated leukapheresis of patients with chronic myelogenous leukemia. Blood 42925, 1973. 5. Hadlock, D. C., I. E. Fortuny, J. J. McCuUough, and B. J. Kennedy: Continuous flow centrifuge leukapheresis in the management of chronic myelogenous leukemia. Br. J. Haematol. 2 9 443, 1975.
Anti-K12 in a Black? To the Editor: In the early 1970s, Mr. Sp., a donor of a commercial blood and plasma facility in South
Volume 19 Numkr 6
