Abstract

Dear Editor, A 72-year-old man was diagnosed with Rai stage II chronic lymphocytic leukemia (CLL) in January 2002 by another hospital. After an initial observation period, the patient’s CLL progressed in January 2004, with lymphocyte counts increasing above 100×10 per liter, accompanied by reduced platelet counts. Although no enlarged lymph nodes were detected, the presence of borderline splenomegaly was noted. The patient underwent physical examination, bone marrow biopsy, and a computed tomography scan. Further cytogenetic and immunophenotypic studies showed the presence of 13q deletion, low CD38 expression, and a lowrisk ZAP 70 constellation, indicative of a favorable prognosis. In view of the presence of moderately elevated serum creatinine levels of unknown etiology, first-line single-agent chemotherapy with reduced-dose fludarabine was administered. Serum creatinine levels increased after two cycles and, as the patient’s lymphocyte count responded well, chemotherapy was stopped in February 2004. The patient’s renal function, as indicated by his serum creatinine levels, did not deteriorate further from February 2004 to the end of December 2004. However, at the beginning of 2005, his renal function progressively deteriorated and he developed renal failure in March 2005, at which time a Cimino shunt was established and hemodialysis was initiated. In September 2005, the patient was transferred to our hospital for continuation of hemodialysis and clinical oncology follow-up. He presented with a lymphocyte count of 59×10 per liter. Repeated chest X-ray and abdominal ultrasound showed no significant lymph nodes or splenomegaly; constant monitoring for cytomegalovirus (CMV) infection did not reveal signs of reactivation and the patient’s lymphocyte count increased slowly until it reached 172×10 per liter in February 2007. Further treatment with cytostatic chemotherapy was ruled out because of the patient’s renal failure and because he was undergoing chronic hemodialysis. We decided to treat the patient with the humanized anti-CD52 monoclonal antibody alemtuzumab (MabCampath®, Bayer Schering Pharma AG, Berlin, Germany) via subcutaneous (SC) administration. Dose escalation of alemtuzumab was carried out over the first 6 days: 10 mg on day 1, 20 mg on day 3, and 30 mg on day 6. Thereafter, alemtuzumab was administered at 30 mg on days 8, 10, 13, and 15. All SC injections of alemtuzumabwere administered after hemodialysis. Alemtuzumab therapy was accompanied by the usual recommended premedication and anti-infective prophylaxis [1] consisting of sulfamethoxazole 400 mg–trimethoprim 80 mg and famciclovir 250 mg administered once daily after each hemodialysis procedure (Monday, Wednesday, Friday). Allopurinol 100 mg once daily was also administered after each hemodialysis procedure for prevention of hyperuricemia. The effects of alemtuzumab therapy on the patient’s lymphocyte count from February 28, 2007 (day 1) to March 28, 2007 (day 29) are shown in Fig. 1. During posttreatment follow-up, the patient’s lymphocyte counts increased steadily from 2.9×10 per liter on April 2, 2007 to 7.5×10 per liter on November 5, 2007 and 7.4×10 per liter on February 18, 2008. The patient’s platelet count increased from 138×10 per liter on February 28, 2007 to 152×10 Ann Hematol (2009) 88:399–400 DOI 10.1007/s00277-008-0630-5

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