|LETTER TO EDITOR
|Year : 2014 | Volume
| Issue : 3 | Page : 380-381
Bendamustine induced tumor lysis syndrome with acute renal failure in chronic lymphocytic leukemia
R Naithani1, A Bhat1, A Bhasin2
1 Division of Bone Marrow Transplantation and Hematology, Max Hospital, Delhi, India
2 Department of Medical Onclolgy, Nephrology, Max Hospital, Delhi, India
|Date of Web Publication||10-Dec-2014|
Dr. R Naithani
Division of Bone Marrow Transplantation and Hematology, Max Hospital, Delhi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Naithani R, Bhat A, Bhasin A. Bendamustine induced tumor lysis syndrome with acute renal failure in chronic lymphocytic leukemia. Indian J Cancer 2014;51:380-1
|How to cite this URL:|
Naithani R, Bhat A, Bhasin A. Bendamustine induced tumor lysis syndrome with acute renal failure in chronic lymphocytic leukemia. Indian J Cancer [serial online] 2014 [cited 2020 Mar 31];51:380-1. Available from: http://www.indianjcancer.com/text.asp?2014/51/3/380/146740
A 52 year male presented with right axillary and bilateral inguinal lymph node enlargement. Liver and spleen were palpable 6and 12cm below costal margin respectively. His Hemoglobin was 7.2 g/dL and total leukocyte count (TLC) was 91.6 × 10 9 /L and platelet of 7 × 10 9 /L. He was diagnosed as chronic lymphocytic leukemia (CLL) Rai stage four. In view of active hepatitis B it was decided to give first chemotherapy with bendamustine alone.
Patient was administered chemotherapy with bendamustine 100 mg/m 2 on days one and two with baseline urea 25.7 mg/dl (range 15-38 mg/dl), creatinine 0.7 (range 0.6-1.3 mg/dl), uric acid 2.8 (range 2.6-7.2 mg/dl) along with hydration 3L/m 2 and allopurinol. Four days after the treatment patient presented with pain all over the body. CBC showed a TLC 38.4 × 10 9 /L. Investigations revealed urea 94.2 mg/dl, creatinine 2.2 mg/dl, uric acid 11.4 mg/dl (2.6-7.2), calcium 7.2 mg/dl (8.2-10.2 mg/dl), phosphorus 5.9 (2.5-4.6 mg/dl). Liver function tests were normal. Blood and urine cultures were sterile. Naranjo ADR probability score (for determining whether an adverse reaction is actually due to the drug rather than the result of other factors) was nine suggesting definite association with bendamsutine.  A diagnosis of tumor lysis syndrome with non-oliguric acute renal failure was made. He was treated with hyperhydration and single dose of rasburicase 1.5 mg. Four hours later uric acid dropped to 5.3 mg/dl. Next day creatinine came down to 1.1 mg/dl, urea to 57.8 mg/dl, and the following day urea dropped to 27.8, creatinine to 0.8, uric acid to 1.9 and remained low during subsequent days. Four weeks later he received 2 nd cycle of chemotherapy with bendamustine and rituximab. He tolerated chemotherapy well this time without any evidence of tumor lysis syndrome.
Bendamustine with rituximab rgimen is generally considered safe and has been used in the treatment of advanced or relapsed CLL with an acceptable side effect profile.  Knauf et al. reported 1.2% incidence of tumor lysis without mention of any renal failure.  Another study reported only one patient who had preexisting renal dysfunction to develop TLS.  Hummel et al. reported a case of recurrent chemotherapy-induced TLS with renal failure in one patient with CLL.  Our patient had high pre treatment WBC, multiple enlarged nodes, hepato-splemegaly suggesting high tumor burden.
The occurrence of tumor lysis in patients with CLL warrants a close monitoring for tumor lysis specially those presenting with high leukocyte counts.
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