acute tumor lysis syndrome in non-hodgkin lymphoma induced by dexamethasone

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American Journal of Hematology 29:115-116 (1988) Acute Tumor Lysis Syndrome in Non-Hodgkin Lymphoma Induced by Dexamethasone Kapil Dhingra and Samuel R. Newcom Grady Memorial Hospital and Division of Hematoiogy/Oncoiogy,Department of Medicine, Emory University School of Medicine, Atlanta Acute tumor lysis syndrome developed in a 30-year-old man with non-Hodgkin lym- phoma after dexamethasone administration. To the best of our knowledge, this case is the first one reported following single agent corticosteroid treatment. Key words: corticosteroids, paraparesis, hyperuricemia, spinal cord compression, azotemia INTRODUCTION Tumor lysis syndrome is a well-recognized complica- tion of aggressive cytoreductive therapy of rapidly prolif- erating neoplasms. Most commonly it has been reported after combination chemotherapy of Burkitt lymphoma [l]. There have been reports of tumor lysis syndrome after single agent chemotherapy with etoposide [2], am- sacrine [3], and interferon [4]. CASE REPORT A 30-year-old white male was admitted with low back pain, progressive paraparesis, and an 8 X 6-cm tempo- roparietal skull mass. Laboratory studies revealed WBC at 7100/p1; hemoglobin 10.8 g/dl, platelets 314,oOO/p1, serum glutamic-oxalacetic transaminase 35 IU/L, serum alkaline phosphatase 168 IU/L, lactate dehydrogenase (LDH) 263 U/L, serum calcium 11.5 mg/dl, phosphorus 4.3 mg/dl, blood urea nitrogen (BUN) 13 mg/dl, creati- nine 1.3 mg/dl, and uric acid 9.3 mg/dl. A test for serum antibodies against human immunodeficiency virus-1 was negative. A myelogram revealed a high-grade block at T-12 through L-1. Computerized axial tomography (C-T) demonstrated massive retroperitoneal and mesen- teric lymphadenopathy with bilateral hydronephrosis. A biopsy of the epidural mass showed diffuse large cleaved cell lyphoma, which had cell markers of a B-cell neo- plasm. Dexamethasone (10 mg intravenously every 6 hours) was initiated to reduce edema at the level of the spinal cord compression. Seventy-two hours after dexa- methasone was begun, the patient became oliguric and azotemic (Fig. 1). Dexamethasone was stopped, and the patient was treated with allopurinol and intravenous fluids containing sodium bicarbonate. A brisk diuresis ensued after 24 hr. Physical examination and C-T scan of the head revealed marked reduction in the size of the skull mass. The patient had full recovery of renal function, received radiotherapy to the epidural lymphoma, com- pleted six cycles of combination chemotherapy, and re- mains in complete remission 18 months after diagnosis. COMMENTS Acute tumor lysis syndrome was formally recognized in 1980 [l]. In patients with Burkitt lymphoma who developed this syndrome, it was observed that a large tumor bulk, high serum LDH (greater than 600 IU/L) and inadequate urinary output correlated with major met- abolic complications [ 13. In patients undergoing diuresis and receiving allopurinol, this syndrome developed infre- quently. Our patient was at high risk for development of tumor lysis syndrome only because of massive retroperi- toneal and pelvic lymphadenopathy, because he had nei- ther an elevated LDH nor inadequate urinary output. We suggest that patients with aggressive lymphomas be monitored carefully for complications of tumor lysis when corticosteroids are prescribed. Patients with known risk factors such as large tumor burden, high serum LDH, or inadequate urinary output should be given con- current allopurinol therapy and vigorous oral hydration before and during treatment. Received for publication March 5, 1988; accepted June 9, 1988. Address reprint requests to Dr. Samuel R. Newcom, Emory Univer- sity School of Medicine, 69 Butler St., S.E., Atlanta, GA 30303. 0 1988 Alan R. Liss, Inc.

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Page 1: Acute tumor lysis syndrome in non-Hodgkin lymphoma induced by dexamethasone

American Journal of Hematology 29:115-116 (1988)

Acute Tumor Lysis Syndrome in Non-Hodgkin Lymphoma Induced by Dexamethasone

Kapil Dhingra and Samuel R. Newcom Grady Memorial Hospital and Division of Hematoiogy/Oncoiogy, Department of Medicine, Emory University School of Medicine, Atlanta

Acute tumor lysis syndrome developed in a 30-year-old man with non-Hodgkin lym- phoma after dexamethasone administration. To the best of our knowledge, this case is the first one reported following single agent corticosteroid treatment.

Key words: corticosteroids, paraparesis, hyperuricemia, spinal cord compression, azotemia

INTRODUCTION

Tumor lysis syndrome is a well-recognized complica- tion of aggressive cytoreductive therapy of rapidly prolif- erating neoplasms. Most commonly it has been reported after combination chemotherapy of Burkitt lymphoma [l]. There have been reports of tumor lysis syndrome after single agent chemotherapy with etoposide [2], am- sacrine [3], and interferon [4].

CASE REPORT

A 30-year-old white male was admitted with low back pain, progressive paraparesis, and an 8 X 6-cm tempo- roparietal skull mass. Laboratory studies revealed WBC at 7100/p1; hemoglobin 10.8 g/dl, platelets 314,oOO/p1, serum glutamic-oxalacetic transaminase 35 IU/L, serum alkaline phosphatase 168 IU/L, lactate dehydrogenase (LDH) 263 U/L, serum calcium 11.5 mg/dl, phosphorus 4.3 mg/dl, blood urea nitrogen (BUN) 13 mg/dl, creati- nine 1.3 mg/dl, and uric acid 9.3 mg/dl. A test for serum antibodies against human immunodeficiency virus- 1 was negative. A myelogram revealed a high-grade block at T-12 through L-1. Computerized axial tomography (C-T) demonstrated massive retroperitoneal and mesen- teric lymphadenopathy with bilateral hydronephrosis. A biopsy of the epidural mass showed diffuse large cleaved cell lyphoma, which had cell markers of a B-cell neo- plasm. Dexamethasone (10 mg intravenously every 6 hours) was initiated to reduce edema at the level of the spinal cord compression. Seventy-two hours after dexa- methasone was begun, the patient became oliguric and azotemic (Fig. 1). Dexamethasone was stopped, and the patient was treated with allopurinol and intravenous fluids

containing sodium bicarbonate. A brisk diuresis ensued after 24 hr. Physical examination and C-T scan of the head revealed marked reduction in the size of the skull mass. The patient had full recovery of renal function, received radiotherapy to the epidural lymphoma, com- pleted six cycles of combination chemotherapy, and re- mains in complete remission 18 months after diagnosis.

COMMENTS

Acute tumor lysis syndrome was formally recognized in 1980 [l]. In patients with Burkitt lymphoma who developed this syndrome, it was observed that a large tumor bulk, high serum LDH (greater than 600 IU/L) and inadequate urinary output correlated with major met- abolic complications [ 13. In patients undergoing diuresis and receiving allopurinol, this syndrome developed infre- quently. Our patient was at high risk for development of tumor lysis syndrome only because of massive retroperi- toneal and pelvic lymphadenopathy, because he had nei- ther an elevated LDH nor inadequate urinary output.

We suggest that patients with aggressive lymphomas be monitored carefully for complications of tumor lysis when corticosteroids are prescribed. Patients with known risk factors such as large tumor burden, high serum LDH, or inadequate urinary output should be given con- current allopurinol therapy and vigorous oral hydration before and during treatment.

Received for publication March 5, 1988; accepted June 9, 1988.

Address reprint requests to Dr. Samuel R. Newcom, Emory Univer- sity School of Medicine, 69 Butler St., S.E., Atlanta, GA 30303.

0 1988 Alan R. Liss, Inc.

Page 2: Acute tumor lysis syndrome in non-Hodgkin lymphoma induced by dexamethasone

116 Brief Report: Dhingra and Newcom

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DEXAMETHASONE CHEMOTHERAPY

Fig. 1. Simultaneous and sequentlal changes in serum chemlstries reflecting tumor lysls during dexamethasone administration.

REFERENCES

1. Cohen LF, Balow JE, Magrath IT, Poplack DG, Ziegler JL: Acute tumor lysis sydrome: A review of 37 patients with Burkitt’s lym- phoma. Am J Med 68:486-491, 1980.

2. Thomas MR, Robinson WA, Mughal TI, Glode LM: mmor lysis syndrome following VP-16-213 in chronic myeloid leukemia in blast crisis. Am J Hematol 16:185-188, 1984.

3. Vogler WR, Morris JG, Winton EF: Acute tumor lysis in T-cell leukemia induced by amsacrine. Arch Intern Med 143:165-166, 1983.

4. Fer MR, Bottino GC, Sherwin SA, Hainsworth JD, Abrams PG, Foon KA, Oldham RK: Atypical tumor lysis syndrome in a patient with T-cell lymphoma treated with recombinant leukocyte inter- feron. Am J Med 77:953-956, 1984.

5 . Livingston RB, Carter SK: “Single Agents in Cancer Chemother- apy.” New York:IFJ/Plenum 1970, pp 337-358.

6. Bloomfield CD: Glucocorticoid receptors in leukemia and lym- phoma. J Clin Oncol 2:323-328, 1984.

7. Bloomfield CD, Peterson BA, Zaleskas J, Frizzera G, Smith KA, Hildebrandt L, Gajl-Peczalska K, Munck A: In vitro glucocorti- coid studies for predicting response to glucocorticoid therapy in adults with malignant lymphoma. Lancet 1:952-955, 1980.

8. McClean JW, Kiely-Grandbois K, Hurd DD, Peterson BA, Bloomfield CD: Glucocorticoid toxicity in patients treated for non- Hodgkin’s lymphoma. Proc Am Soc Clin Oncol 2:217, 1983 [abstr] .