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Tumor Lysis Syndrome at the Beginning of Thalidomide Therapy for Multiple Myeloma

Polyclinique Francheville, Périgueux, France
Hôpital Haut-Lévèque, Centre Hospitalier Universitaire Bordeaux, Pessac, France

To the Editor:In August 2000, a 59-year-old white female presented a multiple myeloma (MM; immunoglobulin A lambda stage IIIA in Durie and Salmon classification) treated successively by three courses of vincristine, adriblastine, and dexamethasone treatment,¹ vertebral L1 radiotherapy (24 Gy), and double high-dose chemotherapy with melphalan (140 and 200 mg/m²) supported by autologous peripheral-blood progenitor-cell transplantation. The patient was considered in very good response ( 75%) after completion of these treatments. Seven months later, relapse occurred and thalidomide treatment started.

At this time, the baseline work-up showed 90% plasma cells in bone marrow, serum paraprotein in immunoglobulin A lambda was 0.44 g/L with 0.83 g/L Bence-Jones paraprotein urinary excretion. Serum creatinine level was 159 µmol/L with normal calcemia. Uric acid was 387 µmol/L (normal range, 178 to 357 µmol/L). No other treatment was given in association with thalidomide.

Six days after start of thalidomide treatment at the dose of 200 mg/d, she developed anuria and a 9-kg weight gain. Simultaneously, the serum creatinine level increased to 504 µmol/L with hyperphosphoremia (3,295 µmol/L; normal range, 810 to 1,620 µmol/L), hyperuricemia (696 µmol/L), and acidosis without hypercalcemia.

Thalidomide treatment was stopped, and symptomatic treatment including continuous intravenous furosemide, urate oxydase, and alcalinization started. The serum creatinine level decreased to 168 µmol/L and concurrently increased body weight of 9 kg. Thalidomide therapy was thereafter reinitiated at the dose of 100 mg/d. At this time, bone marrow showed only 40% plasma cells. Patient ultimately died 2.5 months later from MM evolution.

The major route of elimination of thalidomide is nonrenal,² and in a group of asymptomatic human immunodeficiency virus-infected subjects, there were no clinically significant changes in biochemical or hematologic parameters monitored after two single oral doses of thalidomide.³ In the study of Singhal et al,⁴ an increase of 50% or more in serum creatinine levels was observed in eight of 84 patients but was related to progressive disease.⁴

In our case, the onset of renal failure with hyperphosphoremia and hyperuricemia immediately after beginning of thalidomide treatment and the observed response on the bone marrow infiltration strongly support the hypothesis of acute renal failure related to a tumor lysis syndrome. Because the use of thalidomide is likely to increase in MM and other lymphoproliferative disorders,⁵ we suggest that patients treated with thalidomide, especially those with pre-existent renal dysfunction, should be closely monitored at the beginning of therapy.

REFERENCES

1. Barlogie B, Smith L, Alexanian R: Effective treatments of advanced multiple myeloma refractory to alkylating agents. N Eng J Med 310: 1353-1357, 1984[Abstract]

2. Chen TL, Vogelsang GB, Petty BG, et al: Plasma pharmacokinetics and urinary excretion of thalidomide after oral dosing in healthy male volunteers. Drug Metab Dispos 17: 402-405, 1989[Abstract]

3. Noormohamed FH, Youle MS, Higgs CJ, et al: Pharmacokinetics and hemodynamic effects of single oral doses of thalidomide in asymptomatic human immunodeficiency virus-infected subjects. AIDS Res Hum Retroviruses 15: 1047-1052, 1999[CrossRef][Medline]

4. Singhal S, Mehta J, Desikau R, et al: Antitumor activity of thalidomide in refractory multiple myeloma. N Eng J Med 341: 1565-1571, 1999[Abstract/Free Full Text]

5. Dimopoulos MA, Zomas A, Viniou NA, et al: Treatment of Waldenstrom’s macroglobulinemia with thalidomide. J Clin Oncol 19: 3596-3601, 2001[Abstract/Free Full Text]

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