Thalidomide in the treatment of relapsed multiple myeloma

被引:148
作者
Rajkumar, SV [1 ]
Fonseca, R [1 ]
Dispenzieri, A [1 ]
Lacy, MQ [1 ]
Lust, JA [1 ]
Witzig, TE [1 ]
Kyle, RA [1 ]
Gertz, MA [1 ]
Greipp, PR [1 ]
机构
[1] Mayo Clin, Div Hematol & Internal Med, Rochester, MN USA
关键词
D O I
10.4065/75.9.897
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: To describe the efficacy of therapy with thalidomide, a drug that has antiangiogenic properties, in patients with relapsed multiple myeloma, Patients and Methods: We studied 16 patients (median age, 64 years) who received thalidomide for relapsed myeloma at the Mayo Clinic in Rochester, Minn, between November 1998 and August 1999, Treatment consisted of thalidomide given orally at a dose of 200 mg/d for 2 weeks, then increased by 200 mg/d every 2 weeks, up to a maximal dose of 800 mg/d, Results: The stage of myeloma at treatment was Durie-Salmon IIIA in 9 patients (56%) and IIIB in 7 (44%). The median time from myeloma diagnosis to initiation of thalidomide therapy was 32 months. In 4 patients (25%) prior stem cell transplantation had failed, and 14 (88%) had received 2 or more prior chemotherapeutic regimens before institution of thalidomide, All patients were evaluable for response. Four (25%) achieved a partial response to therapy, with a greater than 50% reduction in the serum or urine M protein level. Responses lasted 2, 4+, 8, and 10+ months. Major adverse effects included constipation, sedation, rash, and peripheral neuropathy, Conclusion: Thalidomide is an active agent in the treatment of patients with advanced myeloma.
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页码:897 / 901
页数:5
相关论文
共 28 条
[1]   A prospective, randomized trial of autologous bone marrow transplantation and chemotherapy in multiple myeloma [J].
Attal, M ;
Harousseau, JL ;
Stoppa, AM ;
Sotto, JJ ;
Fuzibet, JG ;
Rossi, JF ;
Casassus, P ;
Maisonneuve, H ;
Facon, T ;
Ifrah, N ;
Payen, C ;
Bataille, R .
NEW ENGLAND JOURNAL OF MEDICINE, 1996, 335 (02) :91-97
[2]  
BARLOGIE B, 1986, BLOOD, V67, P1298
[3]   Total therapy with tandem transplants for newly diagnosed multiple myeloma [J].
Barlogie, B ;
Jagannath, S ;
Desikan, KR ;
Mattox, S ;
Vesole, D ;
Siegel, D ;
Tricot, G ;
Munshi, N ;
Fassas, A ;
Singhal, S ;
Mehta, J ;
Anaissie, E ;
Dhodapkar, D ;
Naucke, S ;
Cromer, J ;
Sawyer, J ;
Epstein, J ;
Spoon, D ;
Ayers, D ;
Cheson, B ;
Crowley, J .
BLOOD, 1999, 93 (01) :55-65
[4]  
Bellamy WT, 1999, CANCER RES, V59, P728
[5]   THALIDOMIDE IS AN INHIBITOR OF ANGIOGENESIS [J].
DAMATO, RJ ;
LOUGHNAN, MS ;
FLYNN, E ;
FOLKMAN, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (09) :4082-4085
[6]  
Dankbar B, 1998, BLOOD, V92, p681A
[7]   Seminars in medicine of the Beth Israel Hospital, Boston - Clinical applications of research on angiogenesis [J].
Folkman, J .
NEW ENGLAND JOURNAL OF MEDICINE, 1995, 333 (26) :1757-1763
[8]   Tumour angiogenesis and prognosis [J].
Fox, SB .
HISTOPATHOLOGY, 1997, 30 (03) :294-301
[9]   Thalidomide selectively modulates the density of cell surface molecules involved in the adhesion cascade [J].
Geitz, H ;
Handt, S ;
Zwingenberger, K .
IMMUNOPHARMACOLOGY, 1996, 31 (2-3) :213-221
[10]   Thalidomide costimulates primary human T lymphocytes, preferentially inducing proliferation, cytokine production, and cytotoxic responses in the CD8+ subset [J].
Haslett, PAJ ;
Corral, LG ;
Albert, M ;
Kaplan, G .
JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 187 (11) :1885-1892