Nozza Andrea, Siracusano Licia, Armando Santoro
Department of Medical Oncology and Hematology, Istituto Clinico Humanitas, Milan, Italy.
Clin Ther. 2006 Jun;28(6):953-9. doi: 10.1016/j.clinthera.2006.06.009.
Multiple myeloma (MM) is a hematologic neoplasia characterized by the monoclonal proliferation of bone marrow plasma cells. Renal failure occurs in 20% to 30% of MM patients at diagnosis and in >50% with an advanced form of the disease. For those with advanced MM, often a high-risk group of patients with poor prognosis, salvage treatment for renal failure needs to avoid nephrotoxic drugs.
We report a case of a 78-year-old white male (weight, 90 kg) presented to the Department of Medical Oncology and Hematology, Istituto Clinico Humanitas, Rozzano, Milan, Italy, with refractory MM immunoglobulin G kappa (IgGkappa), Durie-Salmon Stage IIA, with progressive renal failure after an oral melphalan, prednisone, and thalidomide regimen (4 mg/m2.d, 40 mg/m2.d for 7 days every 6 weeks, and 100 mg/d, respectively). The patient had documented increments of serum monoclonal component (M-protein), anemia, and renal failure with Bence Jones proteinuria (serum creatinine, 2.9 mg/dL; creatinine clearance, 30 mL/min; hemoglobin, 10.9 g/dL; serum IgGkappa M-protein, 3.9 g/dL; proteinuria 3.5 g/d;light-chain level in urine, 1.2 g/L). After 2 cycles with bortezomib at a reduced dose (1.0 mg/m2 twice weekly for 2 weeks followed by a 10-day rest period) to evaluate tolerability and renal toxicity, the patient completed another 3 cycles at the standard dose (1.3 mg/m2) in combination with dexamethasone (20 mg on the day of bortezomib administration and the day after). This led to an improvement of the renal function with a reduction of serum and urinary M-protein (serum creatinine 1.4 mg/dL; serum IgGkappa M-protein, 2.9 g/dL; proteinuria, 2 g/d; kappa light-chain level in urine, 0.7 g/L). The patient developed thrombocytopenia but did not suffer from some of the more severe adverse events associated with bortezomib, such as infection or peripheral neuropathy, even at full dose.
We report an elderly patient with refractory MM and progression with renal failure who responded to bortezomib treatment. Bortezomib was well tolerated in this patient.
多发性骨髓瘤(MM)是一种血液系统肿瘤,其特征为骨髓浆细胞的单克隆增殖。20%至30%的MM患者在诊断时出现肾衰竭,而疾病晚期患者中这一比例超过50%。对于晚期MM患者,这通常是一组预后较差的高危患者,肾衰竭的挽救治疗需要避免使用肾毒性药物。
我们报告一例78岁白人男性(体重90kg),因难治性MM免疫球蛋白Gκ(IgGκ)、Durie-Salmon IIA期,在接受口服美法仑、泼尼松和沙利度胺方案(分别为4mg/m²·d、40mg/m²·d,每6周7天,以及100mg/d)后出现进行性肾衰竭,就诊于意大利米兰罗萨诺市伊斯特托临床医院的医学肿瘤学和血液学系。患者有血清单克隆成分(M蛋白)增加、贫血及肾衰竭伴本-周蛋白尿的记录(血清肌酐2.9mg/dL;肌酐清除率30mL/min;血红蛋白10.9g/dL;血清IgGκ M蛋白3.9g/dL;蛋白尿3.5g/d;尿轻链水平1.2g/L)。在以降低剂量(1.0mg/m²,每周两次,共2周,随后休息10天)使用硼替佐米2个周期以评估耐受性和肾毒性后,患者以标准剂量(1.3mg/m²)联合地塞米松(硼替佐米给药当天及次日各20mg)完成了另外3个周期的治疗。这导致肾功能改善,血清和尿M蛋白减少(血清肌酐1.4mg/dL;血清IgGκ M蛋白2.9g/dL;蛋白尿2g/d;尿κ轻链水平0.7g/L)。患者出现血小板减少,但即使在全剂量时也未出现一些与硼替佐米相关的更严重不良事件,如感染或周围神经病变。
我们报告了一例患有难治性MM且伴有肾衰竭进展的老年患者,其对硼替佐米治疗有反应。该患者对硼替佐米耐受性良好。