Izumi Mayuko, Tsunemine Hiroko, Suzuki Yasuhiro, Tomita Akihiro, Kusumoto Toshiko, Kodaka Taiichi, Itoh Kiminari, Takahashi Takayuki
Department of Hematology, Shinko Hospital, 4-47 Wakihama-cho, 1-chome, Chuo-ku, Kobe, 651-0072, Japan.
Int J Hematol. 2015 Aug;102(2):238-43. doi: 10.1007/s12185-015-1775-3. Epub 2015 Mar 21.
We report here the successful treatment of cold agglutinin-associated refractory hemolysis with bortezomib in a patient with Waldenström's macroglobulinemia (WM). A 78-year-old man was referred to our hospital with cold hemagglutinemia of unknown cause. Laboratory examination revealed a hemoglobin concentration of 6.9 g/dL, serum IgM concentration of 1904 mg/dL, and a titer of cold hemagglutinin of over ×8192. Serum immunoelectrophoresis demonstrated monoclonal protein of the IgM-κ type. A bone marrow aspirate showed many lymphoplasmacytic cells, which were positive for CD19, CD20, CD38, and cytoplasmic μ and κ light chains. A diagnosis of WM-associated cold hemagglutinemia was made. Because of red blood cell transfusion-dependency, we treated him with intravenous fludarabine, oral melphalan-prednisolone, cyclophosphamide, and melphalan, and two courses of R-CHOP in sequence with a marked decrease of serum IgM (928 mg). We then started weekly bortezomib plus dexamethasone (BD) therapy, as he was still transfusion-dependent. Soon after the initiation of BD, he achieved transfusion independence, with a further decrease in serum levels of IgM and marked improvement of anemia. Interestingly, his marrow abnormal lymphocytes were later found not to carry the MYD88 L265P mutation. The successful treatment with bortezomib for WM lacking this mutation is discussed.
我们在此报告用硼替佐米成功治疗1例华氏巨球蛋白血症(WM)患者的冷凝集素相关难治性溶血。一名78岁男性因不明原因的冷凝集素血症转诊至我院。实验室检查显示血红蛋白浓度为6.9 g/dL,血清IgM浓度为1904 mg/dL,冷凝集素滴度超过×8192。血清免疫电泳显示IgM-κ型单克隆蛋白。骨髓穿刺显示许多淋巴浆细胞,其CD19、CD20、CD38以及胞质μ和κ轻链呈阳性。诊断为WM相关冷凝集素血症。由于患者依赖红细胞输血,我们先后用静脉注射氟达拉滨、口服美法仑-泼尼松龙、环磷酰胺和美法仑对其进行治疗,并连续进行了两个疗程的R-CHOP治疗,血清IgM显著下降(928 mg)。由于他仍依赖输血,随后我们开始每周给予硼替佐米加地塞米松(BD)治疗。开始BD治疗后不久,他就不再依赖输血,血清IgM水平进一步下降,贫血明显改善。有趣的是,后来发现他骨髓中的异常淋巴细胞未携带MYD88 L265P突变。本文讨论了用硼替佐米成功治疗缺乏该突变的WM。