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Case Report Allogeneic Bone Marrow Transplantation for Advanced Waldenstrom’S Macroglobulinemia

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Case Report Allogeneic Bone Marrow Transplantation for Advanced Waldenstrom’S Macroglobulinemia Bone Marrow Transplantation, (1999) 23, 747–749 1999 Stockton Press All rights reserved 0268–3369/99 $12.00 http://www.stockton-press.co.uk/bmt Case report Allogeneic bone marrow transplantation for advanced Waldenstrom’s macroglobulinemia R Martino1, A Shah2, P Romero1, S Brunet1, J Sierra1, A Domingo-Albo´s1,✠, S Fruchtman2 and L Isola2 1Clinical Hematology Division, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; and 2Division of Hematology, Mount Sinai Medical Center, New York City, NY, USA Summary: Patients and methods Waldenstrom’s disease is a lymphoproliferative dis- Case 1 order that is typically treated with plasmapheresis and/or alkylating agents. In young patients, other A 34-year-old female was diagnosed in October 1986 with lymphoproliferative disorders have been treated with Waldenstrom’s macroglobulinemia. The patient presented allogeneic transplantation. Two patients with aggressive with autoimmune hemolytic anemia, a monoclonal IgM Waldenstrom’s disease, who progressed in spite of kappa of 17 g/l, kappa light chains in the urine, involve- multi-agent chemotherapy and autologous stem cell ment of bone marrow, peripheral blood, liver and spleen transplantation, in one case, underwent allogeneic and generalized lymphadenopathy. Lymph node biopsy transplantation from their HLA-identical donors. Both showed diffuse small lymphocytic lymphoma with lympho- remain alive with event-free survivals of more than 3, plasmacytic differentiation. Initial treatment was chloram- and more than 9 years, respectively. Allogeneic trans- bucil, steroids and splenectomy. In January 1988 the patient plantation should be considered for young patients with received combination chemotherapy with CHOP (cyclo- Waldenstrom’s disease. phosphamide, vincristine, adriamycin and prednisone), for Keywords: allogeneic; bone marrow transplant; Walden- a total of six cycles with no response. The monoclonal para- strom’s macroglobulinemia; lymphoplasmacytic lym- protein rose to 50 g/l, with diffuse marrow involvement, phoma; IgM monoclonal paraprotein increased liver and lymph node involvement and B symp- toms. The patient had an HLA-identical brother and was referred for BMT. Pre-BMT she had a 60% marrow infil- tration by CD5+, CD19+, FMC7+, IgM+, kappa+ lymphoid High-dose chemotherapy with autologous stem cell support cells, with immunoglobulin heavy chain gene rearrange- is widely used for the treatment of lymphomas and mye- ment by Southern blot. Generalized lymphadenopathy and 1 loma. In the setting of indolent lymphomas, this therapy hepatic nodules were seen on CT scan. The IgM kappa 2,3 is fraught with a high incidence of disease recurrence. monoclonal paraprotein pre-BMT was 60 g/l, with marked Allogeneic bone marrow transplantation (BMT) is being reduction of normal IgG and IgA. The hemoglobin was increasingly used to treat young patients with poor prog- 105 g/l, platelet count 334 × 109/l, WBC 7.6 × 109/l, with 4 nosis low-grade lymphoproliferative disorders. Walden- 37% neutrophils and 55% lymphocytes, including 10% strom’s macroglobulinemia (WM) is a lymphoplasmacytic lymphoma cells, and the LDH concentration was 749 U/L lymphoma with IgM monoclonal paraprotein. This rare (normal Ͻ460). Conditioning for BMT consisted of high- lymphoid malignancy usually follows an indolent course. dose oral chlorambucil (0.6 mg/kg daily for 4 days), cyclo- As with other low-grade lymphoid malignancies the disease phosphamide (60 mg/kg for 2 days, total dose 120 mg/kg) can have an aggressive course with poor prognostic features and TBI (fractionated over 4 days, total dose 12.5 Gy). that justify innovative or aggressive treatments, including Unmanipulated bone marrow was infused on 4 August 5,6 BMT. To our knowledge, however, there have been no 1989. GVHD prophylaxis consisted of CsA plus short- previous reports of allogeneic BMT for WM. We report course MTX. There were no significant post-transplant two young patients with aggressive WM who received allo- complications. Recovery of 0.5 × 109/l neutrophils occurred geneic BMTs. on day +20 and 50 × 109/l platelets on day +30. There was no acute or chronic GVHD. Donor–recipient chimerism studies were regularly performed after BMT by a PCR- based study of RFLP, with a sensitivity of 5%, and showed Correspondence: Dr LM Isola, Box 1079, Mount Sinai Medical Center, 1 Gustave L Levy Place, New York, NY 10029, USA complete donor chimerism in both peripheral blood and ✠Deceased bone marrow aspirates from 3 months post-BMT onwards. Received 5 November 1998; accepted 3 November 1998 At that time, CT scans showed no lymphadenopathy or BMT for Waldenstrom’s macroglobulinemia R Martino et al 748 liver nodules. Bone marrow biopsy still showed small para- phalan 200 mg/m2 and a peripheral blood autologous stem trabecular lymphoid nodules as described in the nodular PR cell transplant in July 1995 as salvage prior to allogeneic of CLL.7 However, no CD5+, CD19+, kappa+ cells were transplant from his HLA-identical sister. A bone marrow detected by flow cytometry (sensitivity 0.1–1%). No examination following the autologous transplant showed rearranged immunoglobulin heavy chain genes have been residual Waldenstrom’s macroglobulinemia. The unin- detected in the marrow after transplant. This patient volved marrow was hypocellular with a relative increase remains event-free with a Karnofsky performance status of in immature granulocytes and iron stores. The IgM spike, 100% on day 3378 post-transplant. A small serum mono- although lower than previous readings was still present clonal IgM kappa band of 2.25 g/l is still detectable by (5.2 g/l). There was also no appreciable change in the per- immunofixation, with normal IgG and IgA levels. No light sistent adenopathies or soft tissue masses in the abdomen chain proteinuria has been found post-BMT. Table 1 on follow-up CT scans. Repeated packed cell and platelet summarizes the patient’s follow-up after BMT. transfusions were administered due to bleeding episodes and a falling hemoglobin concentration. Before allogeneic BMT, the IgM spike was 5.6 g/l with a normal IgG and Case 2 markedly reduced IgA. The hemoglobin was 6.3 g/dl, plate- A 39-year-old male presented in June 1992 with a history let count 18 × 103/␮l, WBC 3.5 × 109/l, with 76% neutro- of night sweats, fatigue and pallor. A bone marrow aspirate phils and 19% lymphocytes, and the LDH concentration and biopsy showed a lymphoplasmacytic infiltrate consist- was 188 U/L (normal Ͻ460). ent with Waldenstrom’s macroglobulinemia. Serum electro- Conditioning for allogeneic BMT consisted of cyclopho- phoresis showed an IgM kappa monoclonal protein of sphamide (60 mg/kg for 2 days, total dose 120 mg/kg) and 35 g/l. Serum viscosity was 2.1. Urine was negative for TBI (1350 cGy in nine fractions over 5 days plus 1300 cGy Bence–Jones proteins. A CT of the chest, abdomen and boost to the abdomen in four fractions over 4 days). pelvis showed pretracheal, retroperitoneal and iliac chain Unmanipulated marrow was infused on 10 October 1995. adenopathy (up to 1.5 cm). A bone survey showed no focal GVHD prophylaxis consisted of CsA plus solumedrol. lesions. His initial treatment consisted of plasmapharesis Recovery of neutrophils Ͼ0.5 × 109/l occurred on day +13 and chlorambucil followed 4 months later by three cycles of and platelets Ͼ20 × 109/l on day +22. The last IgM level, combination chemotherapy (cyclophosphamide, vincristine measured a year after the transplant, was 0.45 g/l. Follow- and prednisone). The patient received two cycles of 2-CDA ing the transplant, the patient developed chronic extensive for progressive anemia in December 1993. At the time, a GVHD with varying degrees of skin, joint, mouth, lungs CT scan showed cervical, axillary, medistinal and retrocru- and liver GVHD. However, he is currently alive on day ral adenopathy and a 5.5 × 6 cm mass in the head of the 1014 post-BMT with a Karnofsky performance status of pancreas, but no focal liver lesions. A repeat bone marrow 70% and no CT evidence of lymphoma or abnormal protein biopsy showed hypercellular marrow with atypical pleo- in the serum. morphic plasmacytoid cells with prominent nucleoli with admixed lymphocytes and plasma cells. Flow cytometry showed an abnormal monoclonal (kappa+) B cell population Conclusions comprising 25% of the gate. These B cells were positive for CD19, CD20, CD22 and DR, and negative for CD10, This report presents two cases of long disease-free survival CD34 and CD5. The SIg staining was brightly positive. The following allogeneic BMT for Waldenstrom’s macroglobu- IgM kappa monoclonal protein was 17.4 g/l. The patient linemia. Both positive outcomes are in line with a recent received two cycles of fludarabine in January 1995 without review of the IBMTR data concerning the use of allogeneic any response followed by two cycles of MINE (mesna, BMT for low grade lymphoid malignancies.8 One of our ifosfamide, mitoxanthrone, etoposide) chemotherapy in patients (No. 2) had undergone an autologous stem cell June 1995. By then he had hepatomegaly, splenomegaly transplant with persistence of disease. His subsequent allo- and bulky adenopathy at the porta hepatis. He received mel- geneic BMT resulted in complete resolution of the mono- Table 1 Patient outcome after transplantation Case Dis status/chimerism Dis status/chimerism Dis status/chimerism Dis status/chimerism EFS (days at 1–3 months at 3–6 months at 12 months at last follow-up post-BMT)/KfS 1 nPR/CDCa CR/CDCa CR/CDCa,b CR/CDCa,b (100 mo+) 3373/100% Serum IgM Serum IgM Serum IgM serum IgM kappa 21.4 g/l kappa 12.1 g/l kappa 9.95 g/l kappa 2.25 g/l 2 nPR/CDC CR/CDC — CR/CDC (36 mo+) 1014/70% Serum IgM — Serum IgM — kappa 2.65 g/l kappa 0.45 g/l Dis = disease; CR = complete remission; nPR = nodular CR; CDC = complete donor chimerism; EFS = event-free survival; KfS = current Karnofsky performance status.
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