Cases reported "Multiple Myeloma"

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1/27. Development of IgG lambda multiple myeloma in a patient with cutaneous CD30 anaplastic T-cell lymphoma.

    We report a patient with an epidermotropic cutaneous T-cell lymphoma which transformed into an anaplastic cutaneous CD30 T-cell lymphoma. Repeated relapses required prolonged systemic puva therapy. Two years after diagnosis, the patient had several episodes of infections of the respiratory tract. serum electrophoresis now revealed significantly reduced polyclonal immunglobulin production and an additional band in the gamma fraction corresponding to IgG lambda monoclonal gammopathy. Thereafter, the patient suffered a pathologic fracture of the dorsolateral 5th rib on the right side and an accumulation of monoclonal plasma cells in the bone marrow confirmed the diagnosis of multiple myeloma (IgG lambda). Accordingly, 6 cycles of cytoreductive chemotherapy (alkeran, decortin) were given. After one year of steady state disease the patient lost weight and bone pain increased while only a few papular eruptions were detectable. radiography showed multiple small osteolytic areas. A few months later he died with signs of bone marrow insufficiency.
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2/27. Acute promyelocytic leukaemia complicating multiple myeloma: evidence of different cell lineages.

    The association of leukemia and multiple myeloma is well described usually as a complication of chemotherapy but also in the absence of chemotherapy or at diagnosis. Such leukemias are typically acute myeloid leukemia (AML), particularly myelomonocytic subtype, and cases of acute promyelocytic leuke (APL) are rarely reported. Controversy exists as to whether myeloma and AML originate from a single haematopoietic progenitor or arise from different cell lineages. We report a case of a 58 year old female who developed APL 10 months following diagnosis of nonsecretory light chain (kappa) myeloma which had been treated with local spinal irradiation and low dose oral melphalan and prednisone. Clonality had originally been demonstrated by light chain restriction (kappa) of her bone marrow plasma cells whilst immunoglobulin heavy chain and T cell receptor genes were germ line. At development of APL cytogenetics revealed t(15;17) and PML-RAR fusion gene was detected by RT-PCR. The patient was treated with all-trans retinoic acid (ATRA) and received 2 cycles of consolidation chemotherapy with idarubicin. Following this therapy the t(15;17) and PML-RAR were both undetectable whilst the clonal population of kappa staining plasma cells persisted. This particular patient represents a rare case of APL complicating multiple myeloma with persistence of the myeloma clone but disappearance of PML-RAR alpha rna following therapy. This case study appears to support the argument that the APL and myeloma originated from distinct cell lineages.
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3/27. Ischemic heart disease associated with vincristine and doxorubicin chemotherapy.

    OBJECTIVE: To report the ocurrence of ischemic heart disease (IHD) in a patient with multiple myeloma treated with vincristine and doxorubicin. CASE SUMMARY: A 46-year-old man developed a Q-wave inferior and right-ventricle myocardial infarction with postinfarction angina after receiving his third cycle of vincristine and doxorubicin for immunoglobulin a multiple myeloma. angiography showed two small filling defects consistent with thrombi in the distal right coronary artery. DISCUSSION: IHD may be a serious but uncommon complication of treatment with several chemotherapeutic agents. It is likely that chemotherapy played a role in the development of IHD in our patient. Several putative mechanisms for vascular toxicity have been associated with chemotherapy. CONCLUSIONS: Chemotherapy with vincristine and doxorubicin may play a role in the ocurrence of IHD. physicians should possess an awareness of this potentially serious complication of chemotherapy.
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4/27. multiple myeloma and mycosis fungoides in the same patient: clinical, immunologic, and molecular studies.

    The coexistence of multiple myeloma (MM) and mycosis fungoides (MF), and hence of both B- and T-cell neoplastic clones, is a rare event. We describe a case of plaque-stage MF associated with IgG lambda MM. The clinical onset of MF preceded that of MM, supporting the hypothesis that MF predisposed to the development of the B-cell proliferative disorder. The skin tumor cells were found to originate from CD4( ) t-lymphocytes, characterized by a V beta 8 receptor and no proviral human T-lymphotropic virus (HTLV)-I monoclonal integration. They also displayed a polarized Th1-type cytokine profile containing mRNAs for interleukin (IL)-2, interferon (IFN)-gamma, and tumor necrosis factor (TNF)-beta, but not for IL-4, IL-5, or IL-10. The CD8( )/CD57( ) suppressor-cytotoxic subpopulation was significantly increased in the peripheral blood and was associated with MM progression. Expression of p16INK4A, a gene from the ink family that inhibits cyclin-dependent kinases and regulates the cell cycle, was lacking in MF cells and bone marrow (BM) plasma cells. The p16INK4A gene was silenced by hypermethylation, suggesting that it plays a role in the early phase of the pathogenesis of both diseases. Thus, a lymphoid precursor cell presumably contains aberrations that induce the development of both clonal diseases in a multistep process.
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5/27. Massive hepatomegaly: a presenting manifestation of multiple myeloma.

    We report a 50-year-old woman presenting with isolated massive hepatomegaly. liver histology showed dilated sinusoids within which some atypical cells, probably of hematopoeitic origin, were identified. bone marrow was densely packed with similar atypical cells with high nucleo-cytoplasmic ratio, which tested positive for plasma cell markers. Plasma protein electrophoresis showed a distinct M spike in the gamma globulin fraction and skeletal survey revealed multiple lytic lesions in the skull and pelvic bones. Thus, a final diagnosis of multiple myeloma was made. The patient has received six cycles of chemotherapy and is doing well.
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6/27. syndrome of inappropriate secretion of antidiuretic hormone after infusional vincristine.

    A 77-year-old woman with refractory multiple myeloma was treated with a 4-day continuous intravenous infusion of vincristine and doxorubicin and 4 days of oral dexamethasone. Nine days after her second cycle she presented with lethargy and weakness associated with hyponatremia. Evaluation revealed the syndrome of inappropriate secretion of antidiuretic hormone, which was attributed to the vincristine infusion. After normal serum sodium levels returned, further doxorubicin and dexamethasone chemotherapy without vincristine did not produce this complication.
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7/27. Reversible ageusia after chemotherapy with pegylated liposomal doxorubicin.

    OBJECTIVE: To report a case of reversible ageusia in a patient with multiple myeloma receiving pegylated liposomal doxorubicin. CASE SUMMARY: A 67-year-old man with a history of arterial hypertension and persisting left bundle-branch block was diagnosed with multiple myeloma. He was initially treated with cyclophosphamide 200 mg/m(2) (days 1-4), pegylated liposomal doxorubicin 20 mg/m(2) (day 1), and dexamethasone 40 mg (days 1-4) (CLAD). That treatment was followed by high-dose melphalan therapy and autologous peripheral stem-cell transplantation. The disease recurred 18 months later, and renal failure developed. The patient was again treated with the CLAD protocol. After the first cycle, almost complete ageusia occurred, along with weight loss and severe depression. Chemotherapy was continued, but pegylated liposomal doxorubicin was replaced by conventional doxorubicin. Within 12 weeks, the patient's sense of taste returned to normal. DISCUSSION: Pegylated liposomal anthracyclines are increasingly being used as a less cardiotoxic alternative to conventional doxorubicin in first- and second-line therapy of multiple myeloma. Whereas cardiotoxicity and unspecific reactions are seen less frequently, palmar-plantar erythrodysesthesia is a common reaction to pegylated liposomal anthracyclines. No other reasons for ageusia in our patient could be identified. Based on the Naranjo probability scale, ageusia was rated as a probable reaction to pegylated liposomal doxorubicin. CONCLUSIONS: As with all new and innovative drugs, thorough documentation of infrequent adverse events is necessary. We would like to raise awareness for ageusia, which appears to be a rare but severely impairing adverse reaction to a relatively new pharmacologic agent.
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8/27. Tumour lysis syndrome in multiple myeloma after bortezomib (VELCADE) administration.

    Bortezomib (VELCADE) is a proteasome inhibitor, which has been recently used for the treatment of relapsed/refractory multiple myeloma (MM) with encouraging results. Tumour lysis syndrome (TLS) has been described during chemotherapy for many haematological malignancies, such as acute lymphoblastic leukaemia and high-grade lymphomas. TLS is very rare in MM with ten reported cases, including approximately 1% of patients receiving high-dose chemotherapy with stem cell support (ASCT). We report here a patient with refractory MM and deletion 13q, who had received more than four lines of previous treatment, including two ASCT, and had relapsed. The patient received bortezomib, as a single agent, at a dose of 1.3 mg/m(2) twice per week for 2 weeks, in a 3-week cycle, and developed TLS after the second dose of cycle one. Bortezomib therapy, due to the rapidity of its action, may result in TLS in myeloma patients who have rapidly proliferative disease with a high tumour burden. Therefore, TLS should be looked for during the first cycle of bortezomib treatment and suitable precautions should be considered.
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9/27. Sustained remission including marked regression of a paravertebral plasmacytoma in a patient with heavily pretreated, relapsed multiple myeloma after treatment with bortezomib.

    Despite advances in systemic and supportive therapies, multiple myeloma (MM) has remained an incurable disease, which underlines the need for novel approaches to therapy. Recent data indicate that the proteasome-inhibitor bortezomib has marked activity with manageable toxicity in relapsed and refractory MM. We here report on a patient suffering from heavily pretreated and refractory MM with a paravertebral tumor manifestation. After three cycles of bortezomib, the patient achieved near-complete remission, as well as a nearly complete regression of the paravertebral tumor. This case further documents that bortezomib is an effective novel therapy for MM.
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10/27. Combination of bortezomib, thalidomide, and dexamethasone in the treatment of relapsed, refractory IgD multiple myeloma.

    The use of the proteasome inhibitor bortezomib has been recently introduced into the treatment of relapsed, refractory multiple myeloma (MM). We here demonstrate a case of a patient with IgD MM who was successfully treated with a combination of bortezomib, thalidomide, and dexamethasone. Relapse of the disease occurred following tandem autologous transplantation and was refractory to a salvage therapy consisting of thalidomide, cyclophosphamide, etoposide, and dexamethasone. While the administration of thalidomide was continued, the addition of bortezomib and dexamethasone led to a complete remission after 2 cycles of therapy. The feasibility of this treatment is supported by a recently reported phase I/II trial that used a lower dose of thalidomide in combination with an equal dose of bortezomib. This is the first report of a patient with IgD MM treated accordingly, suggesting that this entity is highly sensitive to the novel therapy.
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