Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-four patients with primary generalized amyloidosis (PGA) and 14 with multiple-myeloma-related amyloidosis (MRA) were studied. The commonest clinical manifestations in PGA were nephrotic syndrome, hepatomegaly and congestive heart failure, and in MRA, low back pain, plasmacytoma and rheumatoid-arthritis-like syndrome. Eight patients with PGA had limited clinical expression of the disease, such as involvement of only kidneys, joints, parotid glands or gastrointestinal tract; in one patient amyloidosis was limited to lymph nodes. Low serum concentrations of total protein and albumin were common. M components were detected in the serum of 91% of patients with PGA and 92% of patients with MRA: 70% of the M components in PGA and 25% of those in MRA had lambda light chains. Bence Jones proteinemia was detected in 56% of the patients with PGA and in 77% of those with MRA. The serum concentration of immunoglobulins was decreased substantially in more than two thirds of the patients with PGA. Proteinuria (greater than 250 mg/24 h) was observed in 78% of patients with PGA and in 93% of patients with MRA. Bence Jones proteinuria was noted in 75 and 77% of patients, respectively. Plasmacytic infiltration of the bone marrow was found in 90% of the patients with PGA. The mean survival time of the patients with PGA was 28 months and of those with MRA, 29 months from the time of diagnosis.
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PMID:Clinical and laboratory findings in primary generalized and multiple-myeloma-related amyloidosis. 126 76

Compared to leukemia, malignant lymphoma and other hematogenous tumors, multiple myeloma rarely metastasizes to the central nervous system. Intracerebral metastasis without involvement of the cranium itself is rarer. We report a case of Ig-G k-type multiple myeloma with metastasis to the left frontal lobe extending to the right basal ganglia without involvement of the cranium. A 71-year-old male complained of exertional dyspnea and lumbago. His laboratory data revealed hyperproteinemia and an abnormal increase in Ig-G (6117mg/dl) in his serum. Serum protein immunoelectrophoresis revealed an IgG k-type band, and Bence-Jones protein was detected in his urine. MMPP, VMCP, VIPP and MP chemotherapy was given, and serum IgG level decreased to a normal range. 21 months after his first admission, incontinence, disorientation, gait disturbance and apathy developed. CT-scan showed an isodense lesion with massive edema in the left frontal lobe and right basal ganglia. On MRI, a Gd-DTPA enhancing lesion was detected extending from the left frontal to the opposite frontal lobe through the splenium. No abnormal skull punched out lesions were noted. Left frontal lobectomy was performed. Histopathology revealed plasmablastic myeloma cells with clear nucleole and eccentric nucleus in the cerebrum. He was diagnosed as having intracerebral metastasis of multiple myeloma without involvement of the cranium. Unfortunately, he died of pancytopenia and pneumonia. Our case suggests the possibility of metastasis via blood into the cerebrum.
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PMID:[A case of multiple myeloma with intracerebral metastasis]. 140 49

We encountered a patient with multiple myeloma who died suddenly, in whom bilateral pulmonary artery thrombosis was found at autopsy. The patient was a 50-year-old woman who had received chemotherapy for multiple myeloma at a local clinic for 4 years, and was transferred to our hospital because of recurrence of multiple myeloma in August 1990. Despite chemotherapy performed after admission, serum globulin level increased and her low back pain worsened, and she was generally restricted to bed. On October 21, she developed sudden dyspnea, became markedly cyanotic, lost consciousness, and then suffered a cardiopulmonary arrest. Autopsy revealed bilateral pulmonary artery thrombosis as well as thrombosis in the pelvic veins. Hyperviscosity due to multiple myeloma and long-term recumbency were the probable causes of pelvic venous thrombosis and subsequent pulmonary artery thrombosis. We report a rare case of bilateral pulmonary artery thrombosis which developed during the course of multiple myeloma and led to sudden death.
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PMID:[Sudden death due to bilateral pulmonary thromboembolism in a patient with multiple myeloma: an autopsy case report]. 144 54

A 73-year-old female patient with myelomatous pleural effusions is described. She was admitted to our hospital with lumbago and emaciation. Laboratory findings revealed cytopenia and hypogammaglobulinemia. Immunoelectrophoresis demonstrated Bence-Jones monoclonal protein in the serum, but not in the urine. Bence-Jones myeloma was diagnosed by the bone marrow aspiration. Chest X-ray film, however, showed bilateral pleural effusions. Fluid cytology revealed numerous immature plasma cells, indicating pleural involvement. Intrapleural administration of alpha-interferon combined with systemic chemotherapy (oral melphalan-prednisolone with alpha-interferon im.) was successful in maintaining the resolution of pleural effusions. Intrapleural alpha-interferon administration seems to be effective in the management of myelomatous pleural effusions.
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PMID:Bence-Jones myeloma with pleural effusion: response to alpha-interferon and combined chemotherapy. 150 23

The patient was a 64-year-old woman who was admitted to our hospital because of lumbago. A diagnosis of multiple myeloma (non-producing type) was made, based on (1) the presence of multiple osteolytic lesions, (2) hypercellular marrow with 64.2% plasmacytoid malignant cells, (3) no monoclonal gamma-globulin was detected in the serum and urine, and (4) abnormal monoclonal gamma-globulin was also not detected in the cytoplasm and membranes of these malignant cells. After several courses of chemotherapy, a pleural effusion infiltrated by myeloma cells developed and the patient's serum contained a markedly increased amylase activity of salivary-type. Amylase activity was also detected in vitro in the supernatant of cultured myeloma cells established from the patient's pleural effusion. The presence of alpha-amylase in the myeloma cells, which were derived from pleural effusion, was demonstrated immuno-histochemically. These observations indicates that amylase was ectopically produced by these myeloma cells. Interestingly, 14 out of 20 metaphases in the cells derived from pleural effusion showed translocation of 1p22 near the region of 1p21, where the amylase gene was assigned.
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PMID:[Ectopic production of amylase by a non-producing type of multiple myeloma]. 169 5

A 78-year-old man was admitted because of lumbago and chest pain. A diagnosis of non-secretory primary plasma cell leukemia was made based on the laboratory findings and his history. However, the plaque-forming cells assay of bone marrow cells revealed secretion of monoclonal immunoglobulin from the myeloma cells. Hyperammonemia was detected in the serum. Although the patient was treated with 4 courses of combination chemotherapy (vincristine, adriamycin, cyclophosphamide, methylprednisolone), he died of respiratory failure five months after diagnosis. Autopsy showed widespread multiple myeloma and prominent infiltration of myeloma cell in the sinusoid of the liver. Recently, there have been a few reports which increased the plasma ammonia concentration with multiple myeloma. This report strongly suggested that liver infiltration of myeloma cell caused hyperammonemia.
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PMID:[Non-secretory primary plasma cell leukemia with hyperammonemia]. 206 85

A 66-year-old female was admitted to our hospital with lumbago. On admission, laboratory examination revealed hemolytic anemia. Direct Coombs' test was positive, and also direct monospecific-Coombs' test by anti-C3d serum was positive. Immunoelectrophoresis showed IgA-lambda type M proteins in serum. Bone marrow aspiration disclosed increased atypical plasma cells. X-ray of skull showed punched-out lesion. From these findings, she was diagnosed as IgA (lambda) myeloma complicating with autoimmune hemolytic anemia. Hemolysis was improved by chemotherapy. It was thought that IgA and C3 were related well to hemolysis in this case.
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PMID:[IgA-lambda type myeloma complicating with autoimmune hemolytic anemia]. 212 9

A 46-year-old man was admitted because of lumbago and numbness of the left leg. Pelvic X-ray showed a large defect in the left sacrum and CT revealed multiple punched-out lesions. Serum IgA was 1,740 mg/dl with a monoclonal component of IgA kappa by serum electroimmunofixation. Bence Jones protein of kappa type was detected in urine. Diagnosis of myeloma was made on the basis of histology of the biopsied sacral tumor. Repeated melphalan/prednisolone intermittent therapy (MP) was done with concomitant administration of natural interferon-alpha (IFN-alpha) 3 X 10(6) U intramuscularly for 67 days. Performance status including gait markedly improved. Normal bone marrow morphology and disappearance of M-protein by electroimmunofixation were achieved after 13 cycles of MP, when pelvic X-ray revealed prominent recalcification. No further treatment was instituted for subsequent 6 months, without any demonstrable M-protein. Complete remission of myeloma is rare with conventional therapies and thus new therapeutic modalities have been waited for. IFN-alpha may promise better responses if appropriately combined with other chemotherapies.
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PMID:[Complete remission in multiple myeloma with natural interferon-alpha (HLBI) and melphalan/prednisolone intermittent therapy]. 221 76

A 77 year-old male was admitted to the hospital because of lumbago and M-proteinemia. IgA (kappa) monoclonal protein (8,100 mg/dl) was demonstrated in serum, and Bence Jones protein (kappa) in urine samples. The bone marrow examination showed an increased number of pathological plasma cells (34. 5%). Multiple osteolytic lesions were evident on X-ray films. A diagnosis of multiple myeloma (MM) was made. He had exudative erythematous skin lesions on his back. His serum was positive for antibody to ATLA. A biopsy specimen from the skin lesions showed Pautrier's micro-abscess which were filled with Leu 3a positive T lymphocytes. 159 base pairs of human T cell leukemia virus I (HTLV-I)/pX position was identified from a cutaneous sample utilizing the polymerase chain reaction method. Thus, a diagnosis of MM superimposed on adult T cell lymphoma was made. An extensive search failed to find any cases complicated with these two diseases except a report by Tagawa et al. concerning a patient with ATL who developed IgA (kappa) MM during a five year follow up. Therefore, this is the first reported case of MM superimposed on ATL.
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PMID:[Multiple myeloma superimposed on adult T cell lymphoma]. 228 74

A 73-year-old man was admitted into the hospital because of lumbago in October, 1986. Laboratory examination on admission showed anemia, an IgA-kappa Bence Jones proteinemia. The bone marrow picture disclosed a marked involvement by the neoplastic cells, followed by leukemic conversion 2 weeks later. The leukemic cells displayed a lymphoblastoid appearance on light microscopy, but rather compatible with plasma cells on electron microscopy, showing some strands of rough endoplasmic reticulum and a prominent Golgi apparatus in the cytoplasm. The cells expressed a wide spectrum of surface markers, including those of plasma cell (PCA-1, OKT10), B cell (B1, sIg) and CALLA. Reverse hemolytic plaque assay disclosed the immunoglobulin production of monoclonal kappa chain, but a heavy chain production was recognized only in a small proportion of the cells. Under the diagnosis of multiple myeloma, he was treated with vincristine, cyclophosphamide, and prednisolone. But he died of renal failure complicating hypercalcemia after only three months of the admission in accordance with previous reports that CALLA-positive myeloma was associated with poor prognosis. This case may also represent the clinical, morphological and phenotypic diversity in multiple myeloma.
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PMID:[CALLA-positive leukemic multiple myeloma of IgA-kappa type]. 250 77


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