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)

Myelodysplastic syndrome (MDS) combined with monoclonal gammopathy or multiple myeloma has rarely been reported. In this article, two siblings, a brother and his sister who showed simultaneous occurrence of MDS and monoclonal gammopathy are reported. The first case, a 73-year-old male, was admitted to our hospital in November, 1987. Analysis of peripheral blood revealed pancytopenia without blast cells. Bone marrow was hypocellular with 14.9% of myeloblasts and 2.8% of plasma cells characterized by 2 to 4 nuclei. Serum IgA level was 635 mg/dl and serum immunoelectrophoresis revealed a monoclonal IgA lambda band. The second case, a 70-year-old female, younger sister of the first case, was admitted to our hospital in January, 1988. Bone marrow was normocellular with 23% of peroxidase-negative myeloblasts and 12.8% of atypical plasma cells. Serum IgG level was 1,901 mg/dl with monoclonal IgG kappa band. Hematological findings have remained unchanged for 12 months. The first case was regarded as hypoplastic MDS with monoclonal gammopathy and the second case was MDS with smoldering myeloma. These cases were very similar with in respect to age, time of onset, clinical course, hematological findings and especially, association with M-protein. There are no reports concerning the familial incidence of MDS with M-protein. These findings supported the hypothesis that an initial event selects a clone of stem cells which retain the capability to differentiate into mature myeloid and lymphoid cells, in these cases B-cells.
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PMID:[Familial occurrence of myelodysplastic syndrome concomitant with monoclonal gammapathy]. 163 65

Epidemiological studies indicating that exposure to organic solvents is a risk factor for haematological malignancies are reviewed. Exposure to benzene is a risk factor for ANLL. A preleukaemic phase with pancytopenia is common and may be associated with a normo- or hypercellular marrow with morphological characteristics suggesting MDS. There are indications that other organic solvents than benzene may be leukaemogenic. Certain chromosome aberrations are characteristic in leukaemic cells from solvent exposed ANLL patients. The average latency time from start of occupational exposure until diagnosis is about 10-11 years. There is epidemiological evidence that exposure to organic solvents may also increase the risk of lymphoproliferative malignancies, i.e. ALL, NHL, HD and myeloma.
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PMID:Exposure to organic solvents and risk of haematological malignancies. 173 76

To study the efficiency of high-dose melphalan in previously untreated patients with advanced myeloma, we performed a Phase I-II trial. Twenty-eight patients were treated at dose level of 60-140 mg/m2. Each patient was first treated with a priming dose of cyclophosphamide (300 mg) followed by high-dose melphalen 1 week later. One course of therapy was given. Patients were then followed without further therapy until relapse. Clinical and laboratory features of the 28 patients in this study included: median age 63, performance status 0-2, hypercalcemia 21%, bone pain 82%, paraprotein types: IgG 76%, Iga 20%, and paraproteinuria 71%. Because none of the patients achieved complete remission (CR) at 60 mg/m2, despite life-threatening toxicity in all patients, the dose level was rapidly increased to 140 mg/m2, a dose previously reported to induce a high percentage of CR. At this dose, CR was achieved in only 1 of 11 patients (9%). This patient had multiple plasmacytomas without generalized bone marrow involvement. One additional patient at 100 mg/m2 achieved CR. Of the whole group, 12 achieved PR. Durations of remissions were generally short: CR 6.3 and 18+ months and PR 2.3-18 month, median 6.9 months. Life-threatening myelosuppression was universal with prolonged pancytopenia. Treatment-related deaths from sepsis were observed in 29% of patients. The median survival of the entire group was 15.6 months. Older patients in this trial did not tolerate high-dose melphalen therapy well; this resulted in a high proportion of toxic deaths and poor overall survival.
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PMID:Phase I-II trial of high-dose melphalan in previously untreated stage III multiple myeloma: Cancer and Leukemia Group B study 8512. 173 10

The authors describe 4 cases of multiple myeloma that developed one or more extraskeletal localizations. They have evaluated the relation between the onset of the extraskeletal localizations and the following myeloma characteristics: tumor burden, clinical phase, chemotherapy response, prognostic significance. All the patients showed these localizations in a plateau phase of myeloma. None of the patients had fever, pancytopenia and in no one the performance status worsened. All patients obtained at least a partial reduction of the localization and only the patient with the retro-orbital localization, got worse and died for myeloma. The other three patients are alive and do not show any sign of progression.
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PMID:[Extraskeletal diffusion of multiple myeloma. A clinico-pathological description of 4 cases]. 176 33

A case of denovo presentation of acute myeloid leukaemia with multiple myeloma is reported in a 32 years old male. He presented with pancytopenia and aleukaemic leukaemia. Bone marrow examination revealed presence of acute myeloid leukaemia and sheets of plasma cells. Serum electrophoresis showed a M protein which was characterised to be Ig lambda with decrease in normal immunoglobulin levels.
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PMID:An association of acute myeloid leukaemia and multiple myeloma: a case study. 176 82

Recent evidence suggests that tumour necrosis factor alpha (TNF) is an autocrine growth factor for the chronic B-cell malignancies hairy cell leukaemia (HCL) and some cases of B-chronic lymphocytic leukaemia (B-CLL). Incubation with TNF in vitro has been shown to increase viability, DNA synthesis and the expression of the protooncogenes myc, fos and jun in the tumour cells from these patients. TNF in vitro also increases expression of TNF-mRNA, suggesting the existence of an autocrine growth loop for TNF in these cells. Current experiments are compatible with the hypothesis that interferon alpha (IFN) interferes with this autocrine growth loop in HCL and B-CLL by stimulating degradation of messenger RNAs (mRNAs) for a number of cytokines including that of TNF. This RNA degradation may be mediated through induction of the enzyme 2,5 oligo-A synthetase with consequent increased synthesis of 2,5 oligo-A which is known to stimulate the activity of a latent ribonuclease capable of degrading cytokine mRNAs. Circulating tumour-derived TNF may also contribute to the pancytopenia in HCL and B-CLL. Whether cytokine autocrine growth loops are important in other B-cell malignancies, e.g. myeloma and non-Hodgkin's lymphoma, and subject to IFN-stimulated breakdown needs further study.
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PMID:Possible mechanism of action of interferon alpha in chronic B-cell malignancies. 193 2

Interleukin-3 (IL-3) is a T-cell-derived colony-stimulating factor (CSF) whose primary targets include relatively early, multipotential, hematopoietic progenitor cells. In this trial, we treated 24 patients with recombinant human IL-3 given by a daily 4-hour intravenous infusion for 28 days. The dose levels were 30, 60, 125, 250, 500, 750, and 1,000 micrograms/m2/d. At least three patients were entered at every dose level. Each participant suffered from bone marrow failure, with the underlying diagnosis being myelodysplastic syndrome (13 patients), aplastic anemia (eight patients), or aplasia after prolonged high-dose chemotherapy (three patients) for multiple myeloma, breast cancer, or acute myelogenous leukemia. Most patients tolerated therapy well, with the most frequent side effects being low-grade fever and headaches. Hematopoietic changes included modest increases in neutrophil counts (eight patients), eosinophil counts (six patients), platelet counts (three patients), and reticulocyte counts (two patients). An increase in blasts occurred in one patient who had refractory anemia with excess blasts in transformation and was reversible once IL-3 was discontinued. In addition, one patient with chronic myelomonocytic leukemia showed an increase in monocytes (and granulocytes). Progression to acute leukemia did not occur. Pharmacokinetic analyses showed a rapid clearance with a mean half-life of 18.8 minutes at the 60 micrograms/m2/d dose, and 52.9 minutes at the 250 micrograms/m2/d dose. Serum concentrations of 10 to 20 ng/mL of IL-3 were achievable at the 250 micrograms/m2/d dose. Our observations indicate that recombinant human IL-3 can be given safely at doses of 1,000 micrograms/m2/d or less. In addition, on the basis of preclinical data and the biologic activity observed in this study, further trials of this molecule, alone and in combination with other growth factors, are warranted in patients with pancytopenia.
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PMID:Phase I study of recombinant human interleukin-3 in patients with bone marrow failure. 204 65

A 43-year-old man was admitted to our hospital because of legs edema and periorbital edema in Dec. 1983. Laboratory findings showed massive proteinuria (3.7 g/day), Bence Jones protein (BJP) in urine, and hypoproteinemia. Peripheral blood examinations were normal and a bone marrow aspiration showed hypocellularity with slight increase of monocytes and plasma cells. Serum immunoelectrophoresis showed two M-components (IgG kappa, IgA lambda). Serum IgG was 1,690 mg/dl, IgA 379 mg/dl and IgM 160 mg/dl. No remarkable findings were obtained in bone survey, Ga-scintigraphy and rectal biopsy, and a diagnosis of diclonal gammopathy with nephrotic syndrome was made. In Aug. 1986, serum IgA started to increase rapidly with concomitant decrease IgG. He died of pneumonia due to pancytopenia in Dec. 1986, when serum IgG was 450 mg/dl, IgA 1,014 mg/dl, and IgM less than 39 mg/dl. Immunoelectrophoresis showed two M-components (IgG kappa, IgA lambda) in serum and BEP (kappa, lambda), IgG (kappa) and IgA (lambda) in urine. An autopsy showed massive infiltration of myeloma cells which were positive for lambda light chain in bone marrow, suggesting a development of myeloma from a diclonal gammopathy in about 3 years.
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PMID:[Diclonal gammopathy (IgG kappa, IgA lambda) with nephrotic syndrome terminating into IgA lambda myeloma after three years--report of a case]. 210 4

A 61 year old woman was admitted to our hospital suffering from severe pancytopenia. Bone marrow aspiration revealed marked hypoplasia with 24.8% plasma cells. There was a small amount of IgA type M protein in serum. Multiple myeloma was ruled out on the basis that 1) the amount of serum IgA-M protein was minimal and no increase was observed, 2) no indication of monoclonality of bone marrow plasma cells was shown by immunofluorescent staining of immunoglobulins, 3) neither bone lesion nor other symptoms related to multiple myeloma were observed. Therefore, a diagnosis of aplastic anemia was made, and bolus methylprednisolone therapy (1,000 mg/day x 3 days) was performed, which brought the patient to complete remission. An oral dose of 15 mg of prednisolone is administered daily now and the remission state is being maintained. Bolus methylprednisolone therapy is performed quite often for the treatment of aplastic anemia. However, there are few reports in which remission was reached with the use of glucocorticoids alone, most having used androgens or other supportive drugs in conjunction. Here, we will discuss this case of aplastic anemia which responded to repeated bolus methylprednisolone therapy, with minimal side effects, and discuss its effectiveness. In addition, aplastic anemia associated with idiopathic monoclonal gammopathy is not reported, so this case is interesting immunologically.
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PMID:[Aplastic anemia associated with minimal serum M-protein treated successfully with repeated bolus methylprednisolone therapy]. 238 Oct 70

The hematotoxicity of benzene exposure has been well known for a century. Benzene causes leukocytopenia, thrombocytopenia, pancytopenia, etc. The clinical and hematologic picture of aplastic anemia resulting from benzene exposure is not different from classical aplastic anemia; in some cases, mild bilirubinemia, changes in osmotic fragility, increase in lactic dehydrogenase and fecal urobilinogen, and occasionally some neurological abnormalities are found. Electromicroscopic findings in some cases of aplastic anemia with benzene exposure were similar to those observed by light microscopy. Benzene hepatitis-aplastic anemia syndrome was observed in a technician with benzene exposure. Ten months after occurrence of hepatitis B, a severe aplastic anemia developed. The first epidemiologic study proving the leukemogenicity of benzene was performed between 1967 and 1973 to 1974 among shoe workers in Istanbul. The incidence of leukemia was 13.59 per 100,000, which is a significant increase over that of leukemia in the general population. Following the prohibition and discontinuation of the use of benzene in Istanbul, there was a striking decrease in the number of leukemic shoe workers in Istanbul. In 23.7% of our series, consisting of 59 leukemic patients with benzene exposure, there was a preceding pancytopenic period. Furthermore, a familial connection was found in 10.2% of them. The 89.8% of our series showed the findings of acute leukemia. The possible factors that may determine the types of leukemia in benzene toxicity are discussed. The possible role of benzene exposure is presented in the development of malignant lymphoma, multiple myeloma, and lung cancer.
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PMID:Hematotoxicity and carcinogenicity of benzene. 267 98


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