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)

Circulating histamine-releasing factors have been identified in the serum and plasma of chronic-urticaria patients by in vivo skin testing and in vitro histamine release from heterologous mixed leukocytes. Quantitative mast cell studies of serum skin test biopsies and electron microscopy indicate that the serum factors release histamine by mast cell degranulation. Peripheral blood basophils and total cellular blood histamine are reduced in chronic-urticaria patients suggesting that the circulating serum factors cause sustained degranulation. Histamine-releasing activity has been identified by skin testing in ultrafiltered serum fractions less than 30 kDa and greater than 100 kDa. In vitro histamine-releasing activity was confined to ultrafiltered serum fractions greater than 100 kDa and was present in IgG purified from some chronic-urticaria sera by protein G affinity chromatography. The dose-response relationship and kinetics of histamine release in vitro were similar to those of anti-human IgE. 'Desensitisation' of basophils by prior incubation with anti-IgE in the absence of calcium and competitive inhibition studies with myeloma IgE serum indicated that histamine-releasing autoantibodies in chronic-urticaria sera and purified IgG have the properties of anti-IgE. Plasma exchange in 4 patients with active chronic urticaria refractory to antihistamine therapy showing in vivo and in vitro histamine-releasing activity was followed by temporary remission of disease activity in 2 of them. It is possible that chronic urticaria is an autoimmune disease.
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PMID:Histamine-releasing autoantibodies in chronic urticaria. 172 16

Three patients with multiple myeloma were treated with recombinant alpha-interferon (r IFN-alpha 2b Intron AR) along with combination chemotherapy i.e. melphelan and prednisolone. In one case it was given as an initial therapy, while the other two patients had refractory and relapsing disease respectively. IFN-alpha 2b was given in the dose of 2 x 10(6) Mu/m2 by subcutaneous injection thrice in a week for six months in two patients and for three months in one patient. All three patients experienced improvement in bone pains; partial response with reduction in the paraprotein level was seen in one patient; while there was no radiological, biochemical or haematological improvement in two patients. Side effects noted were flu like syndrome in all three patients and urticaria in one patient. They were treated symptomatically and did not require cessation of interferon therapy.
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PMID:Recombinant alpha-interferon therapy in multiple myeloma. 209 May 74

The prevalence of autoantibodies of immunoglobulin G (IgG) and immunoglobulin M (IgM) classes directed against myeloma immunoglobulin E (IgE) were determined in distinct subsets of urticaria, using an enzyme immunoassay. IgG anti-IgE antibodies were found in five of nine patients (55%) with cold urticaria, four of eight patients (50%) with urticarial vasculitis, and three of six patients (50%) with chronic urticaria. IgM anti-IgE antibodies were found exclusively in cold urticaria (two of nine patients, 22%). Heating of these sera increased the binding to IgE, suggesting immune complex formation. Several positive sera were capable of inducing histamine release from normal peripheral basophils and caused a wheal-flare response upon intradermal injection. Sera containing such autoantibodies from three cold urticaria patients were studied for passive transfer of cold sensitivity. One serum containing IgG anti-IgE gave a strongly positive transfer test at 5 h but not 48 h, suggesting a pathogenic role for the IgG.
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PMID:Prevalence and functional role of anti-IgE autoantibodies in urticarial syndromes. 244 92

We report a case of IgG multiple myeloma with selective complete Clq deficiency. The patient was a 75-year-old Japanese woman who exhibited urticaria on the arm and an absence of serum hemolytic complement activity (CH50). Further studies revealed no vasculitis in the urticarial lesion but showed selective complete deficiency of Clq without low molecular weight Clq precipitin. Addition of highly purified Clq restored the CH50 level of the patient's serum to normal. It is suggested that this abnormality was a primary Clq deficiency. We discussed a relationship between the Clq deficiency and myeloma and reviewed the literature.
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PMID:Complete Clq deficiency associated with IgG multiple myeloma. 278 87

The First National Health and Nutrition Examination Survey (NHANESI), conducted in 1971-1975, included a cohort of 6913 adults for whom history of smoking, allergies, and other factors was obtained. These persons were traced (with 93% success) approximately 10 years later by the NHANESI Epidemiologic Followup Survey, and incidence of malignancy in the interim period was determined. Primary allergy variables were physician-diagnosed asthma, hay fever, hives, food allergy, or other allergies. Excluded were persons with a prior history of cancer and cases of nonmelanoma skin cancer. After adjustment by logistic regression for age, sex, race, and smoking history, allergic history was found to increase the risk of subsequent malignancy (risk odds ratio = 1.40, 95% confidence interval = 1.10-1.77). The specific allergy type with the strongest cancer risk was hives. The cancer group with the strongest allergy association was lymphatic-hematopoietic (leukemia, lymphoma, myeloma). The risk odds ratio of developing leukemia, lymphoma, or myeloma for persons with hives history was 7.89 (95% CI = 3.13-19.89). These findings suggest that a history of allergy does not protect against subsequent cancer, and may be a risk factor. The possibility is raised that a history of hives may be a particular risk factor for lymphatic-hematopoietic malignancies.
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PMID:Allergy and risk of cancer. A prospective study using NHANESI followup data. 338 43

Aclacinomycin A (ACM-A), an anthracycline analog, was given to 17 patients with solid tumors and to one patient with multiple myeloma, in a phase I clinical trial. A single dose of 60-120 mg/m2 was given every 3 weeks. Dose-limiting toxicity was myelosuppression, especially thrombocytopenia. Granulocytopenia was variable and did not always recover by Day 21 in time for the next ACM-A treatment. Other toxic effects were nausea, vomiting, urticaria, and elevation of hepatic enzymes. Alopecia was not a side effect, even in patients receiving multiple courses of ACM-A. Nine patients were monitored with 24-hour continuous ECG recordings (Holter) on 19 ACM-A treatment days. The incidence of premature atrial and ventricular beats was significantly increased following ACM-A administration. In addition, one patient developed episodes of high-degree atrioventricular block and complete heart block after each of four ACM-A doses, necessitating the insertion of a pacemaker. No antitumor responses were seen in the ten patients who had measurable disease and who had received two or more courses of ACM-A. The recommended doses for solid tumor phase II studies are 100 mg/m2 as a single dose every 4 weeks for patients with high performance status and minimal prior chemotherapy and 60 mg/m2 every 4 weeks for all other patients. Until the acute cardiac effects of ACM-A are further understood, we recommend that all patients receiving ACM-A be monitored by ECG recordings.
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PMID:Phase I trial of aclacinomycin A. 695 61

9,10-Anthracenedicarboxaldehyde bis[(4,5-dihydro-1H-imidazol-2-yl)hydrazone] dihydrochloride (bisantrene) is a new anthracene bishydrazone derivative which was entered into a Phase I clinical trial (one dose weekly for 3 weeks) because it showed significant antitumor activity in a number of animal tumor models and in vitro in the human tumor stem cell assay. When possible, patients were entered into the phase I study if their tumors showed in vitro sensitivity to bisantrene and resistance to standard agents, using a human tumor stem cell assay. Thirty-one patients were treated with bisantrene over a 10-month period, starting at a dose of 70 mg/sq m/week. The appearance of leukopenia determined the dose-limiting toxicity of bisantrene. The maximally tolerated dose appeared to be 200 mg/sq m in that three of five patients tolerated these weekly-for-3-weeks doses while experiencing only mild or moderate leukopenia. In contrast, the 220-mg/sq m dose caused moderate to life-threatening leukopenia after just two weekly doses in four of five patients. Local bisantrene toxicity included mild to severe arm swelling, phlebitis, pain, urticaria, and erythema in 68% of the patients. In general, these toxicities were well tolerated and rapidly reversible, but two patients had severe local swelling for up to 6 months. In this Phase I trial, bisantrene showed clinical antitumor activity against both hematological cancer (i.e., lymphoma and myeloma) and solid tumors (i.e., bladder, lung, and renal cancer and melanoma). Of importance, four of the six responses occurred in patients whose therapy was selected on the basis of in vitro sensitivity to bisantrene using the human tumor stem cell assay. One patient with disseminated melanoma had complete disappearance of an axillary node metastasis (for more than 6 months) while developing a brain metastasis, suggesting that bisantrene does not concentrate in the central nervous system.
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PMID:Phase I clinical investigation of 9,10-anthracenedicarboxaldehyde bis[(4,5-dihydro-1H-imidazol-2-yl)hydrazone] dihydrochloride with correlative in vitro human tumor clonogenic assay. 703 74

Cryoglobulins are proteins that precipitate when cooled and dissolve when heated. Cryoglobulinemia may be classified into Type I (monoclonal), Type II (mixed), and Type III (polyclonal). About 5 to 10% of myeloma proteins and 7 to 20% of primary macroglobulinemia proteins are cryoprecipitable (Type I cryoglobulin), and more than half of these have no symptoms attributable to cryoglobulin nature of their M-component. The most common symptoms of Type I cryoglobulinemia include Raynaud's phenomenon, necrosis of the toes or legs, vascular purpura, and urticaria. In Type I cryoglobulinemia due to plasma cell dyscrasias, treatment is directed primarily at the underlying disease. Plasmapheresis and cryofiltration may be helpful particularly when this can be combined with effective chemotherapy.
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PMID:[Cryoglobulinemia]. 769 15

Since several forms of autoimmunity have been associated with urticaria, we performed a detailed survey of autoantibodies in patients with idiopathic subacute and chronic urticaria. Sera from 25 consecutive patients referred for evaluation of urticaria were tested for the presence of autoantibodies and compared to sera from seventy-five control samples examined from individuals being treated for other allergic diseases. Study patients ranged in age from 15 to 73 years, with a mean of 48. One patient had a diagnosis of inflammatory bowel disease and one had multiple myeloma, but otherwise there were no other diagnoses of disease specifically involving immunity other than atopy. No study patients had a concurrent diagnosis of autoimmune thyroid disease. The test sera were examined for autoantibodies and for antibodies to H. pylori. Antibodies to thyroid peroxidase (TPO) were found significantly (p < 0.01) more common in urticaria (20%] than in controls (0%). Rheumatoid factor(RF) was also found in significantly (p < 0.05) increased in urticaria (16%) compared to controls [0%). Neither H. pylori antibody nor other autoantibodies were present in significant numbers of urticaria patients when compared to controls. Tested autoantibodies included those to thyroglobulin, sDNA, SSA/SSB, ENA, cardiolipin, beta2-glycoprotein I, myeloperoxidase, proteinase-3, smooth muscle, ANA, human lysosomal-associated membrane protein, and bactericidal permeability increasing protein. Thus, patients with urticaria were somewhat more likely to have a thyroid autoantibody to TPO or to have RF. This survey demonstrates that while some markers of autoimmunity may be increased in urticaria patients, broad nonspecific autoimmunity is not found.
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PMID:Are autoantibodies present in patients with subacute and chronic urticaria? 1143 65

Plasma cell leukemia (PCL) is a very rare variant of multiple myeloma (MM) occurring in about 2% of newly diagnosed patients. Plasma cell leukemia may develop during the course of MM (secondary PCL) or it can occur without any prior sign of MM (primary PCL). We report a case of aggressive primary PCL with unusual clinical, cytogenetic and molecular features. A 36-year-old male patient was first seen because of fever and bone pain. On the skin of his chest, back, abdomen, and palpebras, there were nodular infiltrations resembling urticaria. White blood cell count was 10.8 x 10(9)/l with 41% plasmacytes. Bone marrow aspiration was hypercellular, 93.5% of cells were atypical plasmacytes and plasmablasts. The cytogenetic analysis of G-banded chromosomes in bone marrow cells yielded the trisomy 8. The skin biopsy specimen showed intensive infiltrates of uninucleated blastic cells similar to those found in the bone marrow. Immunophenotyping of bone marrow and skin neoplastic cells showed CD45+, CD45Ro+, CD68+, CD38+ and cytoplasmic kappa light chain +. The neoplastic cells stained negatively for lambda light chain, CD3, CD20, CD30, EMA, CD15, CD34, CD56 and factor VIII. The pattern of IgL genes rearrangement in the bone marrow aspirate, peripheral blood mononuclear cells, and skin specimens was examined by PCR analysis. All studied specimens showed three different IgK gene configurations suggesting that the neoplastic cells originated as a result of oligoclonal lymphoproliferation process. The patient received two courses of VAD (vincristine, doxorubicin, dexamethasone) without improvement and three courses of CHOP with only temporary stabilization of the disease. He died 5 months after the diagnosis of PCL because of disease progression and pneumonia.
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PMID:Aggressive primary plasma cell leukemia with skin manifestations, trisomy 8 and molecular oligoclonal features. 1214 88


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