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)

A patient (E.M.) with marked eosinophilia and hyperimmunoglobulin E (IgE) has been followed for 4 years. Peripheral blood eosinophilia reached levels in excess of 18,000 cells/mm3 and serum IgE concentration increased to more than 210,000 units/ml (about 0.48 mg IgE/ml). The IgE has both lambda and kappa light chains and is therefore considered polyclonal. The patient has an increase in peripheral blood lymphocytes which stain for surface IgE. Transfer of the patient's plasma (plasmsEM) to a rhesus monkey did not induce peripheral boood eosinophilia. The half life of IgEEM in a rhesus monkey was 2.2 days, which is similar to the half life of myeloma IgE in human subjects. The condition was not associated with defined morbidity except for mild persistent pruritus. Various studies revealed no evidence for atopic parasitic, immune deficiency or neoplastic disease.
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PMID:Massive polyclonal hyperimmunoglobulinemia E, eosinophilia and increased IgE-bearing lymphocytes. 4 11

IgE antibodies can produce a late inflammatory response 6--12 h after allergen challenge which is characterized by diffuse edema, erythema, pruritus, tenderness and heat. That IgE is involved in inducing the late reaction was shown by the abolition of both immediate and late responses by passive transfer tests: (1) by heating atopic serum at 56 degrees C for 4 h; (2) by removing IgE from the atopic serum by a solid phase anti-IgE immunoabsorbent, and (3) by competitively inhibiting the binding of IgE antibodies to cells by an IgE myeloma protein. Also, both responses were induced by affinity chromatography-purified IgE antibody followed by antigenic challenge. Very similar lesions could be induced by intradermal injection of Compound 48/80. The late phase is characterized by edema and a mixed cellular infiltration, predominantly lymphocytic but also containing eosinophils, neutrophils and basophils. Direct immunofluorescent staining did not show deposition of immunoglobulins or complement components, except IgM in two of 15 and C3 in one of 15 patients, respectively.
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PMID:Late cutaneous reactions due to IgE antibodies. 33 13

IgE antibodies are usually thought to induce only immediate skin reactions. We have shown that the intradermal injection of a number of different allergens can produce a prolonged inflammatory reaction after the immediate wheal and flare in most sensitive subjects. This late inflammatory response occurs 6-12 h after challenge and is characterized by diffuse edema, erythema, pruritus, and heat. Both immediate and late responses can also be seen after passive sensitization of skin sites in nonatopic subjects. That IgE is involved in inducing the reaction was shown by the abolition of both immediate and late responses by passive transfer tests in the following experiments: (a) heating atopic serum at 56degreesC for 4 h, (b) removing IgE from the atopic serum by a solid phase anti-IgE immunoabsorbent, and (c) competitively inhibiting the binding of IgE antibodies to cells by an IgE myeloma protein. In addition, both responses were induced by affinity chromatography-purified IgE antibody, followed by antigenic challenge. Very similar lesions could also be induced by intradermal injection of Compound 48/80, thus suggesting a central role in the reaction for the mast cell or basophil. Histologically, the late phase is characterized by edema and a mixed cellular infiltration, predominantly lymphocytic but also containing eosinophils, neutrophils and basophils. Direct immunofluorescent staining did not show deposition of immunoglobulins or complement components, except IgM in 2 of 15 and C3 in 1 of 15 patients. This finding indicates that the late phase does not depend on the deposition of immune complexes. The results of the study suggest that IgE-allergen interaction on the surfaces of mast cells or on infiltrating basophils causes both immediate and late cutaneous responses.
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PMID:The late phase of the immediate wheal and flare skin reaction. Its dependence upon IgE antibodies. 78 99

Cutaneous lesions are present in up to 40% of patients with primary and myeloma-associated systemic amyloidosis and occur as a result of tissue deposition of immunoglobulin light chain material derived from a circulating paraprotein. The occurrence of waxy, purpuric mucocutaneous lesions provides a crucial early pointer to underlying occult plasma cell dyscrasia; the combination of the symptoms of the carpal tunnel syndrome, macroglossia, and specific mucocutaneous lesions is highly characteristic. Although secondary systemic (reactive) amyloidosis rarely gives rise to clinically evident cutaneous lesions, it may be etiologically related to a number of chronic dermatoses. Lesions of nodular primary localized cutaneous amyloidosis are indistinguishable from those of primary and myeloma-associated systemic amyloidosis, and they result from local plasma cell infiltration. Macular and papular (lichen amyloidosus) variants of primary localized cutaneous amyloidosis may have a familial or racial basis and are characterized by a tendency for keratinocytes to undergo filamentous degeneration and apoptosis. The prognosis of patients with plasma cell dyscrasia-related systemic amyloidosis remains poor, since there is little response to therapy with cytotoxic agents, colchicine, or dimethylsulfoxide. Colchicine is the drug of choice in the prevention and treatment of the renal amyloidosis associated with familial Mediterranean fever, and dimethylsulfoxide may be useful in the management of patients with secondary systemic amyloidosis. Macular amyloid and lichen amyloidosus generally follow a chronic course with intractable pruritus; there have been isolated reports of the beneficial effect of dermabrasion, topical dimethylsulfoxide, and therapy with the aromatic retinoid, etretinate.
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PMID:Amyloid and amyloidosis. 327 77

We describe the case of a young man of Calabrian origin, who came to our observation for the appearance of erythematous pustular, intensely itching, lesions on the arms, trunk and, in a less extent, on the face. The blood count revealed a differential cell count of 16.8% eosinophils. Serum IgE levels were elevated (1000 IU/ml), and T cell subsets showed an increase in CD8+ and a decrease in CD4+ with an inversion of CD4+/CD8+ ratio (= 0.78). The result of the following investigations were either normal or negative: anti-(ds)DNA antibody, anti-nuclear antibody, anti-smooth muscle antibody, anti-striated muscle antibody, serological tests for viral, bacterial, fungal and parasitic diseases and cultural examination of the material from lesion. Histopathological examination of a biopsy specimen from the left arm showed the presence of abundant perivascular inflammatory infiltrate in the dermis and inflammatory infiltrate, with numerous eosinophils, around sebaceous glands. Taken together, all these data suggest the diagnosis of eosinophilic pustular folliculitis, a dermatosis of unknown etiology, with a histopathological picture identical to Ofuji's disease. Eosinophilic pustular folliculitis can be associated with HIV infection or haematological diseases (as non-Hodgkin lymphomas, myeloma, etc.); it was also reported in adult immunocompetent healthy individuals and in children. On the basis of our findings, we propose that this case should be classified as an idiopathic form, as we were not able to demonstrate any associated disease.
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PMID:[Eosinophilic pustular folliculitis and Ofuji disease. A case report]. 750 2

Generalized or localized itch without primary skin manifestations may be the presenting symptom of serious internal diseases. Five characteristic cases of pruritus are discussed: Hodgkin's disease, primary sclerosing cholangitis, polycythemia vera, iron deficiency (with pica), and uremia. Other important causes must be considered; all forms of cholestasis, including primary biliary cirrhosis, drug-induced, pregnancy-related, and extrahepatic cholestasis; other hematologic and malignant disorders such as non-Hodgkin's lymphoma, leukemia, multiple myeloma, solid tumors, and myelodysplastic syndromes; metabolic and endocrine diseases, most notably diabetes mellitus, hyperthyroidism, hypothyroidism, and carcinoid syndrome; focal neurologic diseases such as brain tumors, cerebral infarctions and multiple sclerosis; adverse drug reactions without rash; infectious diseases, especially parasitic and HIV infections. A diagnostic laboratory screening for pruritus of undetermined origin is suggested.
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PMID:[Pruritus--also a challenge in internal medicine]. 852 44

Sweating aggravates itch in atopic dermatitis, but the mechanism is unclear. In this study, we examined the involvement of type I hypersensitivity in the aggravation of atopic dermatitis by sweating. Skin tests with autologous sweat were positive in 56 of 66 patients (84.4%) with atopic dermatitis, but only in 3 of 27 healthy volunteers (11.1%). Sweat samples from both patients and healthy volunteers induced varying degrees of histamine release from basophils of patients with atopic dermatitis. However, the histamine release was impaired by removal of IgE on the basophils. Incubation of basophils with myeloma IgE before sensitization with serum of patients blocked the ability to release histamine-induced sweat. IgE antibody against antigen(s) in sweat may be present in serum of patients with atopic dermatitis. Key words:
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PMID:IgE-mediated hypersensitivity against human sweat antigen in patients with atopic dermatitis. 1243 Jul 31

We present a case of a patient who presented concomitantly with generalized pruritus, brownish sclerodermatous plaques, sclerodactyly and a monoclonal band for IgG-kappa. The patient was diagnosed as having multiple myeloma by bone marrow examination. The rapidly progressive evolution with acute anuric renal failure, malignant hypertension and the skin sclerosis seem to be related to the neoplastic disorder. The scleroderma-like changes have to be differentiated from systemic scleroderma.
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PMID:Multiple myeloma with scleroderma-like changes. 1598 4

Multiple myeloma is a disease in which angiogenesis is postulated to be a target for therapy. Based on this hypothesis, we conducted a phase II trial of ZD6474 (Zactima; a VEGFR inhibitor) 100 mg p.o. daily in patients with relapsed multiple myeloma. The primary efficacy endpoint was objective response as assessed by reduction in M protein. There were 18 patients with a mean age of 64 years. One patient was ineligible and one was not evaluable. Overall, ZD6474 was well tolerated and pharmacokinetic testing demonstrated that adequate drug levels were achieved. The most common drug-related adverse events were nausea, vomiting, fatigue, rash, pruritus, headache, diarrhea, dizziness, and sensory neuropathy, all of which were Grade I-II in severity. There were no drug-related serious adverse events. Laboratory adverse events were infrequent: one patient had Grade III anemia, and there were no Grade III changes in biochemistry. No significant QTc interval changes were seen. There were no responses in M protein levels. In conclusion, ZD6474 was well tolerated at a dose of 100 mg per day and achieved plasma levels predicted to inhibit VEGF signaling. However, this was not reflected in clinical benefit since none of the patients had a reduction in M protein.
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PMID:A phase II study of ZD6474 (Zactima, a selective inhibitor of VEGFR and EGFR tyrosine kinase in patients with relapsed multiple myeloma--NCIC CTG IND.145. 1679 11

Clinical manifestations of liver involvement in multiple myeloma (MM) are uncommon. Rare cases of MM present as acute liver disease. We report a case of a 55-year-old woman with MM who presented with painless jaundice, mild pruritus, and abnormal liver function tests resembling acute cholestatic hepatitis without the stigmata of chronic liver disease. Initial laboratories included elevated liver function tests (aspartate aminotransferase 74 U/L and alanine aminotransferase 45 U/L) and an elevated white blood cell count of 19,600 cells/microL with 33% circulating plasma cells. Myeloma parameters demonstrated an immunoglobulin G lambda monoclonal protein with lambda light-chain Bence-Jones proteinuria. Bone marrow was hypercellular with 70% plasmacytosis. A liver biopsy revealed a diffuse portal and sinusoidal infiltration of plasma cells with lambda light-chain restriction. In this report, we review the literature of liver involvement in MM.
Clin Lymphoma Myeloma 2007 Sep
PMID:Liver involvement in multiple myeloma. 1802 72


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