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 biological response modifier (BRM) has been defined as an agent able to modulate effector mechanisms or mediators of host defence. Some antibiotic molecules have been shown to display a BRM like activity, being able to enhance immune responses (certain cephalosporins), to synergize with the immune effectors (macrolides, quinolones) or alternatively, to depress immune functions (tetracyclines or antimycotic drugs). The BRM-like activity of different antibiotic molecules has been widely reported in in vitro studies as well as ex vivo in experimental animal models. Only recently some Authors have approached the problem by investigating whether the in vivo administration of antibiotic was able to affect different immune effector functions, either in healthy subjects or in patients. The main question in the field is the possible clinical impact of the connections between antibiotics and the immune system, particularly in subjects with acquired immunodeficiency in whom the impairment of the immune responses leads to increased susceptibility to infectious processes. Ex vivo data seem to suggest that cefodizime, one of the newest third-generation cephalosporins, is able to enhance phagocyte and mononuclear cell functions in healthy volunteers, thus confirming the possibility of combining an antibacterial efficacy with the ability to restore or enhance immune responses. Comparable data in studies investigating the effect of cefodizime on immune functions in immunocompromised patients such as elderly subjects, hemodialyzed or diabetic patients, BPCO subjects, patients undergoing surgical stress and patients with multiple myeloma are more important from a practical clinical point of view.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immune response to antibiotics in patients with secondary immunodeficiencies]. 786 Dec 3

In vitro data have demonstrated autologous T-lymphocytes with anti-tumour activity in multiple myeloma (MM). Therefore a phase I/II trial was conducted to study the feasibility, the effect on several immunological parameters, and the tumour response induction of low-dose recombinant interleukin-2 (rIL-2) in MM patients. 18 MM patients of advanced stages in progress, who had failed on standard chemotherapy received 9 x 10(6) IU/m2 rIL-2 twice daily on days 1 and 2 and 0.9 x 10(6) IU/m2 twice daily for 5 subsequent days per week subcutaneously from days 3 to 56 (repeated every 12 weeks until progression). Patients were treated for between 8 and 1086 + d (mean 241 d) without serious side-effects. 6/17 patients experienced tumour response (2/17 objective tumour mass reduction, 4/17 long-lasting stable disease following tumour progression before initiation of rIL-2 treatment). During therapy the number of eosinophils increased 15-fold, CD4+ T lymphocytes were activated as demonstrated by enhanced CD25 antigen expression, and CD56+ NK cells expanded in the peripheral blood. Furthermore, a diminished pre-treatment ratio of CD4+/CD8+ lymphocytes was normalized during rIL-2 treatment. NK cell activity and lymphokine activated killer (LAK) cell activity was significantly enhanced. Endogenous IL-2 production and elevated soluble IL-2 receptor serum concentrations were induced. Low-dose rIL-2 can stimulate immune enhancement in MM despite the characteristic tumour-induced immunodeficiency. The treatment has proven though limited efficacy in advanced MM. Because most of the responders experienced termination of tumour progression rather than tumour regression, rIL-2 maintenance of chemotherapy-induced remissions should be investigated.
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PMID:Low-dose recombinant interleukin-2 therapy in advanced multiple myeloma. 787 83

A clinical course of herpes zoster in hematological patients (chronic lympholeukosis, lymphogranulomatosis, acute leucosis, myeloma disease, chronic agranulocytosis) is presented. These patients exhibited a more severe course of herpes zoster that is caused by immunodeficiency state. It is judicious to treat the patients with reaferon.
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PMID:[Herpes zoster in hematology patients]. 819 11

Infection with human immunodeficiency virus type 1 (HIV-1) primarily involves a subgroup of T-lymphocytic cells, but other cell types are also invaded by the virus, including cell lines within the haematopoietic system. Together with infectious, inflammatory and neoplasic processes, invasion of haematopoietic tissue explains the haematological alterations which are seen during the course of infection with HIV-1. Anaemia develops in the large proportion of patients. Thrombocytopenia frequently occurs during the course of the disease, but may be seen in some patients already at the time of diagnosis, where the condition may be misdiagnosed as "idiopathic" thrombocytopenic purpura. Neutropenia is seen in all disease stages, but is most severe in patients with advanced disease. Bone marrow changes include varying degrees of dysplasia in one or more cell lines, which in some patients may mimic a myelodysplastic syndrome. The number of plasma cells is always increased. In many patients the bone marrow stroma exhibits an increased amount of reticular fibres. HIV-1 infection is associated with an increased risk of non-Hodgkin malignant lymphoma. Acute myelogenous leukaemia and myelomatosis have been described in patients with advanced disease. Treatment of the above mentioned haematological abnormalities aims primarily at reducing replication of HIV-1, thereby diminishing suppression of haematopoiesis by the virus infection, and at controlling the opportunistic infections during the course of the disease. Specific antiviral therapy (AZT) is most successful in correcting thrombocytopenia. The possibility of bone marrow suppression mediated by a toxic drug effect should always be considered in this patient group.
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PMID:[Hematological changes associated with human immunodeficiency virus (HIV-1) infection]. 831 70

Although a normal or increased anion gap (AG) is commonly used to help assess acid-base balance, decreased AG has aided in the diagnosis of halogen ingestion and myeloma. Substantially increased levels of IgG cause a decrease in the AG. Patients with polyclonal increases in immunoglobulins, especially hepatic cirrhosis, also exhibit decreased anion gaps. Patients with human immunodeficiency virus (HIV) infection commonly show polyclonal increases in immunoglobulins. A case is reported of a patient with HIV infection who exhibited a decreased AG associated with increased polyclonal IgG (63 g per L). Unlike the electrophoretic profile of patients with hepatic cirrhosis, which commonly shows a beta-gamma-globulin bridge, reflecting a decreased immunoglobulin degradation, the profile of the patient with HIV infection was consistent with an increased immunoglobulin synthesis. Examination of sera from 18 additional HIV positive patients indicated that, in general, the AG of HIV infected patients with normal renal function is significantly higher than in normal persons. The significance of this finding is as yet unclear. Nevertheless, decreased AG was associated with increased IgG. This may complicate the use of the AG in evaluating HIV infected patients because of frequent elevations in IgG. These relationships are now in the process of further investigation. Nevertheless, it is suggested that, with appropriate history and physical, identification of a decreased anion gap in conjunction with a polyclonal increase in gamma-globulin may be reason to consider a work up for infection by HIV.
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PMID:Human immunodeficiency virus infection and anion gap. 837 29

There is growing evidence that in multiple myeloma (MM) tumor-directed immune responses exist, might influence tumor progress and could be putative targets for immunotherapeutic approaches. Peripheral blood T lymphocytes are capable of suppressing monoclonal immunoglobulin production of autologous myeloma plasma cells in vitro. This activity can be enhanced by stimulation with mitogens, OKT3 monoclonal antibody or interleukin 2 (IL-2), and is obviously mediated by cytolytic T lymphocytes as demonstrated in a cytotoxicity assay using purified MM plasma cells as targets. The lytic activity is significantly higher when the effectors are prestimulated with irradiated autologous MM plasma cells. Based on these results 18 MM patients of advanced stages with tumor progress received 9 x 10(6) IU/m2 recombinant IL-2 (Proleukin) twice daily on days 1 and 2 and 0.9 x 10(6) IU/m2 twice daily for five subsequent days per week s.c. from days 3-56 (q 12 weeks). During therapy the number of eosinophils increased 15-fold, CD4+ T lymphocytes were activated as demonstrated by CD25 antigen expression and CD56+ natural killer (NK) cells expanded in the peripheral blood. NK cell activity and lymphokine-activated killer cell activity were significantly enhanced. IL-2 therapy induced endogenous IL-2 production and elevated soluble IL-2 receptor serum concentrations. Tumor response was observed in 6/17 evaluable patients. These data indicate that low-dose IL-2 treatment can stimulate immune enhancement in MM patients despite their characteristic tumor-induced immunodeficiency, and has proven to have limited efficacy in advanced MM patients.
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PMID:Tumor-directed cytotoxicity in multiple myeloma--the basis for an experimental treatment approach with interleukin 2. 852 May 15

A 58-year-old man was admitted to our hospital because of recurrent pulmonary infections that began three years previously. Laboratory data showed hypogammaglobulinemia and a chest computed tomogram showed diffuse bilateral micronodular shadows and an anterior mediastinal tumor. Immunodeficiency with thymoma (Good's syndrome) was diagnosed. After undergoing a thymectomy, he received intravenous gamma-globulin injections once a month for prophylaxis. Good's syndrome occurs rarely in Japan. A solid tumor-like shadow is not necessarily observed in routine chest X-ray studies, and hypogammaglobulinemia is one sign of this syndrome. The hypogammaglobulinemia of Good's syndrome should be carefully differentiated from that of other immunodeficiency diseases such as common variable immunodeficiency, the acquired immunodeficiency syndrome, chronic lymphocytic leukemia, non-Hodgkin's lymphoma, and multiple myeloma (non-secretory type).
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PMID:[Immunodeficiency with thymoma (Good's syndrome) similar to sino-bronchial syndrome]. 881 Jul 67

Necrotizing fasciitis is a rare but often fatal soft-tissue infection primarily involving the superficial fascia and fat tissue resulting in extensive undermining of surrounding tissues. Skin is initially spared, but as necrotizing fasciitis spreads, all the soft-tissue components, including the skin, become involved. The progression of necrotizing fasciitis is often fulminant, and the prognosis depends to a large extent on the rapidity of correct diagnosis and surgical treatment (debridement). Most of the patients affected with necrotizing fasciitis have some risk factors: chronic general or local diseases, leukopenia, immunodeficiency diseases, malignancies, and an age of 50 years or more. The author reported the occurrence of necrotizing fasciitis in a 69-year-old man with multiple myeloma during the granulocytopenic phase after chemotherapy. The successful treatment of necrotizing fasciitis in the present case relied not only on surgical debridement, but also on G-CSF administration.
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PMID:[Multiple myeloma complicated by necrotizing fasciitis]. 896 Jun 67

A 63-year-old Japanese male with a four-year history of asymptomatic hypogamma-globulinemia is presented. On admission, he had a mild bone marrow plasmacytosis at about 10% of the total nucleated cells, but had no anemia, no paraproteins nor bone lesions. Flow cytometric analysis showed a predominant proliferation of kappa chain-positive cells in the bone marrow and peripheral blood, and an increase in the proportion of natural killer cells in the peripheral blood. Furthermore, coexistent meningioma and transitional cell carcinoma of the bladder were subsequently found 9- and 15-months after the admission, respectively. We considered that a myeloma-induced, possible latent immunodeficiency may have allowed the additional tumor growth, and that this process may have been controlled by the cytotoxic subset of immune effector cells.
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PMID:Asymptomatic multiple myeloma with concomitant neoplasms of two different origins. 898 71

Bilateral multiple parotid calculi, which are uncommonly diagnosed in the normal population, have never been reported in patients infected with human immunodeficiency virus. Herein we report a case of bilateral parotid sialolithiasis in a patient who had acquired immunodeficiency syndrome and was affected by multiple myeloma. The possible etiopathogenesis in view of the alterations of immunity, oral pH, and salivary composition that are observed in multiple myeloma and in human immunodeficiency virus infection are discussed.
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PMID:Bilateral parotid sialolithiasis in a patient with acquired immunodeficiency syndrome and immunoglobulin G multiple myeloma. 915 14


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