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)

Ninety-eight neutropenic patients were randomized to receive piperacillin and gentamicin in combination with either teicoplanin or flucloxacillin. Sixty-seven of these patients, most of whom had myeloma, were given this combination as prophylaxis 5 d after high dose chemotherapy, 35 receiving flucloxacillin and 32 receiving teicoplanin. Of 31 patients with leukaemia who were febrile and neutropenic following induction chemotherapy or bone marrow transplantation, 18 received flucloxacillin and 13 received teicoplanin. For those given flucloxacillin, the mean number of days to change of antibiotics was 7.8 in the prophylaxis group and 5.1 in the treatment group. In the teicoplanin arm, the mean number of days to change antibiotics was 6.8 in the prophylaxis group and 6.1 in the treatment group. Two patients in the flucloxacillin arm developed drug rashes. Four patients developed rigors after teicoplanin administration and one asthmatic became wheezy. One patient had a progressive rise in creatinine, but overall the patients having teicoplanin did not have any appreciable increase of renal toxicity compared to the flucloxacillin arm. Blood cultures were positive prior to commencement in the treatment group in nine patients, and during treatment in six patients. Organisms grown were Gram-positive in 14 patients. Teicoplanin appears to be as effective as flucloxacillin when each is used in combination with piperacillin and gentamicin in the treatment of neutropenic patients, with similar rates of toxicity.
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PMID:Teicoplanin compared to flucloxacillin for antibiotic treatment of neutropenic patients. 214 55

A single rising dose tolerance trial of rDNA interferon-alpha 2 (IFN-alpha 2) was conducted in eight patients with the diagnoses of non-Hodgkin's lymphoma (NHL), multiple myeloma, and chronic lymphocytic leukemia (CLL). Patients received a total of six i.m. doses at weekly intervals as follows: 1, 3, 10, 30, 60, and 100 x 10(6) IU. Patients were monitored at each dose level for serum IFN activity, anti-IFN antibodies, immunomodulation, clinical toxicity, and response. All patients exhibited clinical toxicity, including fever, chills, fatigue, headache, anorexia, mild-to-moderate leukopenia, nausea, and vomiting. Toxicity was dose-related, with significant side effects occurring in all patients at levels of 10 x 10(6) IU and above and some evidence of tachyphylaxis at higher doses. All side effects, including leukopenia and thrombocytopenia, were of short duration and were resolved within 3-5 days. Fevers, rigors, myalgias, and fatigue were partially alleviated by premedication with acetaminophen or hydrocortisone. Pharmacokinetic data indicated mean peak serum IFN titers greater than 90 at a dose of 10 x 10(6) IU and greater than or equal to 200 at doses greater than or equal to 30 x 10(6) IU 8 h after injection. No anti-IFN antibodies were detected. However, the serum levels achieved at higher doses were not linear, possibly indicating in vivo degradation. Total T cells, B cells, monocytes, and T subsets monitored by flow cytometry with monoclonal antibodies remained essentially constant throughout the trial. Although some patients demonstrated minor augmentations of antibody-dependent cellular cytotoxicity (ADCC) and natural killing (NK) activity at the lowest IFN-alpha 2 doses, the majority of patients demonstrated decreases in NK activity after higher IFN doses. No correlation between immunomodulation and clinical response to IFN was observed. At higher dose levels, the predominant immunomodulatory effect of IFN-alpha 2 was suppression of NK, ADCC, and blastogenic responses to T-cell mitogens and recall antigens. B-cell functional deficits as well as radioresistant T-helper and radiosensitive T-suppressor function assessed in a pokeweed mitogen-driven immunoglobulin secretion assay appeared unaffected by IFN administration. One myeloma patient showed progression and was discontinued after 60 x 10(6) IU. There were four patients (3 NHL, 1 myeloma) who achieved partial remission (greater than or equal to 50% tumor reduction) and three (1 CLL, 2 NHL) who showed objective tumor responses of less than 50%. These data suggest that rDNA IFN-alpha 2 is well-tolerated and may have significant antitumor activity against lymphoproliferative malignancies. Clin
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PMID:Immunomodulation by recombinant interferon-alpha 2 in a phase I trial in patients with lymphoproliferative malignancies. 660 23

Treatment options for lymphoproliferative disorders, including chronic lymphocytic leukemia (CLL), increasingly are based upon molecular targets, taking advantage of the immense research output over the past several years elaborating genetic abnormalities, downstream signaling, cell-surface immunobiochemistry, and microenvironmental stimuli. The latter targets have been particularly useful for the treatment of multiple myeloma, transforming a previously uniformly, fatal disease to one of a more chronic and potentially curable disorder. Subsequently, new treatment approaches are less likely to be based on the more classic types of cytocidal therapy, which, although successful and essential for the more aggressive disorders that are immediately life-threatening, tend to be less so, with respect to quality of life, risk versus benefit ratio and overall curability for the indolent diseases. Because the majority of newer agents are not available to the clinicians practicing in the community, a number of treatment options developed over the past two decades are capable of significantly improving the quality of life of patients with advanced CLL. The initial clinical approach to the patient should be based on performance status, age, comorbidities, and increasingly on prognostic factors elucidated over the past three decades. Initially, both simple laboratory studies and easily measurable clinical manifestations were used to guide the clinician (lymphocyte count, anemia, thrombocytopenia, enlarging lymph nodes, splenomegaly, hepatomegaly), and clinical staging systems were developed. At present a cadre of biologic factors, including cytogenetic alterations, gene expression profiles with subsequent immunoglobulin abnormalities, and expression of CD38 and Zap-70, are now available and are standard decision-making criteria to treat a patient with CLL. An initial period of observation allows the clinician along with the patient to gather all the information necessary to make an informed treatment decision. Frequently, a "watch and wait" approach, which for CLL does not appear to harm the patient, is the most appropriate decision. Complications of CLL, such as autoimmune hemolytic anemia and idiopathic thrombocytopenic purpura, will lead to treatment at least temporarily in those patients who might otherwise have not needed therapy. Frontline therapy will range from easily administrable single-agents to combination chemoimmunotherapy regimens. Experimental protocols, utilizing "post state of the art" treatments, are available in the form of research protocols at major treatment centers. At the present time, it is premature to recommend bone marrow ablative therapy as initial treatment unless the prognosis appears grave and the patient can withstand the rigors of this approach.
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PMID:Update on chronic lymphocytic leukemia: overview of new agents and comparative analysis. 2349 26