Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.1.1 (asparaginase)
 2,695 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This 35-year-old housewife was initially treated with vincristine, prednisolone and L-asparaginase for acute lymphoblastic leukemia (ALL, L1 by FAB classification) in 1988 and entered into complete remission. Ten months later she underwent bone marrow transplantation (BMT) from her HLA-identical and MLC-negative sister. The conditioning regimens consisted of busulfan 4 mg/kg/day for 4 days orally and cyclophosphamide 60 mg/kg/day for 2 days intravenously followed by cyclosporine and prednisolone for graft-versus-host disease prophylaxis. Fifty days after BMT, she suffered interstitial pneumonitis and a gastric ulcer, and was treated with a high dose of methylprednisolone and cimetidine. She experienced transient improvement, but soon cough, dyspnea and epigastralgia became worse. The specimens obtained by transbronchial alveolar lavage (BAL) and endoscopic gastric biopsy showed many giant cells containing inclusion bodies which were identified as cytomegalovirus (CMV). This time ganciclovir was started in addition to prednisolone. Then she gradually improved and after repeated BAL and the gastric biopsy after treatment showed no inclusion body in the specimen. Although leukocytopenia was significant for this patient, ganciclovir is considered to be useful for controlling CMV infection in both the lungs and stomach.
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PMID:[Good response to ganciclovir in a patient of cytomegalovirus (CMV) interstitial pneumonitis and gastric ulcer following allogeneic bone marrow transplantation for acute lymphoblastic leukemia]. 774 99

L-asparaginase is widely used in the treatment of acute lymphoblastic leukemia in children and adults. Use of L-aspa E. Coli as well as Erwinase is not possible in all cases because of the side effects, mainly allergic reactions and disfunction of pancreas. Recently, the new form of the enzyme PEG-L-asparaginase was introduced. Binding L-asparaginase E. coli to polyethylene glycol a decreased its toxicity, extended its plasma half-live, not significantly affecting the efficacy. The aim of the study was to examine the results of PEG-L-asparaginase administration in five children with acute lymphoblastic leukemia, and the symptoms of intolerance to L-aspa E. Coli or Erwinase. There were three children with newly diagnosed ALL and two children with first relapse of ALL, treated according to New York Protocol and BFM-90 Protocol for ALL relapses respectively. PEG-L-asparaginase (Oncaspar) was administered in the dose of 2500 IU/m2. According to the protocol four children received 11 courses of treatment with the full dose of the drug. The number of doses for individual patient varied from one to six. The short-lived nettlerash was observed in one patient during two subsequent infusions of the drug. Hydrocortisone and antihistamine drugs were administered. Treatment with PEG-asparaginase was discontinued in one child, who developed dyspnea, nausea, vomiting and face rash during the third dose of the drug. Oncaspar is the valuable drug, which enabled continuation of treatment according to protocol in four out of five children with bad tolerance to routinely used L-asparaginase preparations.
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PMID:[New possibilities of treatment with PEG-L-asparaginase in patients with acute lymphoblastic leukemia sensitized to l-asparaginase E.coli and erwinase]. 1073 74

There is an ever-increasing number of therapeutics used to treat cancer. A recent publication listed 86 currently available antineoplastic medications. Despite this large number, hypersensitivity reactions are not common except with platinum compounds (cisplatin, carboplatin), epipodophyllotoxins (teniposide, etoposide), asparaginase, taxanes (paclitaxel), and procarbazine. Doxorubicin and 6-mercaptopurine are occasionally associated with hypersensitivity reaction. Comparable reactions with other chemotherapeutic agents are. uncommon; many are only anecdotal reports. Reactions associated with individual drugs are discussed in detail. The mechanisms responsible for most of these reactions are not known, as they have generally not been evaluated. The term "hypersensitivity" is widely used in the chemotherapy literature without a common definition. Hypersensitivity is defined here as an unexpected reaction with signs and symptoms not consistent with known toxicity of the drug. Most reactions are coincident with or within hours of drug administration. Almost all are associated with parenteral administration. Symptoms include flushing, alterations in heart rate and blood pressure, dyspnea and bronchospasm, back pain, fever, pruritus, nausea and all types of rashes. Some cases may be due to non-immune mediated release of histamine or cytokines, as many patients can subsequently tolerate re-exposure after pretreatment with steroids and antihistamine, and slow readministration of the drug. This is more compatible with a graded challenge, than desensitization and is generally successful for taxanes, less so for platinum compounds. In most cases hypersensitivity reactions are associated with the specific chemotherapeutic drug. Reaction rates may vary with different forms of the drugs, e.g. pegylated. Occasionally excipients such as Cremaphor EL may induce hypersensitivity reactions.
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PMID:Hypersensitivity reactions to chemotherapeutic drugs. 1272 96

Drug hypersensitivity reactions (HSR) are adverse events resembling allergy which occur at therapeutic doses. Both anticancer chemotherapeutics and monoclonal antibodies have the potential for acute HSR. all infusion reactions involve the immune system; however, some (anaphylactic) are allergic in nature and usually are mediated by immunoglobulin E (IgE), whereas others (anaphylactoid) are not true allergic reactions and are not mediated by IgE. although HSR can be allergic or nonallergic, the clinical manifestations are the same and require prompt, accurate assessment and management to avoid severe adverse events, including fatality. Monoclonal antibodies have a unique side-effect profile that includes the potential for nonallergic HSR caused by cytokine release. Chemotherapeutic agents with the highest potential for acute HSR include the platinum salts, taxanes, procarbazine, asparaginase and the epipodophyllotoxins. From all anticancer agents, rituximab causes the majority of HSR (27%), followed by paclitaxel (10%). The most frequent symptoms in patients experiencing acute HSR include chest pain, dyspnea, wheezing and exanthema for the taxanes, dyspnea and exanthema for platinum salts, chills and rigor for antibodies. Patients with mild-to-moderate acute HSR can be rechallenged following intensified prophylaxis, but rechallenge is usually not recommended following severe HSR.
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PMID:Prevention and handling of acute allergic and infusion reactions in oncology. 2298 83