Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To define the maximum tolerated dose and to study whether recombinant human interleukin-3 (rhIL-3) reduced chemotherapy-induced neutropenia and thrombocytopenia, 20 chemotherapy-naive patients with advanced ovarian cancer eligible for treatment with 6 cycles of carboplatin-cyclophosphamide every 4 weeks (day 1) were entered in a phase I/II open, single-center trial. Cohorts of five patients received during 7 days 1, 5, 10, or 15 micrograms/kg/d rhIL-3 (days 5 through 11) in cycles 1, 3, and 5 by continuous intravenous (IV) infusion or once daily subcutaneous (SC) administration. In control cycles 2, 4, and 6, no rhIL-3 was administered. rhIL-3 significantly increased the recovery of leukocyte, neutrophil, and platelet counts, especially at 5, 10, and 15 micrograms/kg rhIL-3. rhIL-3 also increased basophil, eosinophil, monocyte, and lymphocyte counts at this dose steps. Effects on reticulocytes were limited. No difference in efficacy between SC and IV rhIL-3 treatment was found. Chemotherapy postponement for insufficient bone marrow recovery was necessary in 22 of 45 control cycles versus 2 of 49 rhIL-3 cycles (P less than .001). Platelet transfusions were required in 7 of 45 control cycles versus 3 of 50 rhIL-3 cycles (P less than .5). rhIL-3 up to 10 micrograms/kg/d could be administered without severe side effects. At 15 micrograms/kg/d, rhIL-3 headache was dose-limiting. Other side effects were fever, flu-like symptoms, nausea, skin rash, flushing, facial erythema, and urticaria. Liver toxicity occurred in rhIL-3 and control cycles. rhIL-3 slightly increased tumor necrosis factor alpha, C-reactive protein, and serum amyloid A plasma levels, whereas no effect on IL-6 plasma levels was observed. rhIL-3 administered SC appears to be an interesting hematopoietic growth factor for reduction of chemotherapy-induced myelotoxicity.
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PMID:Effects of interleukin-3 after chemotherapy for advanced ovarian cancer. 151 36

In the last 10 years 63 courses (283 infusions) of porcine FVIII were given to 25 hemophiliacs with high titer alloantibodies and to 5 patients with autoantibodies to factor VIII. Although the product was in general clinically efficacious, adverse effects of treatment were more frequent and severe than previously reported. After 63 courses there was a median percentage fall in baseline platelet count of 54% (range 8-86%); for 10 courses (16%), thrombocytopenia was severe or moderately severe (less than 100 x 10(9)/l), with nadirs of platelet count ranging from 10 to 99 x 10(9)/l (median 67). Allergic reactions were seen in 15 of 30 patients (50%), in 20 of 63 courses (32%), more frequently but not exclusively after the first infusion. Relatively mild symptoms (fever, flushing, urticaria, shivering) occurred in 15 courses; 5 courses, however, were accompanied by more severe anaphylactoid reactions, 2 of which required resuscitation therapy. Allergic reactions were observed both in patients pretreated with steroids or anti-histamines (in 7 of 18 courses, 39%) and in nonpretreated patients (in 13 of 45 courses, 29%). In conclusion, adverse reactions are frequent after porcine FVIII (in 30 of 63 courses, 47%), and can occur also with infusions subsequent to the first. Hence, the recently proposed use of porcine FVIII as home treatment should be implemented with caution.
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PMID:Adverse effects of treatment with porcine factor VIII. 190 52

Side-effects of proguanil reported to the Swedish Adverse Drug Reaction (ADR) register from 1981 to 1988 are described and related to sales figures of the drug in Sweden during the same period. One serious reaction, thrombocytopenia, and 7 minor reactions, mainly urticaria and exanthema were believed to be causally related to proguanil intake in an estimated 60,000 users of the drug. Proguanil can be considered a very safe drug but rare hematological side-effects may possibly occur.
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PMID:How safe is proguanil? A post-marketing investigation of side-effects. 195 33

To determine the maximum tolerated dose (MTD) of trimetrexate glucuronate in combination with cyclophosphamide in patients with metastatic or inoperable nonsmall cell lung cancer (NSCLC), trimetrexate in dosages ranging from 3 to 13.5 mg/m2/day was administered intravenously (IV) to 27 patients for 5 days in combination with cyclophosphamide, 600 mg/m2, on day 1. Patients received between one and six courses of treatment at 3 week intervals, 69 treatment courses in all. Hematological toxicity was mainly mild anemia (81%), leukopenia (67%), and thrombocytopenia (52%). Nonhematological toxicity included nausea and vomiting (67%), mucositis (30%), and urticaria or rash (22%). The incidences of leukopenia and mucositis were dose related. The MTD of trimetrexate in combination with cyclophosphamide was 7.5 mg/m2/day. The dosage chosen for the Phase 2 study, based only on the hematological dose limiting toxicity, was 10.5 mg/m2/day. Of 31 patients with previously untreated metastatic or inoperable NSCLC who have entered in the Phase 2 study, 22 are evaluable for clinical efficacy (World Health Organization criteria, 1979). Treatment was discontinued in four patients because of toxicity. One patient refused further therapy. Four patients are too early to evaluate. Five patients had confirmed partial responses (23%), 12 patients achieved stable disease (54%), and five patients had progressive disease. Results suggest that trimetrexate 10.5 mg/m2/day in combination with cyclophosphamide is active against previously untreated NSCLC. Dose limiting toxicity was mucositis and myelosuppression. An 11 item linear analogue scale assessing quality of life during treatment indicated this combination was well accepted by patients and did not compromise quality of life. The Phase 2 study is continuing.
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PMID:Trimetrexate and cyclophosphamide for metastatic inoperable nonsmall cell lung cancer. 283 17

A phase I study of carboplatin (CBDCA) was performed in 40 children with advanced cancer. A single course of CBDCA consisted of 4 weekly 1-hour infusions followed by a 2-week rest. The starting dose of 100 mg/m2/week was 66% of the maximum tolerated dose in adults. Escalated dose levels given were: 125, 150, 175, and 210 mg/m2. Myelosuppression was dose limiting, with thrombocytopenia more pronounced than leukopenia. There was no evidence of cumulative toxicity. The maximum tolerated dose for children with solid tumors was 210 mg/m2/week X 4. Other side effects included transient nausea and vomiting at the higher dose levels and non-dose-related, reversible changes in creatinine clearance. One patient developed hives. No hepatic toxicity was seen. Among the 28 evaluable patients with solid tumors, one of ten with osteogenic sarcoma had complete disappearance of a lung nodule for 15+ months. Two of four patients with medulloblastoma had partial responses by clinical and computerized tomographic scan for 4 and 10 months. All three responders had received prior cisplatin therapy. CBDCA has major advantages over cisplatin in terms of reduced toxicity. Responses observed in patients previously treated with cisplatin are encouraging. The recommended phase II dose for children with solid tumors is 175 mg/m2/week X 4 with a 2-week rest.
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PMID:Phase I study of carboplatin (CBDCA) in children with cancer. 352 46

Excluding the most frequent kinds of problems seen with the nonsteroidal antiinflammatory drugs (NSAID)--gastritis, peptic ulceration and renal effects--published reports indicate that these drugs may cause a wide variety of rare adverse reactions. The most serious of these are hypersensitivity reactions: blood dyscrasias (aplastic anemia, thrombocytopenia, agranulocytosis, hemolytic anemia), erythema multiforme and hepatitis. Aseptic meningitis and anaphylactoid reactions may strike patients with underlying immunologic abnormalities; urticaria, bronchospasm and proctocolitis may affect aspirin-sensitive patients. Other unusual reactions include several kinds of bullous dermatitis, febrile reactions, pneumonitis, esophageal ulceration, parotitis, pancreatitis and neurological or psychological effects.
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PMID:Rare adverse reactions to nonsteroidal antiinflammatory drugs. 398 96

We report our experience with 8 patients with Felty's syndrome who were treated with D-penicillamine for a mean of one year. Six of the 8 patients experienced improvement in their neutropenia. Cutaneous ulcers healed in 4 of 6, while recurrent infections cleared in 3 of 5 patients. The drug was withdrawn in 6 patients--lack of response in one, thrombocytopenia in one, urticaria in one, rash in one, and granulocytopenia in 2. One of the latter 2 patients developed pancytopenia and died. Although D-penicillamine is effective in treatment of Felty's syndrome, its side effects can be serious and potentially lethal. Its use should be limited to patients who have failed other treatments.
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PMID:D-penicillamine in Felty's syndrome. 405 91

The most important side effects during AHLG-treatment of 34 children suffering from juvenile chronic arthritis, collagenoses, autoimmune chronic hepatitis, aplastic anaemia and acute lymphoblastic leukemia are: Thrombocytopenia, urticaria, fever, anaphylactic reaction. They all are reversible a short time after cessation of AHLG-administration.
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PMID:[Side effects of therapy with antihuman lymphocyte globulin]. 623 25

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

The general features of allergic drug reactions in man have recently been reviewed by Parker (85). By definition allergic drug reactions are produced by specific immunologic processes. Allergic drug reactions must be distinguished from adverse reactions due to overdosage, normal pharmacologic action, toxic metabolite formation, idiosyncrasy, nonspecific release of pharmacologic effector molecules, or drug interactions. The clinical manifestations of drug allergy are quite protean. In addition to classical manifestations of allergy such as serum sickness, anaphylaxis, contact dermatitis or urticaria, drug allergy may produce hemolytic anemia, thrombocytopenia, granulocytopenia, hepatitis, nephritis, pneumonitis, vasculitis, or neuritis where a single organ or cell type is affected. While many drugs produce reactions with suggestive of allergy, definitive experimental evidence either for or against mechanism is usually not available. Some of these reactions may involve allergic mediators released or produced nonimmunologically through pharmacologic, osmotic, or toxic effects on cells involved in immune inflammation (mast cells, basophils, phagocytes, and lymphocytes) or through nonspecific activation of effector molecules in extracellular fluid such as the complement proteins. Drugs may also induce the formation of autoantibodies through mechanisms that are largely obscure, but may in some instances involve the direct participation of the drug as a hapten and in other instances occur indirectly through a pharmacologic or toxic action on the cells responsible for immune homeostasis.
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PMID:Allergic reactions in man. 704 Nov 44


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