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)

Concomitant use of the monoclonal antibody-purified factor IX concentrate (Mononine, Armour Pharmaceutical Company, Collegeville, Pa.) and two antifibrinolytic agents, epsilon-aminocaproic acid (EACA; Amicar, Immunex, Seattle, Wash.) or tranexamic acid (AMCA; Cyklokapron, Kabi Pharmacia, Piscataway, N.J.) was examined for safety and efficacy in patients with hemophilia B. In a retrospective review of 19 patients treated with monoclonal antibody-purified factor IX and EACA on 35 occasions, bleeding was successfully controlled and no instances of clinical thrombotic complications were reported; one instance of urticaria resolved without additional treatment. The use of EACA or AMCA in combination with monoclonal antibody-purified factor IX was also examined prospectively in a study of 9 patients. Bleeding was effectively controlled and no thrombotic events were detected clinically with either antifibrinolytic agent. No significant changes in hematocrit or hemoglobin were detected, and there was no evidence of thrombosis as evaluated clinically and by sensitive molecular markers. It was concluded from both the retrospective and prospective data that monoclonal antibody-purified factor IX concentrate in combination with an antifibrinolytic agent does not activate the coagulation cascade and is a safe and effective treatment for prevention and control of oral bleeding in hemophilia B patients.
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PMID:Concomitant treatment with factor IX concentrates and antifibrinolytics in hemophilia B. 757 94

During the course of replacement therapy, 22-30% of patients with severe hemophilia A develop alloantibody to factor VIII. Autoantibodies to coagulation factors rarely occur in elder individuals with previously normal hemostatic mechanisms or in patients with various underlying disorders. Although the great majority of the acquired inhibitors are directed to factor VIII, the antibodies may arise to every coagulation factor. The inhibitor antibodies directly inactivate specific clotting factor, or occasionally, they bind to a nonfunctional site, resulting in increased plasma clearance. In the last decade, we experienced 12 hemophilia A and 3 hemophilia B patients who developed factor VIII and factor VIII and factor IX inhibitor, respectively, 9 patients with autoantibody to factor VIII (acquired hemophilia), and 4 patients with acquired von Willebrand syndrome. Among 12 factor VIII inhibitors, 4 patients were identified to have inversion in the factor VIII gene, 1 with 4 bases deletion, and 1 with missense mutation resulting in G479R. Four of 9 patients with acquired hemophilia had underlying disorders of autoimmune hemolytic anemia, macroglobulinemia, urticaria, and pharyngeal cancer at the development of factor VIII inhibitor. Antibody to von willebrand factor was detected in 3 of 4 patients with acquired von Willebrand syndrome.
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PMID:[Immune coagulation disorders (excluding antiphospholipid syndrome]. 1176 64