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Hereditary or acquired deficiencies of protein C or its cofactor, protein S, have been associated with tissue necrosis following warfarin administration. Not all patients with these conditions develop necrosis, and tissue necrosis occurs in patients without these defi-ciencies. Inherited resistance to activated protein C has been described in many patients with venous thromboembolic disorders but has not yet been evaluated as a risk factor for tissue necrosis. The risk associated with these conditions, both for recurrent thrombosis and for adverse reactions, is difficult to evaluate since it does not appear to be the same for everyone. Decisions about testing and therapy must be made on an individual basis. It has been reported that concomitant anticoagulation therapy with heparin for 5 to 7 days during initiation of therapy with COUMADIN may minimize the incidence of tissue necrosis. Warfarin therapy should be discontinued when warfarin is suspected to be the cause of developing necrosis and heparin therapy may be considered for anticoagulation. Miscellaneous: Text Continues Below
polycythemia vera, vasculitis, and severe diabetes. Minor and severe allergic/ hypersensitivity reactions and anaphylactic reactions have been reported. In patients with acquired or inherited warfarin resistance, decreased therapeutic responses to COUMADIN have been reported. Exaggerated therapeutic responses have been reported in other patients. Patients with congestive heart failure may exhibit greater than expected PT/ INR response to COUMADIN, thereby requiring more frequent laboratory monitoring, and reduced doses of COUMADIN (Warfarin Sodium). Concomitant use of anticoagulants with streptokinase or urokinase is not recommended and may be hazardous. (Please note recommendations accompanying these preparations.) PRECAUTIONS Periodic determination of PT/ INR or other suitable coagulation test is essential. Page: << Prev | 1 | 2 | 3 | 4 | 5 | Next >>
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