Diminished Response to Recombinant Factor Vila in a Patient with Idiopathic Thrombocytopenic Purpura
Autor: | Zale P Bernstein, Walter S. Schroeder, Melissa S. Baxter, Yijun Cheng |
---|---|
Rok vydání: | 2006 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Drug Resistance Factor VIIa 030204 cardiovascular system & hematology Multiple dosing law.invention 03 medical and health sciences 0302 clinical medicine Refractory law Humans Medicine Pharmacology (medical) Platelet Aged Purpura Thrombocytopenic Idiopathic Platelet Count business.industry Factor VII medicine.disease Thrombocytopenia Thrombocytopenic purpura Recombinant Proteins Surgery Purpura 030104 developmental biology medicine.anatomical_structure Coagulation Recombinant DNA Female medicine.symptom business Artery |
Zdroj: | Annals of Pharmacotherapy. 40:2053-2058 |
ISSN: | 1542-6270 1060-0280 |
DOI: | 10.1345/aph.1h331 |
Popis: | Objective: To describe the hypotheses that may explain a diminished hemostatic response in a patient receiving multiple doses of recombinant coagulation factor Vila (rFVIIa) for off-label treatment of bleeding events. Case Summary: A 70-year-old female with a significant history of idiopathic thrombocytopenic purpura (ITP) was admitted for coronary artery bypass grafting surgery. The patient developed thrombocytopenia and persistent hemorrhage postoperatively that was refractory to conventional therapy for ITP. She experienced an initial hemostatic response to rFVIIa after receiving 3 doses. During her second trial of rFVIIa a few days later, the duration of hemostatic effect was approximately half that of the first. The patient then received rFVIIa almost daily over the following 9 days to which she remained unresponsive, ultimately resulting in death. All doses in this patient were 9.6 mg (101 μg/kg), except the last, which was 4.8 mg (50.5 μg/kg). Discussion: Several hypotheses may explain this patient's resistance to rFVIIa therapy. Two involve depletion of platelets or coagulation factors essential for rFVIIa efficacy. Another involves development of an antibody to rFVIIa. The last involves acidemia, which may interfere with the pharmacologic effect of rFVIIa. Conclusions: The combination of persistent thrombocytopenia and exhaustion of coagulation factors is the likely cause leading to resistance to rFVIIa therapy in this patient. |
Databáze: | OpenAIRE |
Externí odkaz: |