Adalimumab‐induced platelet antibodies resulting in severe thrombocytopenia
| Autor: | Frank H J Wolfhagen, Henk-Jan Boiten, Peter E. Westerweel, Sufia Amini |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Blood Platelets
Male medicine.medical_specialty 030226 pharmacology & pharmacy Gastroenterology 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Crohn Disease Mesalazine Internal medicine medicine Adalimumab Humans Pharmacology (medical) Platelet 030212 general & internal medicine Aged Pharmacology Tumor Necrosis Factor-alpha business.industry Autoantibody Thrombocytopenia Infliximab Discontinuation Bone marrow suppression chemistry Monoclonal business medicine.drug |
| Zdroj: | British Journal of Clinical Pharmacology. 87:3619-3621 |
| ISSN: | 1365-2125 0306-5251 |
| Popis: | Anti-tumour necrosis factor-α (TNFα) agents are effective in diseases including Crohn's disease but may cause cytopenias. The mechanisms involved in anti-TNFα agent-induced thrombocytopenia are scarce. We report a 73-year-old male with Crohn's disease for which he currently used adalimumab, an anti-TNFα agent. He had received mesalazine and infliximab before the treatment of adalimumab. No comorbidities were present. Routine laboratory tests revealed a deep thrombocytopenia (thrombocytes 24 × 109 /L), after which adalimumab was discontinued. Bleeding symptoms included cutaneous haematomas and mild epistaxis. Direct monoclonal antibody-specific immobilization of platelet antigens revealed autoantibodies specific to glycoprotein IIb/IIIa and glycoprotein V platelet receptors. There was no bone marrow suppression. Other causes of the thrombocytopenia were ruled out. The platelet count normalized after adalimumab discontinuation. No further interventions were required. Monitoring thrombocyte levels after initiating anti-TNFα agents is recommended, which could lead to prevention of this potentially fatal phenomenon. |
| Databáze: | OpenAIRE |
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