Adalimumab-induced platelet antibodies resulting in severe thrombocytopenia.
Henk-Jan BoitenSufia Nadjib AminiFrank H J WolfhagenPeter E WesterweelPublished in: British journal of clinical pharmacology (2021)
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.
Keyphrases
- rheumatoid arthritis
- juvenile idiopathic arthritis
- disease activity
- monoclonal antibody
- bone marrow
- ulcerative colitis
- high glucose
- hidradenitis suppurativa
- diabetic rats
- drug induced
- single cell
- systemic lupus erythematosus
- mesenchymal stem cells
- dendritic cells
- oxidative stress
- sleep quality
- stress induced
- smoking cessation
- combination therapy