Immune-mediated adalimumab-induced thrombocytopenia for the treatment of ulcerative colitis

Objective: Tumor-necrosis factor (TNF)-α inhibitors including adalimumab have been widely used for patients with inflammatory bowel diseases refractory to conventional treatment. Neutropenia is the most common side effect of TNF-α inhibitors, but thrombocytopenia is rarely presented. Few cases have been reported on TNF-α-induced thrombocytopenia, but the pathophysiology has not been fully understood. Herein, we explore the pathophysiology of adalimumab-induced thrombocytopenia through the clinical course and treatment options for a patient that developed thrombocytopenia after administration of adalimumab. Methods: We report a singular case of a patient with refractory ulcerative colitis who developed retinal hemorrhages due to thrombocytopenia after receiving adalimumab. The patient’s platelet count continued to drop despite discontinuation of adalimumab and platelet transfusion administration. Thrombocyopenia stabilized only after receiving intravenous immunoglobulin and prednisone. Laboratory tests identified anti-platelet IgM, but no antibody reactivity was seen against platelets in the presence of adalimumab (anti-platelet-adalimumab complex). Results: The patient’s response to immunosuppressants and lack of antibody against adalimumab-platelet complexes (drug-induced thrombocytopenia or type II hypersensitivity reaction) suggests that adalimumab can induce destruction of platelets through the formation anti-platelet antibodies. This is likely caused by immune system derangement in the setting of a chronic inflammatory state, as seen with ulcerative colitis, including an antigenic mimicry of adalimumab against a surface epitope of platelets or adalimumab-induced T-cell apoptosis. Conclusion: Physicians are to be aware of a life-threatening complication of adalimumab, immune-mediated thrombocytopenia for the treatment of ulcerative colitis.