Previous treatment with leflunomide and adalimumab (Humira®) had failed and been discontinued months before etanercept was started. No other medications were used, and even methotrexate and hydroxychloroquine were discontinued by her rheumatologist when

etanercept was commenced. One week after the injection, she reported malaise, lassitude, and low-grade fever; those symptoms persisted over 2 weeks. A sudden appearance of high fever and rash led to her admission. On admission, she was febrile and tachycardic but stable, with unrewarding examination GM6001 except for gingival bleeding, a profuse petechial rash over both legs and polysynovitis, which was not new. Laboratory tests showed hemoglobin (Hb) 7.5 g/dl (normocytic), WBC 1.8 × 109/L with absolute neutrophil count (ANC) 0.7 × 109/L, platelets 3 × 109/L, ESR 172 mm/h, CRP 76.8 mg/dL (normal <6 mg/dL), albumin 26 g/L, and globulins 47 g/L (polyclonal). Serum creatinine, electrolytes, and liver enzymes were normal. Peripheral blood smear confirmed severe pancytopenia Ferrostatin-1 ic50 with absent reticulocytes (0.3 %). Bone marrow aspiration and biopsy revealed BM aplasia (Fig. 1). Methotrexate in serum was undetectable. Chest X-ray, urinalysis, and cultures were normal.

Tests for other causes of cytopenias, including serology for Epstein–Barr virus (EBV), cytomegalovirus (CMV), hepatitis viruses, parvovirus B-19, and HIV were negative. Fig. 1 Patient’s bone marrow biopsy showing stroma and plasma cells (more resistant to drug toxicity) but absence of all other hematopoietic BAY 11-7082 supplier elements, consistent with transient aplasia The patient was treated with platelets Sclareol (four times), packed cells (4 U), granulocyte colony-stimulating factor (Neupogen®) over 5 days, and broad-spectrum antibiotics. She

was discharged on the 12th hospital day, afebrile and stable (absolute neutrophil count [ANC] 10.5 × 109/L), for ambulatory follow-up. One month later, the Hb was 12.4 g/dL, white blood count (WBC) 13.7 × 109/L, and platelets 149 × 109/L. The patient resumed methotrexate treatment uneventfully for more than 6 months of follow-up. 3 Discussion and Review of the Literature When serious adverse events (SAEs) associated with anti-TNFα therapy are considered, attention is usually focused on an increased risk of infections (in particular, reactivation of tuberculosis and opportunistic infections) and malignancy, though the latter remains an unresolved concern [2]. However, anti-TNFα therapy-induced cytopenias constitute another SAE that are potentially life threatening and mandate better recognition. For example, neutropenia was reported in 14.3–18.8 % of patients receiving a TNFα inhibitor [3–5]. In most of the patients, neutropenia occurred after just 2 weeks of treatment, was mild (mean −1.1 × 109/L), transient, and showed spontaneous resolution, allowing the original treatment to be continued in most (81 %) patients.