Life threatening liver disease during treatment with monoclonal antibodies

A 66 year old man with an exacerbation of erythrodermic psoriasis despite several weeks of treatment with efalizumab, a recombinant humanised monoclonal antibody that binds to CD11a and acts as an immunosuppressant, was treated with adalimumab, a fully humanised monoclonal antibody that binds and deactivates tumour necrosis factor α (TNFα). Before starting treatment tuberculosis was excluded. The patient had no risk factors for infectious diseases and had never received blood products. Ten days after starting adalimumab, the patient developed jaundice. Blood tests showed the presence of the surface antigen of the hepatitis B virus (HBV) and higher than normal values of alanine aminotransferase (9.14 µkat/l; normal value <0.85 µkat/l), γ glutamyl transferase (2.92 µkat/l; <1.1 µkat/l), alkaline phosphatase (2.19 µkat/l; <2.15 µkat/l), and bilirubin (155 µmol/l; <20.5 µmol/l). Despite appropriate treatment, he developed progressive coagulopathy (international normalised ratio 2.5), and his serum bilirubin increased to more than 40 times the upper limit of normal (809 µmol/l; <20.5 µmol/l). The coagulopathy normalised over four weeks, whereas bilirubin normalised only after months of effective treatment. Fortunately, the patient did not clinically decompensate during this period of severe liver injury. ### Short answers