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Published 18 February 2009, doi:10.1136/bmj.b508
Cite this as: BMJ 2009;338:b508
Thorsten Kaiser, resident1, Joachim Moessner, professor of medicine, head of department 1, Keyur Patel, assistant professor of medicine 2, John G McHutchison, professor of medicine2, Hans L Tillmann, assistant professor of medicine1,2
1 Medizinische Klinik und Poliklinik II, Universität Leipzig, 04103 Leipzig, Germany, 2 Duke Clinical Research Institute, Durham, NC 27713, USA
Correspondence to: HL Tillmann hans.tillmann@duke.edu
| The first 150 words of the full text of this article appear below. |
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
(TNF
). 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),
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
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