January 2000, Volume 9, Issue 1, Pages 74 - 77

Case report

Liver dysfunction due to apoptosis in a patient with systemic lupus erythematosus Masaya Mukai1, Toshiyuki Bohgaki1, Atsushi Notoya1, Michifumi Kohno1, Masatoshi Tateno2 & Seiichi Kobayashi3 1Division of Clinical Immunology and Hematology, Department of Medicine     2Department of Pathology, Sapporo City General Hospital, Sapporo, Japan     3Department of Laboratory Technology, College of Medical Technology, Hokkaido University, Sapporo, Japan     Correspondence to: Masaya Mukai , Division of Clinical Immunology and Hematology, Department of Medicine, Sapporo City General Hospital, Kita 11-jo, Nishi 13-chome, Chuo-ku, Sapporo 060-8604 Japan Tel: (+81) 11 726 2211; fax: (+81) 11 726 9541, E-mail: masaya-mukai@hokkaido.med.or.jp

Keywords

systemic lupus erythematosus;   lupus hepatitis;   apoptosis;   programmed cell death;   soluble Fas ligand

Abstract

We report on a 23-year-old Japanese female with a 13-year history of systemic lupus erythematosus (SLE), and two episodes of deterioration followed by treatment with high dose prednisolone. Although she had been recently treated with prednisolone (12.5 mg daily), her liver function became worse in July 1998. Results of a liver biopsy revealed multi-focal hepatic cell death in a severe fatty liver, without any inflammatory cell invasion. The biopsy also showed a positive TUNEL (Tdt-catalysed DNA nick end labelling) reaction indicating apoptosis. Her liver function recovered rapidly following steroid pulse therapy. Serum soluble Fas ligand (sFasL) was found to be elevated to a concentration of 0.395 ng/ml at the time of liver damage, but was less than 0.03 ng/ml before liver damage and after prednisolone treatment. The liver damage in this case appeared to be involved with apoptosis induced by sFasL. Although hepatitis associated with SLE is rare, apoptosis directly related to elevated sFasL levels might cause this complication. Lupus (2000) 9, 74-77

^© Macmillan Publishers Ltd 2000