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Liver dysfunction due to apoptosis in a patient with systemic lupus erythematosus

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 9541masaya-mukai{at}hokkaido.med.or.jp

Toshiyuki Bohgaki

Atsushi Notoya

Michifumi Kohno

Division of Clinical Immunology and Hematology, Department of Medicine, Sapporo, Japan

Masatoshi Tateno

Department of Pathology, Sapporo City General Hospital, Sapporo, Japan

Seiichi Kobayashi

Department of Laboratory Technology, College of Medical Technology, Hokkaido University, Sapporo, Japan

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.

Key Words: systemic lupus erythematosus • lupus hepatitis • apoptosis • programmed cell death • soluble Fas ligand

Lupus, Vol. 9, No. 1, 74-77 (2000)
DOI: 10.1177/096120330000900115


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