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Successful treatment with fenofibrate of autoimmune hepatitis in a patient with rheumatoid arthritis

Autoimmune hepatitis (AIH) is a chronic progressive liver disease that is thought to be caused by dysregulation of the immune system. This syndrome is characterized by elevated serum transaminase activity and circulating organ non-specific autoantibodies (1). The standard treatment for AIH is corticosteroids and azathioprine. Alternative therapy may be required because of failure to achieve remission and intolerance of the side effects of these drugs (2). We describe an AIH patient who received therapy with fenofibrate, a peroxisome proliferatoractivated receptor (PPAR)-a ligand. This treatment was effective in improving the patient’s liver function. This case suggests that fenofibrate could be a feasible alternative therapy for AIH. A 67-year-old man visited our clinic in October 2000, for worsening polyarthritis. Rheumatoid arthritis (RA) was diagnosed at a local clinic when he was 66 years old. Before the diagnosis, he had experienced 12 months of swelling, pain, and stiffness of the wrist joints bilaterally. He was given non-steroidal anti-inflammatory drugs (NSAIDs) for 1 year with no improvement of symptoms, and then he moved to our clinic. At that time, arthritis was noted in his wrist bilaterally, the second and third metacarpophalangeal (MCP) joints bilaterally, and in the right knee joint. His complete blood count showed a normal red blood cell count, leucocytosis (12 600/mL), and mild thrombocytosis (36.4610/mL). Blood chemistry data revealed liver dysfunction [aspartate aminotransferase (AST) 51 IU/L (normal range 10–40), alanine aminotransferase (ALT) 44 IU/L (normal range 5–45), lactate dehydrogenase (LDH) 394 IU/L (normal range 170–370), and alkaline phosphatase (ALP) 1064 mU/mL (normal range 100–280)]. Increases in erythrocyte sedimentation rate (ESR; 95.3 mm/h) and C-reactive protein (CRP; 8.5 mg/dL, normalv0.5 mg/dL) were observed. An RA test was positive and anti-nuclear antibody testing was positive with a titre of 1:160 (speckled pattern), while antibodies for Sm, SS-A/Ro, SS-B/La, and U1RNP were negative. Anti-smooth muscle cells antibody was positive (1:20) and anti-mitochondria antibody was negative. Ultrasonography of the liver revealed mild fibrotic change and no evidence of tumours. Liver biopsy was not performed, as the patient did not give consent. X-rays of his fingers and wrist joints showed joint narrowing but no erosion was noted. Pain on the visual analogue scale (VAS) was 52 mm, Health Assessment Questionnaire (HAQ) score was 1.2 and the painful joint count was 2.3. Treatment with auranofin (3 mg/day) and prednisone (2 mg/day) was started as treatment of RA. After 1 month, his arthritis had improved slightly (CRP fluctuated between 2.1 and 5.7 mg/ dL) but liver function was still abnormal (AST: 28– 49 IU/L, ALT: 21–42 IU/L, LDH: 302–451 IU/L, ALP: 619–1049 mU/mL). In October 2002 treatment with fenofibrate (300 mg/day) was started, in addition to the treatment with auranofin and prednisone, and his liver function gradually improved (see Figure 1). The patient has been followed up for more than 3 years and there have been no adverse reactions to this therapy thus far. Fenofibrate has been shown to have not only a lipoprotein lowering effect but also an anti-inflammatory effect through the inhibition of nuclear factor (NF)-kB signalling in several systems (3–5). Several lines of evidence indicate that AIH is caused