Relapse of Systemic Lupus erythematosus after Extracorporeal Immunoadsorption

Dr. Rob Higgins, Renal Administration, Dulwich Hospital, East Dulwich Grove, London SE22 8PT (UK) Dear Sir, We report the case of a patient in whom an acute exacerbation of systemic lupus erythematosus (SLE) was associated with staphylo-coccal protein A immunoadsorption which had been performed in order to remove antibodies, against human leucoyte antigens. The patient was born in 1966 and developed SLE at the age of 13 years, presenting with arthralgia. Kidney failure developed at the age of 22 years, renal biopsy showing a segmental and proliferative glomerulone-phritis. At the time dialysis was started, he suffered a relapse of SLE with pericarditis and arthralgia. The anti-double-stranded DNA (anti-dsDNA) antibody level was 39.1 (normal range < 7.0) IU/ml. He received oral prednisolone and monthly intravenous cyclo-phosphamide, with a good response. One year later, he received a cadaveric renal transplant. He remained antinuclear antibody positive at a titre of 1/160, but the anti-dsDNA levels were within the normal range. The transplant failed after 2 years, due to biopsy-proven chronic rejection. On haemodialysis, he was well with an anti-dsDNA antibody level of 7.9 IU/ml. He was placed on the transplant waiting list, and immunosuppressive treatment was tailed off. Eighteen months later he had not received a transplant and had 95% panel-reactive antibodies. Therefore, he was considered for immunoadsorption treatment in order to remove antibody and to facilitate renal transplantation. He received immunoadsorption (Citem 10 System; Excorim, Lund, Sweden) for a total of eight sessions over a total period of 4 weeks. The total plasma volume administered was 65.9 litres, ranging in each session from 6.7 to 9.7 litres. Neither cyclophospha-mide nor prednisolone were administered. After 4 weeks of immunoadsorption, he developed malaise which was clinically diagnosed as a viral illness. Immunoadsorption was stopped. There was elevation of alkaline phosphatase (351IU/1, normal range 30-120) and γ-glutamyl transferase (255 IU/1, normal range 5-55) levels. Extensive testing for viral infection was negative (in particular for hepatitis B and C and for cytomegalovirus). The level of anti-dsDNA antibodies was slightly elevated (13.9 IU/ml), but the symptoms were not reminiscent of his previous SLE. Twelve weeks after the last immunoadsorption treatment he developed an acute arthralgia typical of his previous SLE, and the anti-dsDNA level was 74.4 IU/1. He was treated with prednisolone and azathioprine, with improvement in his symptoms and a fall in anti-dsDNA levels. He remains