C1q is thought to play a crucial part in the pathogenesis of systemic lupus erythematosus (SLE).1-3 C1q deficiency and the presence of C1q autoantibodies are associated with increased disease activity in SLE.1 Therefore, C1q is a promising candidate for adsorption of pathogenetic relevant molecules from the plasma of patients with SLE. A C1q immunoadsorbent was developed in 19904 and has been used in several patients.5

Our patient, a 25 year old woman, had a relapsing malar and discoid rash, which extended to almost the whole integument, since January 1999. Accompanying oral and genital ulcers, polyarthritis, and lupus nephritis (histological membranous glomerulonephritis, WHO Va), as well as laboratory abnormalities, led to the diagnosis, SLE.6 Despite treatment with chloroquine (400 mg/day) initially and methotrexate (7.5–15 mg/week) since August 1999 in combination with prednisone (10 …