1992 Volume 15 Issue 5 Pages 475-482
Cyclosporine A (CsA) produces potent immunosuppression through its main inhibitory effect on activation of helper/inducer and cytotoxic T lymphocytes. Although CsA therapy has shown promising results in various diseases associated with disordered immuneregulation (i.e. uveitis, type I diabetes, psoriasis), therapeutic trials for systemic lupus erythematosus (SLE) seem to have been restricted chiefly because of its deleterious nephrotoxicity.
We reported an active case of SLE complicated with avascular bone necrosis of bilateral femoral heads. Our patient received 3mg/kg/day of CsA for the initial six weeks. When CsA dosage was incremented to 6mg/kg (the blood trough level of CsA was 210.6ng/ml at that point), minimal rises of the value of serum β 2-microglobulin and its urinary excretion were observed but returned to the normal level promptly after the dosage was reduced. Hypocomplementemia began to normalize at sixth week and discoid rash disappeared successively. Although hypergammaglobulinemia was not improved after six months of CsA therapy, number of lymphocyte absolutely increased and the titers of the following autoantibodies significantly decreased after several months: anti-nuclear antibody, anti-Sm antibody, anti-RNP antibody, anti-RBC antibody and anti-platelet antibody.
Although the immunological mechanism should be further elucidated, the favorable response observed in our patient might raise the possibility that CsA could induce remission in the group who suffer from side effects caused by long-term use of steroids, including osteoporosis, cataracts and atherosclerosis.
