Within 1 year after the introduction of hydralazine to control malignant hypertension in 1952, the first report appeared of a late-onset ‘collagen disease’ resembling systemic lupus erythematosus (SLE) in 17 out of 211 hydralazine-treated patients. 1 Although procainamide was introduced for the treatment of cardiac arrhythmia at about the same time, it was not until 1962 that Ladd reported a patient who developed lupus-like features after 6 months of procainamide therapy. 2 By 1966 a scattering of cases of lupus-like disease as a side-effect of therapy with isonizid, diphenylhydantoin, sulfamethoxypyradazine, primidone and tetracycline appeared. In the ensuing years a diverse array of more than 50 different drugs has been implicated in the de-novo development of autoantibodies and clinical features similar to those seen in patients with idiopathic SLE.