Treatment of early rheumatoid arthritis with rifampicin.

Following a report that seven of 20 patients with rheumatoid arthritis (RA) had come into clinical and laboratory remission after treatment with rifampicin, and that six of the seven responders had a disease duration of less than three years, 21 patients with classical or definite RA of recent onset were treated with 600 mg rifampicin and 300 mg isoniazid daily for six months. Fourteen of 21 patients completed six months' treatment, but there was no significant improvement in the mean values of the clinical and laboratory parameters measured. The improvement suggested by preliminary studies in patients with early RA is not seen in this larger group. In patients with a disease duration of less than 18 months, however, there was a significant decrease in the erythrocyte sedimentation rate and the serum concentrations of C reactive protein after treatment for six months, although there was no significant clinical improvement. Future studies of this drug in patients with RA should concentrate on this group.

Drug-induced rheumatic syndromes. Diagnosis, clinical features and management.

In order to avoid inappropriate therapy and prolonged morbidity, it is important to recognise when a patient's rheumatic complaints are due to drugs. However, this is often difficult because of the large number of drugs that have been implicated and the diversity of clinical presentations. Arthropathy may be seen with several different syndromes, including drug-induced lupus erythematosus (DILE), serum sickness and gout. The most widely reported of these is DILE, which usually develops after some months or even years of drug therapy. While many authors do not specifically require their presence for the diagnosis of DILE, antinuclear antibodies have been detected in the great majority of reported patients with DILE, whatever the causative drug. In contrast, patients who develop arthropathy soon after commencing a drug rarely have antinuclear antibodies and appear to be distinct from patients with DILE. Apart from arthropathy, a number of other syndromes that appear to have an immunological basis may be induced by drugs. Cutaneous vasculitis is not uncommon and drugs are frequently considered to be the aetiological factor. Whether drugs may cause larger vessel systemic vasculitis is less certain. Rarely, polymyositis and scleroderma-like syndromes have been associated with drug therapy. Corticosteroid-induced osteoporosis is a complication of all the corticosteroid preparations that are widely used at present. However, the development of deflazacort, a so-called 'bone-sparing' steroid, has raised the possibility that the effect of corticosteroids on bone may be separable, at least in part, from the other actions of these drugs. Data have been conflicting with regard to whether there is a 'safe' dose of corticosteroid. Similarly, it is unclear whether prophylactic therapy with agents such as calcium, fluoride and vitamin D is beneficial. Nonetheless, recent findings suggest that approaches will be developed to minimise the risk of osteoporosis in patients who require corticosteroids. There are a number of other ways in which drugs may affect bones. Osteomalacia is a well-known but uncommon complication of treatment with anticonvulsants and occasionally other drugs. The mechanism probably relates to the induction of hepatic enzymes and the consequent increased metabolism of vitamin D in patients with borderline levels initially. Osteosclerosis may also result from drug therapy; usually with fluoride or retinol (vitamin A) and its analogues. With continued research, the true spectrum of drug-induced rheumatic syndromes should become more clearly defined.(ABSTRACT TRUNCATED AT 400 WORDS)

Two distinct quinidine-induced rheumatic syndromes.

Of seven patients with quinidine-induced polyarthropathy, four had positive antinuclear antibodies and could be considered to have had quinidine-induced lupus erythematosus. The remaining three patients had milder symptoms, which occurred soon after the start of quinidine therapy, and did not have antinuclear antibodies. To confirm the association, the latter three patients were rechallenged with quinidine therapy, which caused recurrence of symptoms within 1 week. Antihistone antibodies, which are characteristic of drug-induced lupus erythematosus associated with procainamide and hydralazine therapy, were detected in all patients with quinidine-induced lupus erythematosus. An unusual characteristic of antihistone antibodies seen in two patients was the presence of high levels of IgG antibodies to histone H1 as well as H2A.H2B and H3.H4 complexes, without antibodies to the individual core histones.