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)