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)