The original description of endogenous glucocorticoid excess by Cushing included reference to an ‘increased tendency to fracture’(Cushing, 1932). The introduction of cortisone as a therapeutic agent in the following decade was followed by case reports of vertebral fractures (Curtess et al., 1954). indicating that exogenous hypercortisolism was also deleterious to the skeleton. Since that time, many workers have documented decreased bone mass in steroid-treated patients whether assessed by histomorphometry of bone biopsies (Dempster et al., 1983), metacarpal cortical thickness (Greenberger et al., 1982), or by more sophisticated densitometric techniques (Hahn & Hahn, 1976; Hahn er al., 1979; Rickers et al., 1982; Dykman et al., 1984; Schaadt & Bohr, 1984; Reid et al., 1986; Reid et al., 1988). Prospective studies of bone mass during steroid treatment are fewer in number but confirm that these drugs do cause progressive bone loss. Deding et al.(1977) found a 2.5% decrease in distal forearm bone mineral content during the first 12 weeks of prednisone treatment for haematological or connective tissue diseases. In a similar study, Rickers et af.(1984) found that this rate of loss fell to 0.6% in the second 12 weeks of therapy. Comparable studies in asthmatic patients have found dose-related losses of peripheral trabecular bone of between 1 and 7% per annum (Ruegsegger et al., 1983). Many of these studies did not include a non-steroid-treated control group so the contribution of the patients’ underlying disease to the loss of bone mass is often not known. Adinoff and Hollister (1 983), however, studied fracture prevalence in both steroid-treated and non-steroid-treated asthmatic subjects. They found no evidence of rib or vertebral fractures in the control group in contrast to a fractule prevalence of 11% in asthmatics who had received steroids for at least one year. We also have data indicating that distal forearm bone mineral content is reduced by 17%(P< O-Ol) in steroid-treated asthmatic subjects in comparison with age-and sex-matched asthmatic control patients (Reid et al., in preparation).

Factors determining the rate of bone loss in a particular patient remain to be detennined. Some studies have found that it is related to steroid dose (Chesney et al., 1978a; Hahn, 1978; Ruegsegger et al., 1983), that younger patients are more at risk (Ruegsegger et al., 1983) and that the underlying disease determines susceptibility