Metabolic Unit, Royal National Orthopaedic Hospital, Stanmore, Middlesex, UK
Correspondence to: J. S. Bubbear. E-mail: jbubbear{at}doctors.net.uk
SIR, We read with interest the regional audit by Erb et al. [1] regarding the prevention and treatment of corticosteroid-induced osteoporosis. We also note the recent correspondence on this matter from Miah et al. [2]. Erb et al. reported that 63% of patients from their region were being appropriately treated, according to guidelines published by the National Osteoporosis Society (NOS) [3]. Miah et al. found, however, that only 50% of their patients were being appropriately treated according to more recently published guidelines by the Royal College of Physicians, and the Bone and Tooth society [4], although these were for postmenopausal osteoporosis rather than being specifically targeted at corticosteroid-induced osteoporosis.
We would therefore like to bring to your attention the new guidelines on corticosteroid-induced osteoporosis that were published in December 2002 [5]. These draw on important epidemiological studies in the disease area and also report the effects of various pharmacological agents on reducing the risk of fracture. The guidelines note that risk of fracture increases rapidly after the onset of oral glucocorticoid treatment, and also that there is no safe dose of oral glucocorticoid, with an increased risk of fracture being observed with daily oral prednisolone doses (or equivalent) of 2.57.5 mg/day. The threshold for assessment and intervention has therefore been lowered, and patients are deemed to be at risk of osteoporosis if they are planned to be on any dose of steroid for greater than 3 months. This differs from earlier guidelines where a dose threshold of 7.5 mg/day prednisolone (or equivalent) was used and treatment should be for 6 months or more. In addition, the management guidelines are more aggressive, particularly in older patients and in those with a history of prior fracture. In these patients groups it is advised that treatment to reduce risk of fracture should be initiated at the same time as the corticosteroid therapy, and that there is no need for assessment of bone mineral density (BMD). In younger patients, however, BMD is still recommended to aid in management and the T-score threshold remains the same at 1.5.
It is recommended that these new guidelines are followed in both primary and secondary care. It is also recommended that audit be carried out against these guidelines and the Royal College of Physicians is currently developing an audit tool to assist in this matter. The data from Miah and Erb suggest that a significant number of patients on chronic corticosteroid therapy were being inadequately managed for their osteoporosis risk. We believe that if the patients had been audited against the guidelines published in 2002, then a smaller percentage would have been identified as being appropriately managed. This suggests that all patients on corticosteroids should be reassessed against the criteria proposed in these newer guidelines, with treatment started as necessary. These measures will hopefully reduce the burden of osteoporotic fractures that are associated with corticosteroid use.
The authors have declared no conflicts of interest.
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