Abstract

Since survival of patients with systemic lupus erythematosus (SLE) has improved over the past decades, increasing attention is focused on complications of the disease. Osteoporosis and fractures contribute to damage in the second most frequently involved organ system in SLE: the musculoskeletal system. Recent studies have reported a high frequency of reduced bone mineral density in SLE, and an increased risk of peripheral and vertebral fractures. The incidence of symptomatic fractures is increased 1.2–4.7-fold in patients with SLE. A large population-based study on 4343 patients with SLE and 21 780 age-matched and sex-matched controls, demonstrated previous glucocorticoid use and longer disease duration as important risk factors for symptomatic fractures in SLE. Prevalent vertebral fractures are demonstrated in 18–50% of these relatively young patients, and one in three of these patients has normal bone density.

The aetiology of bone loss in SLE is supposed to be multifactorial, involving clinical osteoporosis risk factors, systemic inflammation, serological factors, metabolic factors, hormonal factors, medication-induced adverse effects and, possibly, genetic factors. A 6-year follow-up study on Dutch patients with SLE revealed that low 25-hydroxyvitamin D serum levels, low body mass index and baseline use of antimalarials were associated with bone loss. In addition, a dose-dependent relationship between glucocorticoid use and bone loss was demonstrated in longitudinal studies in SLE. These findings have implications for daily clinical practice, because vitamin D insufficiency is highly frequent in SLE, antimalarials are regarded as ‘anchor drugs’ for therapy and the majority of patients with SLE are on chronic glucocorticoid treatment.