Disease-related Risk of Vertebral Fracture During Glucocorticoid Treatment of Collagen Vascular Diseases

To the Editor: Collagen vascular diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjögren’s syndrome (SS), systemic sclerosis (SSc)/mixed connective tissue disease (MCTD), polymyositis/dermatomyositis (PM/DM), and microscopic polyangiitis, are chronic and sometimes involve multiple organs, and are thus occasionally life-threatening. Immunosuppressive treatment with longterm high-dose glucocorticoids is necessary, but the treatment causes a high incidence of osteoporosis1,2,3. Recently, we demonstrated that patients treated with longterm high-dose glucocorticoids have a high risk of symptomatic vertebral fractures in collagen vascular diseases, based on the analysis of the Chiba-Shimoshizu Rheumatic Cohort4,5. The chronic and systemic inflammation in patients with RA and SLE has been recognized as causing secondary osteoporosis independently of glucocorticoids6, and many studies demonstrated that patients with RA have lower bone mineral density (BMD) and an increased risk of fracture7,8,9. However, it was not known whether there is a disease-specific or disease-related risk of osteoporotic fracture under glucocorticoid treatment among the collagen vascular diseases. We investigated the disease-specific or disease-related risk for osteoporotic symptomatic vertebral fracture by focusing on women treated with high-dose glucocorticoids for the long term for collagen vascular diseases, subanalyzing a cohort at Shimoshizu National Hospital in Japan. The study subjects were newly treated with an initial dose of > 20 mg/day prednisolone (PSL) equivalent for at least 6 months without prior prophylactic treatment with bisphosphonate, hormone replacement therapy, or selective estrogen receptor modulator to prevent bone loss. We defined glucocorticoid dose increase as the reintroduction of ≥ 20 mg/day of glucocorticoid (PSL equivalent) due to increased disease activity in patients whose doses were once tapered to < 20 mg/day. Symptomatic vertebral fracture was defined as vertebral deformity that was confirmed … Address correspondence to Dr. I. Tatsuno, Department of Clinical Cell Biology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan. E-mail: ichiro-tatsuno{at}faculty.chiba-u.jp