Raloxifene increased bone mineral density in the spine and hips of postmenopausal women using long-term glucocorticoids

Randomized placebo-controlled trial (RCT). ClinicalTrials.gov NCT00371956.

Unclear allocation concealment.*

Blinded (patients, clinicians, and outcome assessors).*

12 months.

Outpatient rheumatology clinics at 2 hospitals in Hong Kong, China.

114 adult women (mean age 55 y) who were postmenopausal for ≥ 12 months; used a stable dose of prednisone, ≤ 10 mg/d or equivalent, for ≥ 6 months to treat rheumatic disease; and were expected to need corticosteroids throughout the study. Exclusion criteria included hypercoagulability risk factors (e.g., positive antiphospholipid antibodies); bone disorders (e.g., osteomalacia, renal osteodystrophy, and hyperparathrydoidism); undiagnosed uterine bleeding; serum creatinine level ≥ 200 µmol/L; history of thromboembolism, allergic reactions, or intolerance to selective estrogen receptor modulators (SERMs); and use of bisphosphonates, parathyroid hormones, SERMS, anticonvulsants, or anticytokine therapy in the past 6 months.

Raloxifene, 60 mg/d (n = 57), or placebo (n = 57). All patients received elemental calcium, 1000 mg/d, and calcitriol, 0.25 µg/d.

Lumbar spine and hip BMD. Other outcomes included new vertebral fractures and adverse events.

94%.

At 12 months, raloxifene increased lumbar spine and total hip BMD more than placebo (Table); groups did not differ for change in femoral neck BMD (data not reported) or new vertebral fractures (Table). The most frequent adverse events were leg cramps (7% vs 0%, P = 0.13), dyspepsia or heartburn (5% vs 9%, P = 0.71), dizziness or vertigo (5% vs 2%, P = 0.61), atypical chest pain (0% vs 7%, P = 0.13), and depression (0% vs 4%, P = 0.48). No arterial or venous thromboemboli were reported.

Raloxifene increased lumbar spine and total hip bone mineral density in postmenopausal women using long-term glucocorticoids for rheumatic disease.