Prevention and Treatment of Bone Disease in Systemic Lupus Erythematosus

Abstract

Opinion statementSystemic lupus erythematosus (SLE), an autoimmune chronic inflammatory disease, can be associated with significant morbidity and mortality of which bone disease such as osteoporosis is a contributor. Patients with SLE are at risk for low bone mineral density (BMD) due to a variety of reasons including inflammation, glucocorticoid use, vitamin D deficiency, premature ovarian failure, increased damage, and traditional risk factors such as age and gender. With better treatments for SLE, survival has improved; therefore, complications from morbidity including osteoporosis need better prevention and treatment strategies. In SLE patients with osteoporosis or those on glucocorticoids who meet guidelines for therapeutic intervention, we prefer bisphosphonates as first-line therapy for most patients. They have proven efficacy in increasing BMD and decreasing fracture risk, known safety profiles, and have a favorable cost-effectiveness profile. The newer agents, teriparatide and denosumab, have not only demonstrated improvement in BMD but also decreased risk of fracture. We typically recommend these medications for some high-risk populations, those who have failed bisphosphonate therapy or those who are intolerant of oral bisphosphonates. Estrogen-containing drugs are not recommended for first-line prevention and treatment of osteoporosis given the elevated risk of cardiovascular disease. Calcitonin has also been used in osteoporosis; however, the bisphosphonates and newer drugs have proven to be more efficacious. Supplementation with calcium and vitamin D is recommended in particular with those patients who are vitamin D deficient and those on glucocorticoids, although data documenting fracture prevention with this strategy is limited. Therapeutic strategies for premenopausal women of child-bearing potential remain controversial because of limited data about safety in subsequent pregnancies. Decisions for these patients need to be made on a case by case basis weighing the risks and benefits to the individual patient. Future therapies targeting different mechanisms within bone resorption and formation are currently under investigation and will significantly add to our limited armamentarium.

Effect of vitamin D and calcium supplementation in patients with systemic lupus erythematosus

“…[31] In addition, long-term use of corticosteroids may induce osteoporosis in patients with SLE by affecting their bone turnover, increasing bone resorption and decreasing bone formation, preventing the formation of collagen and osteocalcin as well as affecting the bone matrix mineralization. [32] Recent studies have shown that low-dose vitamin D and calcium supplementation (<1000 IU vitamin D and <800 mg calcium) does not improve BMD in pediatric SLE patients. [3334] However, long-term supplementation with different doses of vitamin D (400–1200 IU) and calcium (1–1.5 g) can have a better effect on the BMD of postmenopausal osteoporotic women.…”

“…[36] In addition, a high calcium supplementation may improve the bone matrix and, consequently, prevent its destruction. [32]…”

Very high frequency of fragility fractures associated with high-dose glucocorticoids in postmenopausal women: A retrospective study

“…In fact, it is reported that SLE itself is associated with low BMD or osteoporosis (Pineau et al, 2004) (Tang et al, 2013) (Sun et al, 2015). There are some reasons such as inflammation, vitamin D deficiency, and premature ovarian failure for risk of low BMD (Lin & Grossman, 2016). Those mechanisms are occurred in other rheumatic diseases than SLE and may also contribute to very high frequency of fragility fracture in this study.…”