EXPERT ANALYSIS FROM RWCS 2016

MAUI, HAWAII (FRONTLINE MEDICAL NEWS) – Patients with systemic lupus erythematosus (SLE) really need to be placed on bone protection therapy as soon as they start on corticosteroids because their risks of steroid-related osteoporosis and osteonecrosis are so high, Dr. Dafna D. Gladman advised at the 2016 Rheumatology Winter Clinical Symposium.

Investigators for new studies of large cohorts of SLE patients seen at the University of Toronto Lupus Clinic have examined numerous potential predictors of bone comorbidities, but only one independent risk factor emerged: a high cumulative dose of corticosteroids, said Dr. Gladman, professor of medicine and codirector of the clinic.

“The dose of steroids is certainly important. It’s relevant to patient management because we obviously want to try to minimize the amount of steroids that patients with lupus get,” the rheumatologist observed.

The Toronto experience underscores just how common and serious these bone comorbidities are.

Among 1,729 SLE patients in the clinic database, 13.6% developed symptomatic osteonecrosis as defined by clinical symptoms plus positive imaging findings. Overall, 86% were female. The mean age at diagnosis of SLE was 26.6 years, with a mean 8.2-year interval from SLE diagnosis to the first episode of osteonecrosis. The 235 patients with osteonecrosis had a collective 382 affected joints at the time of their first osteonecrosis diagnosis, with an additional 160 joints becoming osteonecrotic later.

Particularly noteworthy was the finding that fully 47% of patients had more than one site involved at the time of their first osteonecrotic event, according to Dr. Gladman.

By far the most frequently affected joints were the hips, followed by knees. Surgery was often required in order to manage the injuries. Indeed, surgery was performed on more than half of osteonecrotic hips, 30% of affected wrists, and 20% of knees.

In a multivariate regression analysis involving 162 SLE patients with osteonecrosis and an equal number of matched controls who had SLE but not osteonecrosis, the only independent predictor of osteonecrosis was a high cumulative dose of corticosteroids; in the osteonecrosis group, it averaged 31 g. Factors that didn’t pan out as predictors included patient age, gender, race, smoking status, current or past use of antimalarial drugs, duration of immunosuppressive therapy, disease severity as reflected by the adjusted mean SLE Disease Activity Index score 3 years prior to osteonecrosis or the last clinic visit, total serum cholesterol, and a history of Raynaud’s, vasculitis, or renal or CNS involvement.

Turning to osteoporosis in SLE patients, Dr. Gladman said that among 286 patients who underwent bone mineral density (BMD) measurement at the time they were first seen in the clinic, 31.5% had an abnormal result. Among the 173 premenopausal females, 17% had a BMD below the lower limit of normal for their age. So did 27% of men below age 50. In postmenopausal women, the prevalences of osteoporosis and osteopenia were 12% and 43%, respectively. One of 10 men over age 50 had osteoporosis, while 8 had low BMD.

Twenty patients had a symptomatic fragility fracture at the time of their BMD test, and, of note, only half of them had an abnormal BMD.

“So the BMD does not actually identify all those patients who are at risk for the adverse outcome of osteoporosis, which will be a fragility fracture,” Dr. Gladman said.

She reported having no financial conflicts of interest regarding her presentation.

bjancin@frontlinemedcom.com

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