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Kids' Age at SLE Onset Sets Osteonecrosis Risk


 

BOSTON — The incidence of steroid-induced osteonecrosis is significantly lower in childhood systemic lupus erythematosus than in adults with the disease, according to the findings of a prospective MRI study. Additionally, among pediatric patients, age of lupus onset is an independent risk factor for the degenerative bone condition, Dr. Junichi Nakamura reported at the annual meeting of the Pediatric Orthopaedic Society of North America.

Characterized by the death of bone marrow and trabecular bone as a result of disruption of blood supply to the bone, osteonecrosis is a well-known complication of systemic lupus erythematosus (SLE) and is often associated with steroid therapy, yet the incidence of steroid-induced osteonecrosis in childhood SLE has not been well established, according to Dr. Nakamura of Chiba (Japan) Children's Hospital.

To assess the relative incidence of the condition in children and adults and to determine associated risk factors in children, Dr. Nakamura and his colleagues prospectively studied 169 patients, including 43 with childhood lupus (aged younger than 20 years at time of diagnosis) and 126 adults with the disease. All the patients fulfilled the 1982 revised American College of Rheumatology criteria for SLE, and all underwent MRI of the knee and hip when steroid therapy was initiated and again after at least 1 year of steroid therapy. The mean follow-up period was 7.8 years, and the follow-up rate was 100%, he said.

In total, 676 joint MRIs were analyzed, including initial and follow-up knee and hip MRIs for each adult and childhood SLE patient, Dr. Nakamura said. “The incidence of osteonecrosis was significantly lower in the childhood SLE group than the adults [31% and 41%, respectively].” During the follow-up period, osteonecrosis developed in 20 hips and 33 knees of 20 childhood SLE patients, and in 95 hips and 112 knees of 74 adult SLE patients, he reported.

Among the childhood SLE patients, age at SLE onset, highest dose of corticosteroid per day, and highest dose of corticosteroid per weight per day were compared between those who did and did not develop osteonecrosis, Dr. Nakamura said. The mean age of SLE onset in the osteonecrosis group was 17.2 years, compared with 13.3 years in the nonosteonecrosis group, representing a significant difference. The highest corticosteroid dose per day and the highest dose per weight per day were statistically similar between the two groups, he said.

In logistic regression analysis, “the incidence of osteonecrosis was significantly lower at the younger age of initial steroid treatment,” said Dr. Nakamura. “The odds ratio for osteonecrosis associated with older age of onset was 1.31.” Dosage was not a risk factor, he said.

In the childhood SLE group, “osteonecrosis never developed before 14 years of age,” said Dr. Nakamura. “The youngest patients with osteonecrosis included a 14.9-year-old with osteonecrosis in the hip and a 15.5-year-old with osteonecrosis in the knee.”

Although the findings should be replicated in a larger investigation, clinicians should be cognizant of the potential increased risk of osteonecrosis in children diagnosed with SLE at a later age, in order to optimize screening and management, Dr. Nakamura concluded.

Dr. Nakamura had no conflicts of interest to disclose with respect to his presentation.

T1 MRI of a 17-year-old girl on steroids shows femoral head osteonecrosis.

STIR shows bone marrow edema, right femoral head collapse 10 years later.

Patient had intertrochanteric curved varus osteotomy of Nishio on right hip.

Collapse of bilateral femoral head had not progressed 9 years after surgery.

T1 (left) and STIR MRI (right) show osteonecrosis of the femoral head in a 15-year-old with SLE. The growth plates of the femoral heads have already closed. Images courtesy Dr. Junichi Nakamura

MRI shows reduction of femoral head osteonecrosis 19 years after steroids.

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