Early intervention 'cornerstone' to managing pediatric glucocorticoid-induced osteoporosis
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Early identification and timely intervention are key to treating children with glucocorticoid-induced osteoporosis, a preventive strategy outlined in five important principles by a speaker at ACR Convergence 2021.
“Vertebral fractures are the hallmark of [glucocorticoid-induced osteoporosis (GIO)] in children with inflammatory disorders,” Leanne Ward, MD, research chair in pediatric bone health at the University of Ottawa and scientific director of the Ottawa Pediatric Bone Health Research Group. This is the first of the principles she discussed.
These vertebral fractures are most likely to occur in the first year of glucocorticoid therapy, according to Ward. She added that glucocorticoid use is significantly associated with both vertebral and non-vertebral fractures. Vertebral fractures in children have been linked to a number of adverse outcomes, including back pain, kyphosis and loss of height, according to Ward.
It is for this reason that Ward urged ongoing vigilance for vertebral fractures in children undergoing steroid therapy. Regular spine X-ray and/or DXA scans are recommended, along with bone mineral density screenings every 6 months for the duration of steroid therapy. “They are frequently asymptomatic,” she said of vertebral fractures. “This necessitates routine screening.”
If screening reveals risk for vertebral fractures associated with glucocorticoid-induced osteoporosis, Ward said that the second principle is to determine whether the child is capable of recovering from osteoporosis on their own, without intervention. “Vertebral body reshaping after a vertebral fracture is a key sign of recovery that mitigates the need for osteoporosis intervention,” she said.
One sign of successful recovery is when the spine reshapes after discontinuation of glucocorticoids. However, she encouraged patience among rheumatologists managing these patients. “This takes time,” Ward said.
Younger children and those with less severely misshapen spines are more likely to recover without intervention than older children and those with more significant damage.
This brought the talk to the third principle, which is to understand which children will require intervention to mitigate the impacts of glucocorticoid-induced osteoporosis. “The classic candidate for GIO treatment is a child with the presence of at least one low-trauma vertebral or long bone fracture,” along with one of a few other criteria. These criteria include being older, having persistent risk factors and an unfavorable disease trajectory. Younger children with significant pain or loss of mobility may also be candidates for GIO intervention.
Intervention may include more regular imaging, glucocorticoid tapering or intravenous bisphosphonate therapy with zoledronic acid, depending on the patient and the severity of her condition.
The fourth principle is that zoledronic acid is associated with adverse events in some two-thirds of patients after the first dose. However, Ward noted that studies have shown that one-quarter of patients treated with placebo also experienced these effects, so careful monitoring of patients is warranted.
“A proportion of children experience disease flares that appear unlinked to osteoporosis treatment in this context,” she added. “That is important to keep in mind.”
The final principle is that there is a synergistic effect of anti-resorptive therapy and growth mediated skeletal modeling on cortical bone, according to Ward. “This provides rationale for not withholding bisphosphonate therapy despite low bone turnover states,” she said. “This is what GIO is – a low bone turnover state.”
With all these principles in mind, Ward closed with straightforward advice for rheumatologists. “My main take-home message here is that early intervention and secondary prevention of osteoporosis in children with persistent risk factors are the cornerstones of pediatric GIO management,” she said.