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Steroids Affect Growth in Nephrotic Syndrome


 

SNOWMASS, COLO. — Glucocorticoid steroid use appears to limit height gains in children with idiopathic nephrotic syndrome, but do not necessarily reduce bone density, Dr. Lenore Buckley said at a symposium sponsored by the American College of Rheumatology.

“The issue of what glucocorticoids do to bone mass in children is an area where we are only just beginning to get some data,” said Dr. Buckley, of the Medical College of Virginia, Richmond.

One cross-sectional study looked at 60 children with isolated idiopathic nephrotic syndrome being treated with glucocorticoids, and compared them with 195 matched controls, mean age 9–10 years. Children treated with glucocorticoids were found to lose height but not necessarily bone density (N. Engl. J. Med. 2004;351:868–75).

In the group treated with glucocorticoids, 26 study participants were black, and 39 control group participants were black, according to the study data.

Previous studies have found that children lose bone mineral density when treated with glucocorticoids. But those studies looked at children with systemic illnesses, such as juvenile rheumatoid arthritis and inflammatory bowel disease, so it is not clear whether their low density was due to their treatment with glucocorticoids or to their systemic condition.

The mean height z score of the children in the control group was positive (0.35), whereas the mean height z score of the glucocorticoid treated children was negative (- 0.17), the study found.

At the lumbar spine, the same bone mineral density per unit area was found in both the control and glucocorticoid treated groups, however.

“For what bone [both groups] have, the density is the same, but [the glucocorticoid group doesn't] have as much bone because they don't grow as much,” Dr. Buckley said. The bone density for the treatment group could be due to the glucocorticoid, which causes weight gain, and weight stimulates bone density growth.

The mean body mass index z score for children with nephrotic syndrome was 1.24, while the score for controls was 0.34. There was also a higher percentage of obese children in the nephrotic syndrome group, compared with the control group (38% vs. 16%, respectively), the study found.

A more detailed look at the children's bone density found that those with nephrotic syndrome had slightly lower trabecular bone density (mean z score - 0.27, vs. 0), but much greater cortical bone density (mean z score 0.87, vs. 0). This situation also suggests that while there may be a process interfering with bone accumulation, there is also some compensation due to weight gain, Dr. Buckley said.

Children with nephrotic syndrome go on and off glucocorticoid treatment, which could allow for some periods of recovery, so these findings may not extrapolate to children treated chronically, Dr. Buckley noted.

“What it tells us is that in the short run, these kids are not at risk for fracture—they have pretty good density,” she said. “But what it doesn't tell us is the risk of fracture in the future.”

Adults not taking glucocorticoids whose rate was one standard deviation below the mean as a child have a four times higher risk of fracture, studies show.

The evidence also shows that adult patients who take glucocorticoids lose bone mineral density early and quickly, and their risk of fracture goes up rapidly. However, over time, it has been found that the loss stabilizes, and when glucocorticoids are stopped there is some recovery, though it is not clear how much recovery and whether patients fracture risk returns to the level it was before glucocorticoid use.

In adults, “we think now that there probably is almost no safe dose of glucocorticoids that couldn't possibly lead to some decrease in bone mass,” said Dr. Buckley.

'In the short run, these kids are not at risk of fracture—they have pretty good density.' DR. BUCKLEY

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