Hi Susan,
When used for replacement therapy (as with CAH), dex has been found to be about 70-80 times more potent than HC. This is compared to the 30-40 times strength that is more commonly listed in drug conversion tables, which is, apparently, more applicable in situations where dex is used to treat an inflammation. In other words, with the 70-80x conversion, you need much less dex to do the job, with a condition like CAH, than was commonly thought, in the past.
Below, are a couple of references discussing this issue in reference to a study recently published by two doctors at Harvard and Yale Medical Schools, called Dexamethasone Treatment of Virilizing Congenital Adrenal Hyperplasia: The Ability to Achieve Normal Growth by Rivkees S and Crawford J. Pediatrics 2000; 767-773.
A review/discussion of this article can be found on the U. Michigan Health System website at http://www.ped.med.umich.edu/ebm/cats/cah.htm . I've included excerpts from a different source below, which also makes mention of the higher conversion factor.
Back in the Fall, Joan W. published yet another abstract, which corroborates these doctors' findings about the 80-1 relative potency. I saved it, at the time, but have since lost it somewhere in my computer---guess I haven't gotten the knack of saving web pages yet. Perhaps Joan will see this and publish the link for that abstract again.
Hope this helps!
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Successful treatment of congenital adrenal hyperplasia (CAH) with dexamethasone (DEX) is reported by Rivkees SA & Crawford JD from New Haven & Boston (Pediatrics 106:767, Oct). The impetus to use DEX for suppression of the pituitary-adrenal axis of children with CAH comes from its long half-life compared with cortisone or hydrocortisone. This report details nearly 20 years of experience in children with CAH due to 21- or 11- hydroxylase deficiency, focusing on 17 boys & 9 girls who were each treated with once daily, morning doses of DEX (mean dose =0.27 ( 0.01 mg/m2/d). Salt-loosers were also treated with fludrocortisone (0.05 ñ0.2 mg/d). Among the boys treated for a mean of 7.3 yr, mean changes in bone age & height age were 7.0 & 6.9 yr, respectively. In girls, mean treatment for 6.9 yr produced changes in bone & height ages of 6.5 & 6.3 yr, respectively. In a subset of patients who had advanced bone age before treatment, predicted adult height improved by ( 7 cm with prolonged DEX treatment. Adult height & predicted adult height of the children treated from an early age were commensurate with mid-parent target heights. The growth performance of these DEX-treated children appears to be better than that reported for children treated with hydrocortisone. Biochemical indices showed evidence of consistent, satisfactory pituitary-adrenal suppression. The investigators note that the widespread avoidance of DEX for treatment of CAH has been based on the mistaken assumption that DEX has greater suppressive effect on growth than other glucocorticoids. They report that when the daily dose of DEX they use is compared with hydrocortisone, DEX is 70-fold more potent. This relative potency is far greater than the 30-fold increased potency of DEX claimed by the pharmaceutical manufacturer. Because of its high potency, the investigators recommend use of a dilute elixir of DEX (0.1 mg/ml). They point out that the need for dosing only once daily is likely to improve compliance & facilitate maintenance of suppression.