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Published 8 January 2009, doi:10.1136/bmj.39588.561840.BD
Cite this as: BMJ 2009;338:a1788
K Jacob, specialist registrar1, P J Trainer, professor of endocrinology1
1 Department of Endocrinology, Christie Hospital NHS Trust, Manchester M20 4BX
drkoshyjacob@gmail.com
| The first 150 words of the full text of this article appear below. |
A 35 year old woman was taking life long glucocorticoid (dexamethasone) and mineralocorticoid (fludrocortisone, Florinef, Squibb) replacement for congenital adrenal hyperplasia caused by 21-hydroxylase deficiency. She started taking topiramate (Topamax, Janssen-Cilag) in March 2005, and the dose was titrated to 100 mg daily for atypical seizures secondary to mesial temporal sclerosis.
Before starting topiramate she had been taking stable doses of dexamethasone (0.25 mg a day) and fludrocortisone (100 µg a day), with biochemical evidence of good control of her congenital adrenal hyperplasia (figure
). Within a few weeks of starting topiramate she complained of tiredness, nausea, weight loss, and muscle aches.
A diagnosis of hypoadrenalism was supported by raised plasma 17- hydroxyprogesterone, adrenocorticotrophin, and plasma renin activity. The rises in 17-hydroxyprogesterone and adrenocorticotrophin indicate an inadequate replacement dose of glucocorticoid (dexamethasone), and the rise in plasma renin activity indicates an inadequate replacement dose of mineralocorticoid (fludrocortisone).
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