The twice daily dosing would not be advisable for a young girl that is active in sport and such at school in my opinion after reading the abstarct below on normal healthy days let alone during a period where there is possible illness and erratic temp.

1: J Endocrinol 2001 Apr;169(1):65-70 Related Articles,  Links 

 
Bioavailability of oral hydrocortisone in patients with congenital adrenal hyperplasia due to 21-hydroxylase deficiency.

Charmandari E, Johnston A, Brook CG, Hindmarsh PC.

London Centre for Paediatric Endocrinology, University College London, London, UK.

The management of congenital adrenal hyperplasia due to 21-hydroxylase (CYP21) deficiency requires glucocorticoid substitution with oral hydrocortisone given twice or thrice daily. In paediatric practice little is known of the bioavailability of oral hydrocortisone tablets used in these patients. The aim of this study was to assess the bioavailability of oral hydrocortisone and to evaluate current replacement therapy in the light of cortisol pharmacokinetic properties. We determined the bioavailability of hydrocortisone following oral and intravenous administration in sixteen (median age: 10.9 years, range: 6.0-18.4 years) adequately controlled CYP21 deficient patients. Serum total cortisol concentrations were measured at 20-min intervals for 24 h while patients were on oral substitution therapy, and at 10-min intervals for 6 h following an intravenous bolus of hydrocortisone in a dose of 15 mg/m(2) body surface area. The area under the serum total cortisol concentration versus time curve (AUC) following oral and intravenous administration of hydrocortisone was calculated using the trapezoid method. The bioavailability was estimated by dividing the corrected for dose AUC after oral hydrocortisone administration by the corrected for dose AUC after the intravenous hydrocortisone administration and was exemplified as a percentage. After oral administration of hydrocortisone in the morning, median serum total cortisol concentrations reached a peak of 729.5 nmol/l (range: 492-2520 nmol/l) at 1.2 h (range: 0.3-3.3 h) and declined monoexponentially thereafter to reach undetectable concentrations 7 h (range: 5-12 h) after administration. Following administration of the evening hydrocortisone dose, median peak cortisol concentration of 499 nmol/l (range: 333-736 nmol/l) was attained also at 1.2 h (range: 0.3-3.0 h) and subsequently declined gradually, reaching undetectable concentrations at 9 h (5-12 h) after administration of the oral dose. After the intravenous hydrocortisone bolus a median peak serum total cortisol concentration of 1930 nmol/l (range: 1124-2700 nmol/l) was observed at 10 min (range: 10-20 min). Serum cortisol concentrations fell rapidly and reached undetectable levels 6 h after the hydrocortisone bolus. The absolute bioavailability of oral hydrocortisone in the morning was 94.2% (90% confidence interval (CI): 82.8-105.5%) whereas the apparent bioavailability in the evening was estimated to be 128.0% (90% CI: 119.0-138.0%). We conclude that the bioavailability of oral hydrocortisone is high and may result in supraphysiological cortisol concentrations within 1-2 h after administration of high doses. The even higher bioavailability in the evening, estimated using as reference the data derived from the intravenous administration of hydrocortisone bolus in the morning, is likely to reflect a decrease in the hydrocortisone clearance in the evening. Decisions on the schedule and frequency of administration in patients with congenital adrenal hyperplasia should be based on the knowledge of the bioavailability and other pharmacokinetic parameters of the hydrocortisone formulations currently available.

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Depending how old your Daughter is, under treatment when she is ill on a long  basis could effect both her advancement in growth, bone age and also be a problem with menstrual cycle or even cause PCOS if she is an adolescent in insufficient treated illness for an extended period.   At some point in the day when her temp shoots up she obviously is cortisol deficient and this means any excess cholesterol is converted to androgens instead.  On a day to day basis this isn’t really that good and espeically not for girls.   There are too may risks asscoaited with hyperandrogenism as you will know anyway such as increased masculinization on top of what would have occured in utero.    Also when there is undertreatment in that way there is also a lesser ability to deal with injury I would imagine.    I would never send Ashley to school in those circumstances if he had a fluctuating temp or complained of discomfort.  That is a signal that things are not quite right really.  Normal healthy children may be ok, they can handle the stress if it occurs, though even then they would probably have a delayed recovery than they otherwise would if they were chilling out for a few days at home and getting some rest until they fully recuperate.    I don’t think that is an old fashioned attitude I have either.  It makes good deal of sense and especially given the circumstances for children with CAH and what can happen in illness at short notice.  That is about all that anyone could advise you really about increasing steroid in times of illness.  It is  down  to the individual parents response basically and we learn as we go along and as we see certain things occurand after a few crisis.

Here is an abstract on Hypoaldosteronism which could result in insuficient treatment for SWCAH if they are ill and it is not dealt with due to the fact that in illness, the body usually makes more aldosterone.  In SWCAH giving extra hydrocortisone covers the child.  Not giving increased meds in illness or mild illness I guess could also cause excess secretion of sodium and elevated potassium:

1: Vitam Horm 1999;57:177-216 Related Articles,  Links 

Hyper- and hypoaldosteronism.

Torpy DJ, Stratakis CA, Chrousos GP.

National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.

Aldosterone participates in blood volume and serum potassium homeostasis, which in turn regulate aldosterone secretion by the zona glomerulosa of the adrenal cortex. Autonomous aldosterone hypersecretion leads to hypertension and hypokalemia. Improved screening techniques have led to a re-evaluation of the frequency of primary aldosteronism among adults with hypertension, recognizing that normokalemic cases are more frequent than was previously appreciated. The genetic basis of glucocorticoid remediable aldosteronism has been elucidated and adequately explains most of the pathophysiologic features of this disorder. A new form of familial aldosteronism has been described, familial hyperaldosteronism type II; linkage analysis and direct mutation screening has shown that this disorder is unrelated to mutations in the genes for aldosterone synthase or the angiotensin II receptor. The features of aldosterone hypersecretion may be due to non-aldosterone-mediated mineralocorticoid excess. These include two causes of congenital adrenal hyperplasia (11 beta-hydroxylase deficiency and 17 alpha-hydroxylase deficiency), the syndrome of apparent mineralocorticoid excess (AME) due to 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) deficiency, primary glucocorticoid resistance, Liddle’s syndrome due to activating mutations of the renal epithelial sodium channel, and exogenous sources of mineralocorticoid, such as licorice, or drugs, such as carbenoxolone. The features of mineralocorticoid excess are also often seen in Cushing’s syndrome. Hypoaldosteronism may lead to hypotension and hyperkalemia. Hypoaldosteronism may be due to inadequate stimulation of aldosterone secretion (hyporeninemic hypoaldosteronism), defects in adrenal synthesis of aldosterone, or resistance to the ion transport effects of aldosterone, such as are seen in pseudohypoaldosteronism type I (PHA I). PHA I is frequently due to mutations involving the amiloride sensitive epithelial sodium channel. Gordon’s syndrome (PHA type II) is due to resistance to the kaliuretic but not sodium reabsorptive effects of aldosterone for which the genetic basis is still unknown. This review aims to provide a survey of the clinical disorders of aldosterone excess and deficiency and their clinical management, with a focus on primary aldosteronism and isolated aldosterone deficiency.

Publication Types:
Review
Review, Academic

PMID: 10232050 [PubMed - indexed for MEDLINE]

Another abstract about salt retention in illness whcih basically does outline the fact that illness and infection exacerbates the salt loss:

1: Eur J Pediatr 1990 Nov;150(1):22-5 Related Articles,  Links 

Sodium chloride supplement at diagnosis and during infancy in children with salt-losing 21-hydroxylase deficiency.

Mullis PE, Hindmarsh PC, Brook CG.

Endocrine Unit, Middlesex Hospital, London, UK.

Eight infants (6 female, 2 male) with salt-losing congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency were studied to determine the sodium deficit at diagnosis and the level of salt supplement required in addition to subsequent hormone replacement. The median sodium deficit at diagnosis was 34 mmol (range 16-78) or 10.5 mmol/kg (range 4-24). A mean sodium supplement of 2.2 mmol/kg per day (range 0.5-4.9), double the amount provided with feeds, was required to maintain plasma sodium concentration and plasma renin activity (PRA) in the normal range for age. We present an equation based on sodium output (urine), sodium input (feeding plus supplement) and plasma sodium concentration to calculate the sodium supplement needed to maintain sodium balance on hormone replacement in this condition and some practical management suggestions. The necessity for salt supplements is often underestimated and the salt-losing tendency exacerbated by infection remains an unnecessary reason for hospitalization during the first months of life. In patients with salt-losing CAH life-long mineralocorticoid treatment is necessary but additional salt supplements are needed to maintain plasma sodium concentration and PRA in the normal range during infancy.

PMID: 2079072 [PubMed - indexed for MEDLINE

 

I could post a few more abstracts, but I really think you should go back to your Doctor for advice.

Cheers

Anne-Marie