From: Holly Jagger <[log in to unmask]>
Listers,
>Does anyone know how Synthroid bloodlevels affect cortisol replacement
>for
>addisons?
Not a direct answer.
But, according to Thyroid Manager ( http://www.thyroidmanager.org/Chapter5/5a-frame.htm ), "Glucocorticoids (hydrocortisone, prednisone, dexamethasone) Inhibit conversion of T4 to T3"
Also be aware, glucocorticoids like hydrocortisone can suppress TSH. They probably wouldn't with the replacement doses you are taking, but you do need to be aware that there is a thyroid effect on the hydrocortisone. Here's something from Thyroid Manager that discusses it -
http://www.thyroidmanager.org/Chapter5/5a-frame.htm
<Quote>
Glucocorticoids. Physiologic amounts, as well as pharmacologic doses of glucocorticoids influence thyroid function. Their effects are variable and multiple, depending on the dose and on the endocrine status of the individual. The type of glucocorticoid and the route of administration may also influence the magnitude of the effect.323 Known effects include (1) decrease in the serum concentration of TBG and increase in that of TTR;324,325 (2) inhibition of the outer ring deiodination of T4 and probably rT3;239,240 (3) suppression of TSH secretion;246,326,327 (4) a possible disease in hepatic binding of T4; and (5) increase in renal clearance of iodide.328,329
The decrease in the serum concentration of TBG caused by the administration of pharmacologic doses of glucocorticoids results in a decrease in the serum total T4 concentration and an increase in its free fraction and the resin uptake test result. The absolute concentration of FT4 and FT4I remain normal. The more profound decrease in the concentration of serum T3 compared to T4 associated with the administration of pharmacologic doses of glucocorticoids cannot be solely ascribed to their effect on serum TBG. It is due to the decreased conversion of T4 to T3 in peripheral tissues. Thus, glucocorticoids reduce the serum T3/T4 ratio and increase that of rT3/T4 in hypothyroid patients receiving replacement doses of thyroid hormone.239 This steroid effect is rapid and may be seen within 24 hours.239,240 In rats, dexamethasone has been shown to decrease T4 to T3 conversion in liver homogenates. 329a
Earlier observations of cortisone-induced depression of uptake and clearance of iodide by the thyroid328,329 now are understood to be the result of steroid suppression of TSH secretion. Pharmacologic doses of glucocorticoids suppress the basal TSH level in euthyroid subjects and in patients with primary hypothyroidism, and decrease their TSH response to TRH.246,326,327,329b The latter effect is less marked in the presence of hypothyroidism.327 Administration of as little as 34 mg. of hydrocortisone over 24 hours can be shown to reduce the pulse amplitude and mean TSH release the nocturnal rise of TSH and the T3 and TSH response to TRH.329b Administration of the glucocorticoid antagonist, mifepristone, produces an increase in TSH that remains within the normal range accompanied by a transient decrease in total but not free T4.329c Normal adrenocortical secretion appears to have a suppressive influence on pituitary TSH secretion because patients with primary adrenal insufficiency have
a significant elevation of TSH.330 In cultures from rat pituitary tumors, hydrocortisone increased the number of TRH receptors 331 Dexamethasone has also been shown to increase the transcription, translation and processing of TRH precursors. 331a,b The mechanism of glucocorticoid action on the hypothalamic-pituitary axis is covered in Chapter 4.
<Unquote>
As for the Florinef, that and hydrocortisone can also affect blood pressure. A few interesting things about florinef (fludrocortisone) below -
http://home.intekom.com/pharm/bm_squib/florinef.html
<Quote>
Thyroid medicine: Metabolic clearance of fludrocortisone is decreased in hypothyroid patients and increased in hyperthyroid patients . Changes in thyroid status of the patient may necessitate adjustment in fludrocortisone dosage.
Estrogens, including oral contaceptives: Fludrocortisone half-life and concentration may be increased and clearance decreased. A reduction in fludrocortisone dosage may be required when estrogen therapy is initiated, and an increase required when estrogen is stopped.
Vaccines: Neurological complications and lack of antibody response may occur when patients taking fludrocortisone are vaccinated (see WARNINGS).
There is an enhanced corticosteroid effect in patients with hypothyroidism and in those with cirrhosis
Since fludrocortisone acetate is a potent mineralocorticoid, most adverse reactions to FLORINEF are caused by this activity and include hypertension, oedema, cardiac enlargement, congestive heart failure, potassium loss and hypokalaemic alkalosis.
Both the dosage and the salt intake should therefore be carefully monitored in order to avoid the development of hypertension, oedema, or weight gain. Periodic checking of serum electrolyte levels is advisable during prolonged therapy; supplemental potassium chloride administration may be needed.
<unquote>
So, it could mean over replacement of thyroid meds, but it could also mean overreplacement of the hydrocortisone / Florinef.
Corticosteroids can artificially lower TSH levels, making it a bit more complicated. I'm sure it's not an easy process to balance all those hormones correctly.
Skipper
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