Hey Randy,
Long post! Don't hesitate to ask more questions when you have them!
I'm no doctor but you've completely failed the ACTH stimulation test in my opinion! Your endo is a moron if he thinks your response is "sluggish". WIth 1000X the ACTH that your pituitary would stimulate your adrenal glands (in the case of a 250 mcg ACTH test), you didn't even stimulate into the normal range for morning cortisol.
GET HARDCOPIES OF YOUR RESULTS AND GO TO ANOTHER ENDO IMMEDIATELY! You may want to request the following tests:
DHEA-S, Aldosterone, renin, sodium and potassium, pituitary panel if you can get it, antiadrenal antibodies, 17-OH progesterone (17-OH-progesterone is the substrate for subsequent 21- and 11-hydroxylation to produce cortisol. The two critical enzymes, 21-hydroxylase and 11-β-hydroxylase, participate in cortisol generation. If hydroxylation, at either position, cannot take place because of enzyme deficiency, cortisol synthesis decreases, accompanied by increased ACTH. Congenital adrenal hyperplasia and adrenogenital syndrome result from lack of normal glucocorticoids and buildup of precursors (mostly virilizing). Lack of 21-hydroxylase is the most common cause of adrenogenital syndrome. Congenital adrenal hyperplasia caused by 21-hydroxylase deficiency is the most common cause of female hermaphroditism.3 It is an autosomal recessive disorder. Basal 17-hydroxyprogesterone levels can be normal in late-onset 21-hydroxylase deficiency presenting as hirsutism. Such patients are described as having dramatically increased 17-hydroxyprogesterone response to ACTH.4 Patients with 21-hydroxylase deficiency have increased 17-ketosteroids, urine pregnanetriol, as well as high 17-hydroxyprogesterone. Prenatal diagnosis of congenital adrenal hyperplasia is possible by HLA typing, by DNA analysis, or by hormone measurements from amniotic fluid, including 17-hydroxyprogesterone.3 Some nonspecificity is seen when amniotic fluid analysis is used.5 Congenital adrenal hyperplasia with adult onset is among the causes of hirsutism and/or infertility.)
http://www.addisonssupport.com/homepage.htm Go to: understanding the Adrenals and Cortisol The chapter from Cecil's Medical text is good. From the LabCorp.com Endocrine Appendix:
ACTH Stimulation Test, One-hour
Screen for Adrenal Insufficiency
The ACTH stimulation test measures the functional integrity of the adrenal glands and their sensitivity to ACTH stimulation.1-5 Individuals with primary adrenal insufficiency fail to produce cortisol levels >18 μg/dL after ACTH stimulation. The test also indirectly assesses hypothalamic and pituitary function. When endogenous ACTH production is impaired by pituitary or hypothalamic dysfunction, the adrenal gland loses its capacity to respond to exogenous stimulation. It should be noted that there is a short period (up to three months) after the onset of pituitary/hypothalamic dysfunction during which the adrenals continue to respond to exogenous ACTH. Recent pituitary surgery or other debilitation of the pituitary/hypothalamic axis can produce misleading results. Generally, peak cortisol values >18 μg/dL at any point during the ACTH stimulation indicate adequate adrenal-pituitary-hypothalamic function. Peak cortisol results between 13 and 17 μg/dL are indeterminate and often become normal when ACTH stimulation testing is repeated. While the standard or low-dose ACTH stimulation test can be diagnostic of adrenal insufficiency when the response is subnormal, some patients with normal results may exhibit adrenal insufficiency in severely stressful situations (eg, surgery or trauma).6
Some investigators recommend measuring serum aldosterone levels along with cortisol. If the cortisol response is insufficient, the aldosterone levels can help localize the deficiency. The aldosterone response in a cosyntropin test is blunted or absent in patients with primary adrenal insufficiency. In secondary or tertiary adrenal insufficiency, aldosterone response is normal (an increase of two times baseline) because the renin-angiotensin axis is not affected by decreased endogenous ACTH.
Protocol: Draw blood for baseline cortisol with or without aldosterone. Inject cosyntropin 250 μg (see note below) IM or IV. (if IV, dilute cosyntropin in 2-5 mL of sterile saline and inject over two minutes). Draw blood for cortisol (with or without aldosterone) at 30 and 60 minutes after injection.
Orderable Tests: 028498 Cortisol x3; 053272 Aldosterone x3
Note: The standard, high-dose ACTH stimulation test involves the administration of 250 μg of cosyntropin. The resultant concentration is super-physiologic (ie, in vast excess to endogenous concentrations of ACTH). Stimulation studies with a more physiologic concentration (1 μg) of cosyntropin have been described.7 This low-dose ACTH stimulation protocol may be more sensitive than the traditional 250 μg test. Cortisol cutoff levels used for the low-dose test are the same as those used for the traditional test. Aldosterone levels during the low-dose test have not been documented. Use of low-dose ACTH has not been documented for testing for CAH.
