Just got my letter back from the Endo I saw 3 weeks ago and he has checked for various things with my bloods - but all "normal" range...
Anyway, the SST was basal cortisol at 332 nmol/L then after injection was 661nmol/L
is this mid range or on the cusp does anyone know?
Thanks.
See my historical posts on this very subject. The nhs has no ranges therefore your tests are always "normal" (which is exactly what suits the nhs) - these tests are one of the biggest nhs farces going. If you look at the print out it actually says something like "no ref ranges extablished"
In general, the NHS doesn't have ranges; though individual laboratories do have interpretation guidance.
For example:
Interpretation
Adrenal insufficiency is excluded if there is a rise in the 30 minute cortisol over the 0 minute cortisol of
>200 nmol/L and the 30 minute cortisol is >550 nmol/L.
pathology.bsuh.nhs.uk/Patho...
The document also lists indications, contra-indications, further considerations, etc.
As labs vary, please folk, DO NOT use these numbers - check with the guidance of the laboratory that did your test.
Rod
Hi joanne, I've had 2 tests, from memory the baseline level has to double or at least reach 500 for them to be satisfied. In my first test mine only rose by a 100 so my GP started me on HC which I stayed on for about a year then with his help weaned myself off. I was sure it was as a result of being hypo for so long that had exhausted my adrenals and I guess it was because my 2nd test was 'normal' as my baseline doubled. There's an article on the BMJ about 'their' levels. - bestpractice.bmj.com/best-p...
Afraid that link gets blocked by a sign-in page.
Rod
Bah, that's frustrating. I got that link from Google. Try this one Rod - the full google link but shortened: bitly.com/1iAJlc1
Just in case others have a problem with access, here's info:
Source: BestPractice.BMJ.com:
Step-by-step diagnostic approach
Addison's disease is difficult to diagnose. It manifests with non-specific signs and symptoms, such as fatigue, weakness, and weight loss, which are also common to other diseases. A high percentage of patients are diagnosed after a life-threatening adrenal crisis. Groups of patients with risk factors for developing Addison's disease should be viewed as being at high risk so that a diagnosis can be established early. Secondary adrenal insufficiency is also associated with severe cortisol deficiency, but otherwise has a different clinical presentation (e.g., no pigmentation and only mild mineralocorticoid deficiency). Therefore, the finding of hypocortisolism is not unique to primary adrenal insufficiency. A history of treatment with glucocorticoid in recent months, or the possibility of hypothalamic-pituitary disease (e.g., concurrent emergence of other secondary pituitary deficiencies, such as thyroid or gonadal deficiencies), should prompt evaluation for secondary adrenal insufficiency.
History
Fatigue and weakness are the most common presenting symptoms. They are usually insidious and may be accompanied by variable degrees of muscle weakness and myalgias.
Anorexia is often present and may lead to significant weight loss. Both are important features in patients with Addison's disease.
Dizziness, arthralgia, and myalgia are less common.
GI symptoms including nausea, vomiting, constipation, and abdominal pain may lead to a misdiagnosis of acute abdomen. Salt craving may be present.
History should be directed at establishing the underlying cause, such as a known history of autoimmune disease, HIV infection, possible tuberculosis infection, and current medication use.
Sudden alterations in glycaemic control and recurrent hypoglycaemia in patients with type 1 diabetes mellitus may suggest autoimmune polyglandular syndrome type 2 with co-existing diabetes and Addison's disease.
Physical examination
Most patients present with significant weight loss secondary to anorexia.
MucosalView image and cutaneous hyperpigmentation,View imageView image which is generalised and more pronounced in areas of increased friction, such as palms, knuckles, and scars, is present in about 95% of patients.
Postural hypotension may be present.
Other signs of autoimmunity, such as vitiligo, Hashimoto's thyroiditis, and pernicious anaemia, may be present.
Women may have significant loss of axillary and pubic hair.
Laboratory evaluation
In an emergency situation, the physician should not wait for the results of blood tests before administering treatment. In this situation, blood is drawn for a random cortisol level if diagnosis is not known, and treatment administered immediately. The following investigations are appropriate when in a less urgent situation.
Morning serum cortisol
The first diagnostic test is morning plasma cortisol level. This is used as a test of exclusion.
A level below 83 nanomols/L (3 micrograms/dL) is highly suggestive of adrenal insufficiency.
A cortisol level above 497 nanomols/L (18 micrograms/dL) effectively excludes Addison's disease.
Cortisol levels of 83 nanomols/L to 497 nanomols/L (3 to 18 micrograms/dL) require further testing with a high-dose ACTH stimulation test to confirm diagnosis.
High-dose ACTH stimulation test
If cortisol levels below 497 nanomols/L (18 micrograms/dL) are found at either 30 or 60 minutes after ACTH stimulation, the diagnosis of adrenal insufficiency is highly likely.
Cortisol levels exceeding 497 nanomols/L (18 micrograms/dL) at 30 or 60 minutes after administration of ACTH (250 micrograms) exclude the diagnosis of primary adrenal insufficiency in most instances; however, some patients with secondary adrenal insufficiency of recent onset or partial ACTH deficiency may manifest a normal response. In situations where this is suspected, patients should either have the stimulation test repeated using a low dose of ACTH (1 microgram), or preferably have a test of the entire hypothalamic-pituitary-adrenal axis (e.g., the insulin tolerance test or the overnight metyrapone test).
Patients with levels slightly below normal should have the test repeated at least once.
Patients who have an abnormal ACTH stimulation test consistent with adrenal insufficiency require further laboratory evaluation to determine the type of adrenal insufficiency.
Serum ACTH level should be measured. If high, the cause is primary adrenal insufficiency. A low value would support a diagnosis of secondary adrenal insufficiency.
If ACTH is inconclusive, a low plasma aldosterone is supportive of Addison's disease.
Ancillary tests
Blood testing for hyperkalaemia, uraemia, hyponatraemia, hypercalcaemia, and eosinophilia should be performed, as these are additional indicators of Addison's disease.
In some patients after diagnosis of primary adrenal insufficiency, the underlying cause is still uncertain. Imaging of the adrenals using CT and MRI can be useful where infection, haemorrhage, or metastatic disease is suspected.
If secondary adrenal insufficiency is suspected, but the cortisol response to ACTH is not diagnostic, a test of the entire hypothalamic-pituitary-adrenal axis may be helpful (e.g., the insulin tolerance test or the overnight metyrapone test). The insulin tolerance test measures the cortisol response to insulin-induced hypoglycaemia. Vigilance is required, due to the fact that hypoglycaemia is an endpoint. The test is contraindicated in older adults and in people with CVD or seizure disorder. The overnight metyrapone test measures the 11-deoxycortisol and cortisol response to metyrapone. Care is required since there is a risk of precipitating adrenal insufficiency, because metyrapone blocks a step in cortisol synthesis.
Plasma renin activity is a further investigation of the renin-angiotensin-aldosterone axis that may be done. In patients with Addison's disease the entire adrenal cortex is involved, and biosynthesis of aldosterone is compromised in addition to that of cortisol. To compensate, renin levels become elevated, but they are ineffective. In contrast, in secondary adrenal insufficiency the renin-angiotensin-aldosterone axis is intact, although slightly less responsive as a consequence of suppressed cortisol concentrations.
Plasma dehydroepiandrosterone (DHEA) and DHEA sulphate (DHEAS) may also be performed. Serum DHEA and DHEAS concentrations are consistently suppressed in both Addison's disease and secondary adrenal failure and in acutely ill patients, so these are tests of high sensitivity but low specificity.
Antibodies directed against the adrenal enzyme 21-hydroxylase are associated with autoimmune Addison's disease, but although sensitive they are not necessary for the diagnosis, or specific. Patients with other autoimmune diseases, such as type 1 diabetes, rheumatoid arthritis, vitiligo, or Hashimoto's thyroiditis, may develop autoantibodies against the adrenal cortex. However, the development of clinical adrenal insufficiency does not occur consistently.
Very Interesting...I had a SST last week, my serum Cortisol was 197 (176-600) so my Endo wanted it done. Haven't got my results back as yet!!
Thanks, looks like mine really are fine then, thats good.
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