As far as I know, the symptoms of primary and secondary Addison's are exactly the same. The only difference is whether the adrenal glands have failed because of failure somewhere else (i.e., pituitary) (secondary), or if they have just quit on their own (primary). I was originally diagnosed with primary Addison's until further tests revealed that my pituitary gland was hypo, which changed the diagnosis to secondary. My growth hormone level and my thyroid were also affected. The treatment did not change once the diagnosis did; I still take 20 mg. of Cortef per day in divided doses. In the beginning, I was also on .1 Florinef, but it was later determined that I didn't really need it, which is most often the case in secondary. I hope this helps to answer your question.

Primary also has adrenal hypoaldosteronism and if untreated you can have symptoms like muscle weakness, extreme salt cravings, and very low blood pressure. You must take florinef and extra salt to compensate.

Secondary doesn't have this problem but may have other hormonal loses such as low growth hormone, elevated prolactin, sex hormone problems and thyroid problems.

Secondary is easy to separate from primary by simply testing the adrenal glands with ACTH. If they respond to the test, you are secondary, if you don't respond with an increase in cortisol you are primary. It's fairly simple to establish which is which.

How were you diagnosed? What tests were used to establish your adrenal insufficiency. If it was just a blood test for cortisol, you need much more than that.

[QUOTE=orion;3124659]Primary also has adrenal hypoaldosteronism and if untreated you can have symptoms like muscle weakness, extreme salt cravings, and very low blood pressure. You must take florinef and extra salt to compensate.

Secondary doesn't have this problem but may have other hormonal loses such as low growth hormone, elevated prolactin, sex hormone problems and thyroid problems.

Secondary is easy to separate from primary by simply testing the adrenal glands with ACTH. If they respond to the test, you are secondary, if you don't respond with an increase in cortisol you are primary. It's fairly simple to establish which is which.

How were you diagnosed? What tests were used to establish your adrenal insufficiency. If it was just a blood test for cortisol, you need much more than that.

Thanks. I know it's kind of a weird question. The truth is I'm not sure how I was diagnosed exactly. I'd been having symptoms that pointed towards Addison's -- salt cravings (only thought of a symptom in retrospect), orthostatic hypotention, fatigue, vomiting, etc. But no noticeable darkening of the skin. I went into the ER for diabetic ketoacidosis. Something about my blood work -- I *think* my electrolytes -- was off.

I remember being told that they couldn't do the Insulin-induced hypoglycemia test. I have no recollection of being given any other specific tests. I think I was diagnosed as Secondary mostly because I didn't have the hyperpigmentation. But, since then, I've read that some of the symptoms I was having were only symtoms of Primary.

I'm currently taking 5mg of prednisone a day.

I also have Type I Diabetes and Hypothyroidism. For various reasons, I haven't been regularly seeing an Endocrinologist, but now I have an appointment with one and I'm trying to have a set of questions/issues ready for her.

Again, thanks for your reply! :)

Secondary is not rare at all. Endos are not good at diagnosing secondaries because they only look for doubling or more on the stim test. Most secondaries will at least double from a low base cortisol value. Endos don't look at how low the base is, just if doubled or not. If triple or more from low base cortisol, then endos think that is fantasic, ignorant of how secondaries usually do on stim tests. See the article I posted on the acth stim test a few months ago.

Endos and most types of docs are not looking for low aldosterone in secondaries because they've been taught secondaries don't have it, but doesn't make sense that absolutely no secondaries out there would not have low aldosterone? No exception? I estimate about half of secondaries have some degree of salt wasting and low renin, low aldosterone.

I haven't figured out why secondaries get the low renin which is an enzyme make in the kidneys. If their renin was at a good level, then their aldosterone would probably be ok since your right, adrenals usually are ok except if they decide to atrophy from lack of renin and acth. I've been seeing low renin in secondaries for several years now, very common. I'm secondary and my renin was below range and my aldosterone was at the very bottom of the range. I suffered greatly before taking florinef with salt.

Note: For women is best to test aldosterone in the first 7 days of their cycle by the way. The middle to late cycle progesterone is high and since aldosterone is made from progesterone, aldosterone can look ok even with symptoms of salt wasting. I've told many women who had salt wasting, but aldosterone looked ok tested in middle of cycle, to retest at the beginning of their cycle and then their aldosterone always come back low.


If low renin, then potassium will be mid point or lower range. Low potassium is a good predictor of low renin I've found.

I've found low renin is a very good predictor of low acth and is the next best thing to use for determining secondary if the patient was started on steroid before having serum acth and acth stim.

labs of real secondary with low aldosterone and renin
Says 10 years treatment for prolactinoma, but I don't find labs for prolactin

morning
aldosterone 1 (1-21)
renin .6 (.6-23)

afternoon
aldosterone 5.5 (1-21)
renin 1.2 (.6-3.0)


sodium 134 (136-145)
potassium 4 (3.5-5.1) most secondaries are low but still in range on both tests. Low potassium is what secondaries get 99% of the time. By this sodium and potassium I would predict they would have low aldosterone and low renin.


DHEA-s 2.4 (3.7-9.5)
ACTH 33 (10-60) should have been well into the 40's

acth stim
base 8.1(8.7-22)
30 min 21
60 min 23.7

stim nearly tripled from very low base value