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I got a copy of the latest ACTH / Cortisol results (Test #3) myself and haven't been in for a follow-up with my Endo, but does this look like Primary Adrenal Insufficiency or am I just jumping to conclusions?

Test #1 - ACTH Stim Test (Done @ 2:00pm):
Baseline Cortisol - 3.2
Baseline DHEA(S) - 461 (110-370) - (135% of range)
Baseline Pregnenolone - 11 (13-208) - (-1% of range)
30 Min Cortisol - 12.7 (Ref >20) - More than doubled, but Low
60 Min Cortisol - 15.2 (Ref >20) - More then doubled, but Low

Test #2 - Saliva Cortisol Panel:
Morning - 7 (13-24) - "Depressed"
Noon - 6 (5-10)
Evening - 4 (3-8)
Midnight - 8 (1-4) - "Elevated"
Cortisol Burden - 25 (23-42)
DHEA - 9 (3-10)

Test #3 - Various Blood Tests:
ACTH - 69 (7-50) - (144% of range)
Cortisol @ 11:00a - 8.8 (4-22 @ 9:00am) - (26% of range)

It also bugs me that my DHEA(S) is High, but my Pregnenolone is Low. I thought Pregnenolone was a precursor to DHEA - does this mean I'm not making enough Pregnenolone from Cholesterol, or am I using it up too quickly to make DHEA/Progesterone/Aldosterone and all their products?

Any insight from anyone?
Well you can add a DHEA supplement first thing in the morning. Issue there is do not exceed 20 mg and if you suddenly get really bad acne.. it is normally from more DHEA than you can handle.

The autoimmune flavor of adrenal insufficiency can be detected with the ACA antibody test. Your Endo may or may not know of it. It is a newer test in endocrine studies from 2006 forward.

As to the fact your ACTH is high and your cortisol low normal. Would point toward your adrenals being the culprite in your insufficiency. I wish I could help you more. My internal medicine MD is treating me. My Endo thinks I am normal.. My TSH is too low for me to have an issue. ;) Glad I have the brains to self-diagnose and keep looking for a good MD.

MG
I've seen at least a thousand acth stims with serum acth over the years I've been doing this and never seen the combo of values you have. Your stim suggests secondary AI. I've never seen a secondary (going by a stim that doubled or more from a low value) with serum acth greater than 43. I've never seen a primary who doubled or more on the stim. I look for upper 40's to low 50's for a good acth. Your DHEA suggests primary. I recommend you read what wrote about interpreting the acth stim and acth serum tests. [url]http://www.healthboards.com/boards/showthread.php?t=472296[/url]


Your pregnenolone suggests hypopituitarism (acth, LH and FSH regulate pregnenolone which breaks down into DHEA, cortisol and sex hormones, so low pregnenolone suggests ACTH, LH and FSH are low).

Very wierd set of tests you have. I'm thinking you should be retested with ITT test instead of ACTH stim though ITT is used to stim, CRH, ACTH, cortisol and growth hormone and I recommend these all be tested in the ITT.

I recommend you get aldosterone and renin tested (fast salt 24 hours) especially if you have salt wasting symptoms (hard to handle outside heat, excessive sweating, excessive urination). Low renin (labs usually give the range for non fasting salt which is around 3-6, non fasting is about 3-24) is what secondaries have 99% of the time. Primaries have high renin. Aldosterone, fasting salt is around 4-22, labs usually give non fasting salt range. Secondaries will have low potassium 99% of the time, though some are in the middle of the range and it could go either way then. Primaries have high potassium, though some are in the middle of the range.

I recommend you also get total and free testosterone, LH, FSH, Estradiol, SHBG, igf-1. In primary hypogonad men, most will be top of the LH and FSH range to just above, secondary hypogonad men, 99% will be low, but in range.

Since thyroid always goes hand in hand with primary and secondary AI, also recommend you get TSH, free T3, free T4, TPO and Tga thyroid antibodies tested. In men, primary hypothyroid will be above 2.2 and higher, secondary is 1.8 or lower. Between 1.8 and 2.2 not so clear which it is if frees are low and hypo symptoms.

Wouldn't hurt to get prolactin tested, but in most cases isn't important to men unless top or above range, then prolactinoma tumor should be investigated. Sometimes hypothyroidism can raise prolactin which usually comes down when thyroid is treated.

Hang in there.
You're welcome. By the way, I've never seen secondary hypo without secondary AI. Not saying secondary hypo can't happen with secondary AI though, but have yet to see an exception.

About twice a year I see Hashi's/secondary hypothyroid combo. This may be antibodies attacking the pituitary and or possible past head injury as the cause. I see this combo in the ratio of 10 women for every 1 man, so maybe seen two other men with this combo over the years. About once every 2 months I see Hashi's with secondary AI. Again tell them possible antibodies attacking their pit (no test for that as far as I know) or they may have damaged their pituitary in a head bump in the past (could be decades earlier).

Make sure you get the renin run with the aldosterone. The renin can be helpful in determining primary or secondary. I've see secondary AI with high renin about once a year for exception (low renin = secondary AI 99% of the time), so very good predictor of secondary. You should have sodium and potassium tests (in CBC) if you want to get an indication of whether your renin could be low or high.
Alright, Hormoneman, you asked for it! (and MG, watch it with the Thread Hijacking! ;))

It all started with Thyroid checks:

Thyroid #1 (Late Jan):
TSH - 1.26 (18.8% of range)
FT4 - 1.15 (25% of range, +6% from TSH)
FT3 - 367 (72% of range, +47% from FT4)

Thyroid #2 (Early Feb):
TSH - 0.825 (8.6% of range)
FT4 - 1.07 (19.2% of range, +10% from TSH)
FT3 - 362 (69.4% of range, +50% from FT3)
Reverse T3 - 24 (Ref: 11-32)
Anti-TPO (for Hashi's) - <10 (Ref: <35)
TSI (for Grave's) - 106 (Ref: <=125)

Saliva Sex Hormones (as part of "Test #2" mentioned in first post):
Free Testosterone - 39 (50-80 pg/mL) - (-35% of range)
Progesterone - 39 (5-95 pg/mL) - (38% of range)
Estradiol - 10 (1-3 pg/mL) - (450% of range)

Addendum to "Test #3" mentioned in first post:
T, Total - 248 (241-827) - (1% of range)
T, Free - 73 (34-194) - (24% of range)
T, Free & Weakly Bound - 166 (84-402) - (25% of range)
Albumin - 5.0 (3.6-5.1) - (93% of range)
SHBG - 14 (8-48) - (15% of range)
LH - 1.8 (1.5-9.3) - (3.8% of range)
FSH - <0.7 "Undetectable" (1.6-8.0)
Prolactin - 6.1 (2.0-18.0) - (25.6% of range)
IGF-1 - 266 (106-255) - (107% of range)
ACTH - 69 (7-50) - (144% of range)
Cortisol @ 11:00a - 8.8 (4-22 @ 9:00am) - (26% of range)

CBC (last week):
WBC - 4.8 (4.0-11.0)
RBC - 4.77 (4.60-6.10)
HGB - 13.4 (13.5-18.0)
HCT - 39.3 (41.0-53.0)
MCV - 82.3 (80.0-98.0)
MCHC - 34.1 (32.0-36.0)
RDW - 14.4 (11.5-14.5)
PLT - 220 (130-400)

CMP (last week):
Glucose, Fasting - 82 (70-100)
Sodium - 142 (135-145)
Potassium - 4.2 (3.5-5.5)
Chloride - 103 (98-107)
CO2 - 27 (23.0-31.0)
Anion Gap - 12 (7-16)
BUN - 11 (5-25)
Creatinine - 0.9 (0.5-1.4)
Calcium - 9.6 (8.7-10.2)
Bilirubin, Total - 0.5 (0-1.0)
Bilirubin, Direct - 0.0 (0.0-0.4)
Total Protein - 7.4 (6.3-8.2)
Albumin - 4.9 (3.5-5.0)
AST (SGOT) - 32 (14-50)
ALT (SGPT) - 35 (21-72)
Alk Phosphate - 97 (50-136)
GGTP - 23 (8-78)
eGFR - >60 (Ref: >60)

Iron / Anemia Profile (Last Week):
Iron - 66 (60-180)
Iron Binding - 400 (200-400)
Percent Saturation - 16.5% (14-55%)
Ferritin, Serum - 8 (25-335)

Lipid Panel (Last week):
Cholesterol, Total - 150 (Ref: <200)
Triglycerides - 211 (Ref: <150)
HDL - 29 (40-59)
LDL - 79 (Ref: <100)
VLDL - 42 (No Ref given)
LDL/HDL Ratio - 2.7 (Ref: <3.55)
TC/HDL Ratio - 5.2 (Ref: <4.97)

Various Other Labs (Last Week):
Vit B12 - 355 (Ref: >240)
RBC Folate - 1150.1 (Ref: >160)
Phosphorous - 3.5 (2.5-4.5)
Uric Acid - 6.0 (3.5-8.0)
Relative Retic - 1.85% (0.1-2.0%)
Absolute Retic - 88 (5-94)

I've read the ACTH "Inperpretation Guide" on other forums (STTM) before, and I too was leaning towards Secondary, but my ACTH vs Cortisol looks like my Pit knows it's too low and is "raising it's voice" (we don't yell/shout in our household :D) to try to get more Cortisol.

Do you have references (that are legal to post here) that state that low Pregnenolone is a marker for Hypopituitarism? I thought since Preg. was a precursor for DHEA, and since my ACTH is probably high all the time, that it is all used up making DHEA and the other Adrenal products, (but not Cortisol for some reason - maybe an enzyme deficiency that is blocking Cortisol synthesis?). Doesn't the high ACTH in response to chronic lower Cortisol make Hypopituitarism less likely? (FSH/LH are low, but we'll get to that later). Also, since Aldosterone isn't ACTH depentent, wouldn't Pregnenolone need to be indepentend of ACTH as well, (or am I out in left field)?

Hopefully in "Round 2" with my Endo, he'll do the Aldosterone/Renin tests, (along with the Estradiol since it was high on the Saliva stuff). I have the "Hard to handle outside heat" thing, but I live in the Southern States, so that doesn't say much. ;) I haven't noticed any "excessive sweating" or "excessive urination", but if it were congenital, (which I suspect it is), then I wouldn't have a good point of reference to compare "excessive" to. Potassium and Sodium look ok. I did have a slightly low Potassium of 2.9 once back in 1994, but that was a while ago.

Sex hormones are another puzzler. As you can see, my T's, SHBG, and my FSH/LH are low, but my IGF-1 and Albumin are high. He didn't check Estradiol (E2), but since it was pretty high on the Saliva testing, I suspect it's pretty high. I read in some Endo training materials that the Hypothalamus can't tell T from E2, so if E2 is high it will lower GnHR and thus drop LH/FSH, and lower T/DHT production. Since low T/DHT means E2 synthesis isn't as repressed, more E2 is produced, the Hypothalamus sees too much sex hormones, and the cycle continues. I don't have Gynecomastia, (male boobies), but I don't think that rules out "Male Estrogen Dominance". It may be something as simple as too much T is being Aromatased into E2, and could I just use something to slow down the conversion, but there isn't a lot of info on this topic that I've found. I've called my Endo and left several messages asking to come in and check E2 and Aromatase rate, but I haven't heard anything back yet.

Thyroid function looks normal, (as far as TSH vs FT4), since it looks like my Thyroid is "following orders" and making as much T4 as the Pit wants. I know the TSH is lowered, but I think that has to do with low Cortisol downregulating Thyroid function instead of Hypopituitarism. The real puzzler is what is causing my FT3 to be +50 percentile higher then my FT4. I thought it was low Cortisol which prevents binding of the T3 at the cell and thus causing an increase in circulating T3, (what I term "Effective Hypothyroidism" since it's there but I can't seem to use it). I also read on a few other boards that E2 and T3 both compete for the same receptors, so high E2 might also explain the extra floating T3, (but I don't have any references other then a few posts on a Body Building forum). I'm still a little unsure as to if the Hypothalamus looks at FT4 or FT3 to regulate the Thyroid, so the relative elevated FT3 could also be a factor in causing the lowered TSH.

Prolactin, WBC, and RBC look good, so I don't suspect a tumor.

Iron, Ferritin, HGB, and HCT are a bit low, but that has to do with giving myself temporary low-iron Anemia, as I stated previously.

(Is it just me, or is this starting to feel like an episode of "House"...) :(
When I went in for the 2nd Thyoid panel, I specifically asked the Nurse for both the Anti-TPO and the TgAB, but they only ran one. I was going to go back to push the issue, but I was too distracted becaused they agreed to do an ACTH Stim test without any resistance.

From my understanding, you have two variants of Thyroid AB problems. Hashi's attacks the Thyroid itself causing spilliage, and Grave's fakes the Thyroid into thinking the Pit has told it increase production.

[quote=(A site I am not able to link to on these Forums)]

Hashimoto’s Thyroiditis is a common autoimmune condition in which one develops an allergy to one’s own thyroid gland. In the early phase when there is destruction of thyroid gland and spillage of thyroid hormone (T4), there is a hyperthyroid effect. In an effort to lower the T4 level in the blood, the pituitary gland decreases the amount of TSH it secretes producing a low TSH. The hyper-metabolic state that occurs usually stresses the adrenal glands and causes adrenal fatigue. When enough destruction has occurred and the thyroid gland can make only a small amount of T4, one goes into a hypothyroid phase. Now one has hypothyroidism and adrenal fatigue. Autoimmune antibodies, Anti Thyroglobulin Antibodies (ATA) and Thyroid PerOxidase Antibodies (TPO), are almost always present on blood testing. The body can eventually counter the hyper-metabolic state by reducing the conversion of T4 to T3 (and increasing T4 to RT3 conversion). Thus metabolically, this is like stepping on the brakes in a car that’s going too fast.
[/quote]

If you look at my FT4 vs TSH, it is only about +8 percentile higher. I assume that if it were Hashi's, the FT4 would be higher and the liver would try to slow things down by pumping up RT3. However, my FT3 is higher then my FT4 and my RT3 looks ok, so there doesn't seem to be a lot of throttling down.

[QUOTE=(Same site as above)]

Grave’s Disease is an autoimmune disease in which an antibody is produced that mimics TSH. It signals the thyroid gland to make T4. As the T4 level rises, the pituitary tries to reduce the T4 level by reducing TSH levels and we get a low TSH. Typically we find elevation of Thyroid Stimulating Immuneglobulin or TSI. Most labs consider a level of 130 or higher as evidence of Grave’s Disease. In reality, we often see the signs of hyperthyroidism begin to appear in a subtle way at a level of 90. At 110 the symptoms are easier to see. By the time we get to 130 the symptoms are usually severe. Unlike Hashimoto’s Thyroiditis, in Grave’s disease the T4 goes into high conversion to T3. This is like driving a car too fast and stepping on the accelerator. This is extremely stressful to the adrenals. [/QUOTE]

My FT4 is pretty good in the 20-25% of range, and my TSI was at 106, so if there is Grave's it is very slight. However, after I figure out the Adrenal / Sex Horemones thing, I will keep an eye on my TSI/TRAb levels.

So, MG, based on your Thyroid knowledge, am I doing ok, or am I totally missing the point?
My DHEA is low normal.. my ACTH is about 200+% of range. So they do not have to be parallel in range.

My cortisol is lower.. and with regards to the ACTH it means as you say.. your pituitary is telling it to make more.. but the adrenals just can not put out. I need to now test the aldosterone and other home made steriods to see if it is an isolated phenomena. You should do the same.

The human adrenal cortex produces aldosterone, cortisol and the so-called adrenal androgens, dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS). We know you are low in cortisol and high in DHEA.

I do not know about the others for you or me. My IM was humoring me when she ran the others and I was right again. Which got a snort and grin and a you know as much if not more than me out of her. I told her not true.. i do not know more about medicine, I am just ground zero to my symptoms and a a.retentive chemist. I am going to have to do some digging into the mechanistic theory you have proposed here. May take me a few days. But it sounds good. ;)

Pregnenolone is a natural hormone made from cholesterol in the body. Pregnenolone is an intermediate in the synthesis of all steroid hormones. It is synthesized inside the mitochondria, the tiny "power plants" found in each cell. Pregnenolone is synthesized from cholesterol and is a precursor for the biosynthesis of steroid hormones. Pregnenolone is the basic precursor for the production of all the human steroid hormones, including DHEA, progesterone, estrogen, testosterone, cortisone, cortisol and aldosterone. Its levels are highest in the brain and studies have shown that it enhances many of our mental functions.

Conclusions: Low pregnenolone can mean a deficiency in any of the hormones it is a precurser for. What minerals and limiting reagents does our body need to convert it to cortisone, cortisol.. etc. Maybe it is a blood chemistry thing aggravating issues. Once again the endocrine system is far from A + B = C.

The thyroid hormone T2 is suspected to be a driving force in this. Since your hormones are off yhou may need to look into your T2 levels. T0-T2 were once thought of as inactive.. however.. T2 has been found integral on a cellular level. SO a good look at the thyroid which is just as tied into the adrenals and pituitary/hypothalumus cogs as well may be helpful. The endocrine sysdtem is a delicate balance of everything.. somethings a fix of the thyroid makes everything else behave.. others require more attention. Who KNOWS.. we have to make hypotheses and run them all out to conclusion.

Here is a tangent for you.;) I am good at those.. it is a blonde moment. I will dig more into the mechanisms.. but you are looking sound given the data you have. Me? I am just screwed up. :D

Dug up this fact from and NIH reference.. "Similar to the adrenal gland, there is an intradermal neuro-immune network involving the local expression of cytokines and neuropeptides. Dysregulation of androgens in the adrenals and/or the skin is associated with acne, hirsutism and androgenic alopecia." I have had an increase in acne of late.. not a normal occurance. Maybe the DHEA supplementation and HC is causing a temporary inbalance.

MG
Your thought process is good. In any reaction chain you have to take into account reactants.. their nature (limiting reagent and what not).. the mechanism/catalyst employed.. and the prooducts.

You do have a similar bucket flow scenario.. but have to take into account that the kidneys will dump excess hormone out in the urine if we make too much.

As to normal cholesterol.. normal pregnenolone production. This is a base assumption assuming that the mechanism creating the pregnenolone is behaving properly. :) My cholesterol is low.. always has been. My MD is fond of telling me to go eat lard. *shivers* Such a nasty thought. He also asks me if I lick salt blocks.. I don't I just have really high triglycerides.. my whole family does. *shrug* We also have to take into account what is normal for the average normal male used in the N A C B limit studies.. may not be normal for us.

It is distracting and kinda fun to see iif we can out think our MDs and come up with the right answer. So far.. I have been right. Now I need more puzzle pieces to play with. I must say the cortisol was needed and my hubby is happy. I am getting my libido back. ;) Now if I could just reset my internal clock so the urges are at a better hour.

My SIL lacks the enzyme responsible for cartilage repair and maintanence. She is 29 and working on arthritis. It is possible to have a genetic flaw in enzyme production. it is possible to also determine if those enzymes are present or not. it is not a common test and may require visiting a research hospital.. but you can do it. I will be interested what you find out. I will share what I find out as well. It is interesting to figure out how you are put together and working on a fundamental level.

I liked the bucket visualization.. well done.
MG
Got a call from the Endo.

He said my T's "Looked good", and that even though my FSH was "undetectable" they only look at my FSH/LH if my T's are "Low". He said that my Total T didn't matter as much as my Free T's, and those "looked ok".

He said my IGF-1 must have been a fluke, and that it really wasn't that high.

Only thing he said he would do was run another ACTH Stim test to verify the results.

Pretty much everything that was High/Low he dismissed, and is probably just doing the ACTH Stim again so he can dismiss any abnormalities and tell me everything looks ok.

I'll bed if my Estradiol and Aldosterone come back high/low, he'll find some other way to dismiss those as well.

I really need to find a new Doc...





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