baseline cortisol question

[dollsie]

Hi everyone,

My mom is having symptoms suggestive of AI. She has Hashi's and Diabetes. I've been pushing her to get a stim test but her endo (he's lousy - totally missed my diagnosis) wanted a random cortisol first. So her blood was drawn at 7:30am at a lab. She got up at 4:30am, had eaten, showered, driven 45 minutes to the lab...she told me that she got lost on the way, was agitated/frustrated, etc.

Her cortisol was 17. What do you think about this? I've seen all kinds of suggested baseline minimums. I remember being told by one endo that women should have a starting morning cortisol at least in the mid 20's, but I need some solid evidence - maybe something I can print out and give to her to take to her next appt. I have  feeling her endo will refuse the stim test without some kind of academic "proof" that it's necessary. Any suggestions?

Thanks in advance,
Leigh

[Idaho Dusty]

Leigh, I can't find anything that will help.  Labcorp's normal am range for women is 4-22 (4?!  can you believe that's "normal" for am!?!?!?).  

Great resources:
labcorp.com
medscape.com
PubMed

I will keep looking.

:) Dusty

[dollsie]

Thanks, Dusty. I know! 4! What are they thinking?! This is one of the reasons my AD was missed at first - I had 5 morning cortisols less than 10 but the docs went by the "normal" reference ranges and said I was fine.

I've been looking and looking but can't find anything about optimal a.m. levels. The only thing I've come across that actually states a morning value in the mid 20's is wikipedia, but I wanted to give her something more legit than that. Thanks for keeping an eye out! I really appreciate it.

How are you doing?

Leigh

[ShannonD]

Leigh,
I will look for the link, but I have read several times that anything less than 18  (even <20) may be abnormal.  A random cortisol, says less than an acth stim test, which is also not very sensitive unless they do 1mcg test with levels of cortisol, acth, dhea, aldosterone at 0, 30, 60, min.  (that is the most sensitive 'picks up most cases' least false negative way to do it.

Anyhow,  my cortisol was similar, it was at 9am and I had gotten up and been walking/driving for hour prior to test.

My internet has been down....so I have been trouble shooting last couple of days.  I will try to find the reference for you, but it may be on stopthyroidmadness web site.  (not that they are the experts....but similar to this site, there are a lot of folks there living with endocrine issues, versus docs, going by the numbers.)

Is your mom hyperpigmenting? low blood pressure? what kind of symptoms is she having? nausea, weakness?
Hope you are finding some answers
Shannon

[dollsie]

Hey Shannon,

Thanks. I'll check out the thyroidmadness site. I've found lots of good info there too...just wanted to give her something her doc would actually pay attention to! She is having lots of weird symptoms: flu-like all the time, nausea, joint/muscle pain, lower back/leg pain, diarrhea, no libido, peeing a lot, weakness. She doesn't think she's hyperpigmented, but the rest of us do (she thinks she just hung on to her tan from the summer). She has dark spots on her lips. She looks thin to me, too.

Her doc raised her synthroid a couple of months ago - she was having thyroid pain and depression, which reminded her of when she first got Hashi's 20 years ago. But as soon as the new dose kicked in, she really went downhill. She also suddenly required 1/2 of her Metformin (for Diabetes) - which means her BG has dropped. Both of these things should have been red flags to her endo, I think. She's also had 3 episodes of high K in the last year, and also high BUN.

She has Hashi's, Diabetes, Raynaud's. I have AD, hypo-t, atrophic gastritis, gluten intolerance, hypogonadism, and vitiligo. So the tendency is definitely there for the polyglandular syndrome. The weirdest part is that I was just diagnosed with Lyme...and she is being tested tomorrow (she found a classic bull's-eye rash a couple of months ago) for the same thing! Like mother, like daughter, I guess!

Thanks again.
Leigh

[galliar]

Try these links:

http://en.wikipedia.org/wiki/ACTH_stimulation_test

http://www.acthstimulationtest.com/interpretation

It appears that a base of around  20 is more normal.  I was diagnosed with Addision's and had different results on different tests.  The one where I walked a couple of miles before the test (don't do this!) started at 12.5.  Another day it is was < 1.  Yet another time it was 6.  ACTH was at 52.  So even a single person can get different results.  Another good thing to test is the rise.  If it doesn't at least double, that is normally a problem.

Are you currently on any steriods?  If you aren't, then the ACTH stimulus test will be easier to evaluate.

[Idaho Dusty]

Hi Leigh,

I'm doing well.  Feeling good!  It's nearly winter here so right now I'm obsessed with trying to figure out a good way to get out of this ice box (I live in Idaho) and away from the snow.  Usually just day dreaming about going somewhere great is enough to get me through one of our winters...

How are you feeling???

:) Dusty

[ShannonD]

Leigh,

Here is yet another reference to read.  The interesting point I thought was that a normal ACTH stim test does not exclude the possibility of mild adrenal insufficiency.  It states that cortisol >25, may exclude adrenal insufficiency, but all spot tests are inconclusive because there is not a good way of determinig how 'steressed' a person's body is, and what might be normal.  

•Interpreting the rapid adrenocorticotrophic hormone test33,34,35,36
◦Two criteria are necessary for diagnosis: (1) an increase in the baseline cortisol value of 7 mcg/dL or more and (2) the value must rise to 20 mcg/dL or more in 30 or 60 minutes, establishing normal adrenal glucocorticoid function.
◦A low aldosterone value of less than 5 ng/100 mL that fails to double or increase by at least 4 ng/100 mL 30 minutes after ACTH administration denotes abnormal mineralocorticoid function of the adrenal cortex.
◦The 30-minute aldosterone value is more sensitive than the 60-minute value because aldosterone levels actually have been shown to decrease in the 60-minute sample.
◦The absolute 30- or 60-minute cortisol value carries more significance than the incremental value, especially in patients who may be in great stress and at their maximal adrenal output. These patients may not show a significant increase in cortisol output with ACTH stimulation.

◦A normal 30- or 60-minute rapid ACTH test excludes Addison disease but may not adequately exclude mild impairment of the hypothalamic pituitary adrenal axis in secondary adrenal insufficiency.


◦In patients with Addison disease, both cortisol and aldosterone show minimal or no change in response to ACTH, even with prolonged ACTH stimulation tests lasting 24-48 hours.
◦When the results of the rapid ACTH test are equivocal and do not meet the 2 criteria mentioned above, further testing might be required to distinguish Addison disease from secondary adrenocortical insufficiency. Plasma ACTH values and prolonged ACTH stimulation tests may be useful in making this distinction.
◦ACTH levels often are elevated to higher than 250 pg/mL in patients with Addison disease. However, ACTH is unstable in plasma, and specimen collection and storage may require special attention. The specimen should be collected in iced anticoagulated plastic containers and frozen immediately.
◦Importantly, note that ACTH levels also may be high in patients recovering from steroid-induced secondary adrenocortical insufficiency and in patients with ACTH-refractory syndromes.
◦ACTH-inducing tests such as metyrapone stimulation and insulin-induced hypoglycemia, which may be useful in the evaluation of some cases of secondary adrenocortical insufficiency, have no role in the diagnosis of Addison disease and may in fact be lethal to the patient with Addison disease.
•In acute adrenal crisis, where treatment should not be delayed in order to do the tests, a blood sample for a random plasma cortisol level should be drawn prior to starting hydrocortisone replacement.
◦A random plasma cortisol value of 25 mcg/dL or greater effectively excludes adrenal insufficiency of any kind. However, a random cortisol value in patients who are acutely ill should be interpreted with caution and in correlation with the circumstances of each individual patient. Random cortisol levels should also be interpreted cautiously in critically ill patients with hypoproteinemia (serum albumin <2.5 g/dL). Approximately 40% of these patients will have baseline and cosyntropin-stimulated cortisol levels below the reference range even though the patients have normal adrenal function (as evidenced by the measurement of free cortisol levels). This phenomenon is because more than 90% of circulating cortisol in human serum is protein bound.
◦Cortisol is known to be elevated by stress, but exactly how high it should rise to constitute a normal response in times of severe stress is not known.
◦An abnormal test result should prompt a proper evaluation of the hypothalamic pituitary adrenal axis after the patient's condition improves before committing a patient to lifelong steroid replacement.
◦In order to perform the ACTH stimulation test in this situation, the patient should be switched to dexamethasone and then tested 24-36 hours later. Dexamethasone does not interfere with the cortisol assay, as does hydrocortisone or prednisone. However, dexamethasone may interfere with interpretation of the random cortisol value drawn after dexamethasone already has been initiated. Dexamethasone also does not have any mineralocorticoid activity, which may be needed in patients with Addison disease.

Let us know what they say.  I imagine your mother might have mild AI, if nothing else....the question becomes, the plus versus minus of using hydrocortisone....because it can be a lifetime of meds.  The other question is would a doc want to prescribe it if she does not 'meet criteria'

There are adrenal extracts or something called isocort, that can 'support' adrenals.  

I certainly think a stim test is a in order.  Especially given your family's history. Hopefully you can get that done.
 
How are you feeling? Any news?
Take care,
Shannon

[ashley]

Leigh,

If your mom had a bull's eye rash then there is no need for a test. The rash is definitive. She should get treatment ASAP. Also, the baseline cortisol is useless - that's the whole point of the stim. test. I hope the endo. will know that.

Have you started antibiotics yet?

Hope you are doing OK,
ashley

[dollsie]

Hi Ashley,

Thanks for the info. I'm so worried about my mom. I passed along all of the ILADS info to her, and when she went to her doc yesterday for the WB, she asked to be started on Doxy immediately. They were fine with it, thank goodness. She also spoke with her endo again and said she wanted the stim test. He's dragging his feet with her, just like he did with me. I can't believe how many endos do this. What are they thinking?! But she said she'll keep pushing for it and thinks he'll work with her. We'll see. To date I STILL haven't found a doc that I'd want her to see. Starting to give up on the endo world altogether...

I'm on oral Doxy until I get my PICC line in (next week). It's not going so well...I'm totally nauseated and was even vomiting non-stop a few days ago. Actually got a little worried at one point that I'd need to use the injectable meds, but it passed and I was o.k. I'm able to tolerate the Doxy at 200mgs/day, but anything above that is a nightmare. But, as much as it upset my stomach, the rest of my body felt better - actually felt totally over-treated on the Dex at one point. I read that Doxy is an anti-inflammatory in high doses, so I guess the Dex really is treating more than the Addison's right now. Maybe that's why I've needed higher doses all along.

I saw a LLMD yesterday who has a great reputation, but the appointment was pitiful. He was in a huge hurry and rushed me to make decisions I wasn't ready for. We didn't talk about a lot of important details. The whole thing was totally off-the-cuff and I was really uncomfortable with it. He also refuses to address anything but Lyme, and seemed inaccessible if something should go wrong (and REALLY expensive). He's not willing to help me if my insurance backs out. He changed his mind about the meds a few times, ended up saying he wanted me on orals instead of IV - this went against everything I've read on ILADS and what the other docs have told me. Honestly, my gut instinct was that he's overwhelmed by my situation and afraid something would go wrong, so he took the least invasive approach. But I want to get better and stop wasting time, and I know my body can handle the IV.

I finally put my foot down about that, and he said he'd start me on Claforan or Primaxin, then add Zithro and Tindamax. This is a much different protocol than what I was expecting. He said it addresses the Lyme, maybe the Bartonella, not the HME. I also got some labwork back yesterday showing off-the-charts antibodies to mycoplasma and HHV-6. So I guess there are more infections than I realized. Blows my mind that all of this was missed at Hopkins last year. Anyway, he didn't address treating either one of these things either, and I have a feeling they may actually be responsible for more of my symptoms than the Lyme. Strange that all of these things are "active" at the same time right now. Very creepy feeling. I blame the high steroid doses for the last 9 months!

So anyway, I think I'll go with the first guy I saw. He is also an LLMD, less experienced (which is why I went to the guy yesterday) but open-minded. He also wants to address things from a holistic perspective, get my hormones straightened out and give my immune system a kick in the right direction. He'll go to bad for me with insurance, and he's accessible. He uses Rocephin/Levaquin almost exclusively but said he'd try other things if I wanted to...not sure what to do about that. I am nervous about the Rocephin b/c of the gallbladder issues, but might just give it a whirl and see what happens. I have a HIDA scan next week  - maybe I should wait until the results of that come back to make a decision about the Rocephin. Or maybe I should just get started and take my chances. What do you think?

Sorry to blabber on, once again! Oh - I meant to ask you, when your D1,25 was high, did you eliminate Vit D from your diet? I'm on the fence about this. My D1,25 is high, D25-OH is low, Ca is in the high-normal range, PTH is in the high-normal range. I've read that Sarcoid and problems like that will usually cause high Ca and low PTH. But it seems like my PTH is trying to get my body to release more D, and maybe the 1,25 is all that I have right now. I think this might be what Dr. F talks about in his article on this, but I'm not sure...

Thanks again.

Leigh

[ashley]

Leigh,

I think the holistic Dr. sounds good - try starting with him. I, too, had many co-infections. Some went away without treatment once the Lyme improved, others had to be treated. I'm sorry about the Doxy - it can be rough, I know. I'm glad, though, that it's antiinflammatory properties are helping you.

No, I never avoided vit D. That protocol always seemed like a nightmare to me and I thought I'd only do it as an absolute last resort. :)

Let me know how things go.

ashley

[Shannon]

Leigh,
Glad to hear that the docs put your mom on the doxycycline, and that you are handling it OK.  Definitely best to find a doctor you are comfortable with.

It has been a while since we were talking about the vitamin D, and calcium etc., but I wanted to show you this exerpt from an article on Dr. Freidman's web site about vitamin D:

The conversion from the 25-OH vitamin D to the 1, 25-OH vitamin D that occurs in the
kidney is catalyzed by parathyroid hormone, also called PTH. Therefore, patients with very
low vitamin D levels will have relatively high PTH levels often with low calcium levels.
This is similar to patients with primary hypothyroidism having elevated TSH levels while
having normal thyroid hormone levels. Additionally, the 25-OH vitamin D form which is
the storage form and is much more abundant that the 1, 25-OH vitamin D form which,
although is active, is less abundant. Therefore, in states of vitamin D deficiency, low levels
of 25-OH vitamin D are found, but the 1, 25-OH vitamin D levels are either normal or
actually slightly high. They are slightly high because the excess PTH that is stimulated by
the low 25-OH vitamin D levels stimulates the conversion up to 25-OH vitamin D to the 1,
25-OH vitamin D. Thus, patients that are vitamin D deficient usually have a low 25-OH
vitamin D level, a high PTH level, a low normal calcium, and a normal or an elevated 1, 25-
OH vitamin D level. However some patients may actually have a high normal calcium as
the elevated PTH and 1, 25-OH vitamin D may cause increased calcium absorption from the
GI track and reabsorption from the kidney. If 25-OH vitamin D levels were not measured,
these patients might have been incorrectly diagnosed with mild hyperparathyroidism as they
have a high normal calcium and a high PTH.

I know that the Marshall Protocol for sarcoid calls for avoidance of vitamin D.  So, who's right for your circumstance?? Tough to know, but unless you were pursuing a full Marshall type protocol, it seems that dietary vitamin D would be OK.

Best of luck to you.
Shannon

[Idaho Dusty]

Leigh,

Most of what you're talking about is way out of my league.  I do want you to know that you are welcome to vent here as much as you like.  You're in a tough position with doctors and your body.  

I think you're on the right path with the holistic doctor.  It's so important to feel like the doctor is listening and cares about you as a person!

Sending positive energy your way,

:) Dusty