I M M U N E S Y S T E M
One more suggestion for you is to test your immunoglobulins (IgG, Total and Subclasses). If you have low levels of antibodies in general, it might make it more difficult to diagnose an autoimmune disease.
6 February 2014
Alpha1 globulin 4 % (2.9-4.9)
Alpha2 globulin 9.3 % (7.1-11.8)
Beta 1 globulin 6 % (4.7 -7.2)
LOW Beta 2 globulin 3.6 % (3.2-6.5)
LOW Gamma globulin 9.9 % (11.1-18.8)
LOW IgA 0.4 g/l (0.7-4) – same result since many years
LOW IgG 6.7 g/l (7-16) – fluctuates most time around 7
IgG subclasses not tested
IgM 1.1 g/l( 0.4-2.3)
HIGH IgE 171 ku/l (0-91) – IgE most years little bit elevated
C3 complement 1.53 g/l (0.9-1.8)
C4 complement 0.36 g/l (0.1-0.4)
rheumatoid-factor 10 IE/ml (0-40)
transglutaminase IgA 0.1 U/ml (0-7)
transglutaminase IgG < 0.7 U/ml (0-7)
2013
White blood cells 7800.00 (4000 – 11000)
Lymphocytes 2031(1200-2300)
T3 cells 1348 /µl (1000 – 1700)
T3 cells 66.4 %(67 – 80)
LOW T4 helper cells 629 /µl (500 – 1000)
LOW T4 helper cells 31.0 % (35 – 55)
T8 cells 615 /µl (350- 800)
T8 cells 30.3 %(20- 38)
LOW ratio T4:T8 1.02 (1.20 - 2.20)
HIGH T8 suppressor cells 13.3 % (< 13)
HIGH NK1 cells 171 /ul (< 160)
HIGH NK1 cells 8.4 % (< 8)
HIGH NK 2 cells 140 /ul (< 70)
HIGH NK2 6.9 % (< 3.0)
NK 3 cells 398 /ul (< 430)
HIGH NK 3 cells 19.6 % (< 19)
HYPOTHALAMUS – PITITARY - ADRENAL - AXIS
I really have to apologize for my lengthy story – but I don't know how to do it otherwise and I need some help, please.
One of my main questions is if there is enough functional cortisol in my body.
Endocrinologists say: Everything is fine and my complaints don’t apply to their specialty (!).
But they look at lab results only and never took in account signs and symptoms, nor did any endocrinologist ever do a physical exam.
They do not consider that my serum cortisol and ACTH is always in the low normal range.
And they do not use saliva cortisol, because it’s “too inaccurate”.
I did saliva cortisol on my own, sent it to a lab that runs such tests.
In my regard
- serum morning cortisol is most of the time in the lower half of normal range
- when given ACTH, cortisol is excellent
- ACTH in serum is always low
- when given CRH, ACTH is good
Thus, there seems to be not enough stimulation from pituitary or hypothalamus.
If the cortisol is low, as it is, and if the pituitary is healthy, the ACTH should be high.
Or is my ACTH low, because there is “enough” functional cortisol in the circulation?
The first time I was tested in a major endocrinological practice in my town: 2011 ACTH-test and 2012 CRH-test. Currently I had a blood draw and a CRH-test in a distant endocrinological practice.
All questioning would be dispensable if 5 mg of Prednisolone and later 25 mg of HC (divided doses) in 2011 to 2012 had yielded better results, when a practitioner allowed a therapeutic trial. I wasn’t able to augment my thyroid hormone supplementation enough regarding my symptoms and the reasoning was that the adrenals may not be able to cope with the thyroid.
Meantime, I learned that adrenal insufficiency in ME/CFS is oftentimes
secondary.
Also, I read (don’t remember exactly, but suppose it has been in the publications of Dr. Baschetti, Italy) that in secondary adrenal insufficiency,
50% of people don’t feel improvement from HC. I would very much like to know if that is true and how it could be explained.
I’ll get back to my experience with Prednisolone/ HC at the end.
Cortisol Saliva Dec 2013
8 AM 1.3 (+) 6 months before 0.42 (RR 0.15-1.00)
Noon 0.26 (-) 6 months before 0.16 (-) (RR not given)
4 PM 0.07 (-) 6 months before 0.13 (-) (RR not given)
8 PM 0.07 (-) 6 months before 0.07 (-) (RR 0.07-0.22 - this is their RR for 2 PM)
Cortisol Serum 9 AM - measured between 1994 to 2014
µg/dl (RR 5-25) 12.3 - 13.4 - 13.7 - 9.77 - 15 - 9.36 - 11.49 - 12.5 - 23.6 - 14.3
I know that serum cortisol doesn’t tell much, but it is what doctors love to test
converted to mmol/l these would be e.g.
µg/dl 12.3 = nmol/l 339.48
µg/dl 9.36 = nmol/l 258.33
µg/dl 23.6 = nmol/l 651.36
Quote: “…include < 3 mcg/dl; 83 nmol/l or exclude > 19 mcg/dl; 524 nmol/l adrenal insufficiency.
However, most patients will have intermediate values and will require dynamic testing.”
Source:
http://www.ncbi.nlm.nih.gov/pubmed/14604069
Cortisol Free in 24h urine Jan 2014
96 (RR 36-137)
ACTH serum measured between 1994 to 2012
pg/ml (RR15-70) 15 - 14 - 11.1 -16.1 - 8,4 - 9,84
I read:
decreased ACTH or at least ACTH that is too low (improper) for the cortisol value points to secondary or tertiary problem
ACTH test July 2011
Cortisol
0 min 20,4 (RR 5- 25)
30 min 34,4
60 min 40,4
ACTH
0 minn 18,51 (RR 15- 90)
30 min 9,06
60 min 2,83
Endocrinologist wrote: „
Clearly exuberant increase of cortisol, ACTH adequate suppressed through ACTH what demonstrates correct pituitary regulation. The present result documents a considerable level of stress in the patient.”
My interpretation: If there is a lot (!) of ACTH, then my adrenals put out cortisol “as it should be”. No Addison’s.
"Secondary adrenal insufficiency is adrenal hypofunction due to a lack of ACTH. Symptoms are the same as for Addison disease, but there is usually less hypovolemia: Diagnosis is clinical and by laboratory findings, including low plasma ACTH with low plasma cortisol. Treatment depends on the cause but generally includes hydrocortisone." Source:
http://www.merckmanuals.com/profess...isorders/secondary_adrenal_insufficiency.html
2012 September
CRH-Test 8 AM, fasting
Cortisol µg/dl
0 min 20,1 (RR 5- 25)
15 min 22,6
30 min 22,9
45 min 22,5
60 min 22,6
ACTH pg/ml
0 min 8,51( RR 15- 90)
15 min 40,22
30 min 26,85
45 min 27,34
60 min 21,51
At that time, I took about 7.5 mg HC (was weaning) 31mcg T3, and HRT.
The endo advised to pause HC only the day of the test and the day before.
Endocrinologist wrote:
"In the CRF test ACTH was stimulated properly through CRH, therefore the pituitary must clearly be excluded as a cause of adrenal cortical insufficiency. From endocrinologic perspective the problems described by the patient cannot be explained through hormonal disturbances. Further diagnostics should not be done."
I read that a significant increase of ACTH in the CRH-test points to tertiary AI (hypothalamus). In other words: Increase of ACTH or cortisol suggests that the pituitary works properly and the problem may lie in the hypothalamus.
2012 September
sodium 137.9 mmol/l (135-155)
potassium 3.82 mmol/l (RR 3.5-5.6)
cortisol 8.72 µg/dl (5- 25)
ACTH 16.13 pg/ml (RR15-70)
DHEA-S 0.11 µg/dl (RR< 2.5 post meno)
HIGH LH 51.99 mIU/ml (RR < 10 post meno)
HIGH FSH 80.1 mIU/ml (RR < 10 post meno)
Renin µU/ml 40.4 (RR7- 40)
Actually I take:
T4 37 mcg + T3 2x 6mcg
some HRT (bioidentical creams, bi-est, progesterone, testo)
potassium 2500 mg/day (I think this equals 35 mEq)
supplements
2014 January 28 – 8 AM laying down
within RR: Creatinine, BUN, urea, Hemoglobin, Hematocrit, RBC, MCH, MCHC, MCV, platelet count, AST/SGOT, ALT/SGPT, albumin, protein, CRP, Sugar, HBA1C, Ferritin, ALT, Triglycerides, HDL, LDL
WBC 5,83 (3.6-9.6)
Sodium 140 mmol/l (132-146)
Potassium 4.6 mmol/l (3.5-5.1)
Calcium 2.2 mmol/l (2.15-2.58)
Phosphorus 0.93 mmol/l (0.81-1.45)
Magnesium 0.96 mmol/l (0.53-1.11)
PTH 37 ng/l (14-72)
LOW 25-OH-D 14,36 - ug/l (20-70)
HIGH Amylase 103 U/l (28-100) – not the first time (autoimmun?)
Lipase 44 U/l (7-60)
Cholesterin 218 mg/dl (50-200)
HIGH Vit B12 1624 pg/ml (197-866)
LOW TSH 0.01 (0.27-2.5)
LOW FT4 9.4 ng/ml (9.3-17) - I take 37 mcg T4
FT3 5.58 pg/ml (3.5-6.5) - I take 2x 6mcg T3
TPO ab 22.4 IU/ml (0-35)
TRAK ab 0.64 U/l (0-1.75)
LOW DHEAS µg/ml 0.4 (RR 0.4-4.3 post meno)
Free Androgenindex 2.7 (RR 0-3.5)
SHBG 95,9 (RR 18-144)
Estradiol pg/ml 209.1 (RR 5-498 post meno)
Progesterone ng/ml 5.6 (RR 0.1-27)
FSH mIE/ml 77.6 (RR 3.5-134)
LH IU/ml 45.3 (RR 1-95.6)
Prolactin ng/ml 15.9 (RR 4.8- 23.3)
Testosterone ng/ml 0.76 (RR 0.03- 0.48 women post meno)
STH µg/l 4.37 (RR 0-6.88)
IGF1 ng/ml 142.4 (29-251)
HIGH Aldosterone 230 ng/ml (29-145) – 8 AM, fasting laying down (I take sodium and potassium, but not the morning of blood draw)
Renin 17.6 ng/l (1.7-23.9)
Aldosteron-Renin-Quotient 13.1 (< 20)
2014 February 6
I'm not sure if the values from February 6 are valid: I had a lot of stress: rose 5:30 AM, went by train 3 hrs, walk 20 min, searching way in foreign town, talked with endo, 11 AM blood draw. During blood draw I was sitting, not fasting, have taken sodium and potassium that morning, because I had gotten no instructions.
Aldosterone 92.1 ng/l (10-160)
Cortisol serum 155.4 µg/l (23-194)
Renin 11.2 ng/l (1.7-24.9)
Aldosteron-Renin-Quotient 8.2 (< 20)
ACTH 12.3 ng/ml (4.7-48.8)
2014 February 18
CRH test 2 PM, 4 hrs fasting, 4 days no HRT
I had stress: 3 hrs by train, 20 min walk, when arriving at the endo they apologized for not having the CRH medication, thus I had to leave and fetch it myself from the pharmacy, stairs up, stairs down (skipped heart beats), no rest, sitting during the test
ACTH pg/ml
0 min 14.10 (RR 4.7-48.8)
30 min 34.0
60 min 8.3
120 min 4.7
Cortisol µg/dl
0 min 224.6 (RR 23- 194)
30 min 251.7
60 min 233.7
120 min 14.78
ALDOSTERONE and POTASSIUM
In 2012 potassium was measured in whole blood (red blood cells) and was found below the lower RR. Since then I take potassium and had to increase to 5 tablets (each 500mg) a day. Since I take that much potassium I rarely have tachycardia and skipped heart beats, as before. The potassium value in red blood cells slowly increased. Potassium in serum is controlled every 4-6 weeks and it is always in the lower half of RR. I would very much like to stop the potassium intake.
Potassium in 24 hr-urine was only slightly elevated lately, meaning that my kidneys loose some potassium, but the nephrologist said that it is not much and therefore cannot explain the high potassium need. No doctor, not the nephrologist, nor endocrinologist can explain hwy I need so much potassium.
The practitioner I consult currently suggest trying an aldosterone blocker, e.g. Spironolactone. On the one hand, I’m eager to stop all that potassium, on the other hand I’m hesitant as long as no one knows why I need so much potassium.
Aldosterone
2014 January pg/ml 230 (RR 29-145) - preanalytics have been correct
2012 June 103 (RR 20-160)
2011 May 174 (RR 20- 150)
2011 July 236.2 (RR 20-160)
With the Aldosterone it is difficult, as it depends on serveral things that have to be respected (activity, sitting/laying while blood is drawn, salt intake ...)
I love (crave) licorice candy, but I don’t eat licorice.
There are publications saying that increased aldosterone is damaging in the long run.
Regarding potassium, I’m researching Gitelman’s Syndrome
http://barttersite.org/what-is-gitelmans-syndrome/
Gitelman’s syndrome is a rare inherited defect in the renal tubule of the kidneys. This defect causes the kidney to waste magnesium, sodium, potassium and chloride in the urine, instead of reabsorbing it back into the bloodstream. Urine calcium levels are lower than normal, despite normal serum values. This syndrome does not cause kidney failure nor does it cause the kidneys to function abnormally. The kidneys are normal. The problem is the reabsorption of important electrolytes and minerals.
PITUITARY
There is one more symptom pointing to the pituitary - ADH: I pee a little too much: about 3300 ml/day. The lab always notes that this is “too much”, but no doctor listened. Also, I have to go to the toilet each night though I do not have heart insufficiency. The phenomenon is described e.g. in A. Cutler ‚Amalgam Illness‘. I drink about the same amount as I pee, but a healthy person pees less, as we leave water through bodily fluids like sweat and others, too. I have little thirst, but I feel dry/ exsiccated all the time.
Therapeutic trial cortisol:
2011 6 months Prednisolone 2.5- 5 mg
2012 6 months HC 25 mg (divided doses)
I definitely felt more energy the first 4, 5 days of taking HC, but in the following days this faded away. As if the pituitary noticed the intake and reduced its stimulation at the same amount.
While taking cortisol, I had more hunger, put on 4 pounds of weight, joint pains (mild) stopped and skin blains disappeared, my commonly low BP (90/70) became normal (120/80) for the first time in years, and the temperature was more stable and not fluctuating from day to day, which, according to Dr. Rind, is a positive sign regarding the adrenals.
But because I missed an overall feeling of well-being and had not more energy, because it was difficult to tell, if there was a benefit at all, because I had difficulties with tachycardia and arrhythmias - the low potassium was not yet detected and the HC aggrevated the situation as it had a mineralocorticoid effect in my case – and because last but not least, I hadn’t been able to increase my thyroid hormone supplementation while on HC, I weaned te cortisol
Afterwards, to the second guess, it might be, that I have been a little bit more active while on cortisol. But, as I said, it’s difficult to tell, was too subtle and could not be felt directly. I remember e.g. that I did several things like painting a wall, what I never repeated since then.
In several books from experienced US and GB authors I almost always read that patients with Adrenal Fatigue felt improvement very soon from HC, oftentimes HC was the missing piece. But I cannot remember that these authors talked about
secondary adrenal insufficiency, therefore this may not apply to secondary?
I also read, that taking Prednisolone or HC is meant to give the adrenals a “rest” so that they may recover. “Giving the adrenals a rest” - in my understanding - would mean, replacing some (or all) of the cortisol that the glands normally produce. And, in turn, this would mean that there is
not more cortisol than before and therefore no more energy, not
before the adrenals
are recovered. Or is this loose thinking?
Before I tried HC, I took all sorts of adrenal support, vitamins, licorice, glandulas .. but never felt improvement.
One may even be resistant to cortisol – receptor-resistance.
Jeffries:
Myth #4: There is a perfect way to test for cortisol deficiency.
Facts: Again, there is no such thing as a perfect test. Cortisol is particularly difficult to test because blood levels can vary by the minute. Some people are even resistant to the effects of this hormone.5,6 So, even “normal” levels may not be enough to keep some people healthy. In his book, Dr. Jefferies addresses this difficulty and recommends that a “therapeutic trial” is often the best approach.7 Jefferies is reported to have told his students, “When in doubt, treat the patient.”
THYROID
Lab values see above 28 Jan 2014
I have a goiter and had a partial thyroidectomy in 1991 because I was diagnosed having a “diffuse autonomy” though no one realized then that the endocrinologist had changed my thyroid medication from plain T4 to T4+Iodine, so it may have been “the iodine”.
Whole family has a goiter, but they don’t know of antibodies or if there is inflammation.
2013 September
scintigram: struma, nodules, cysts (same as last year)
cysts punctuated: no malignancy
from 7/06 to 3/12 my thyroid grew from 22ml to 44ml
From 3/12 I took T3 only (25 mcg) because I had had a very high RT3 of 1293,6 pg/ml (RR 215-637). With T3 only RT3t soon came back to normal.
In 2012 with T3 only my thyroid did no longer enlarge.
There are always three sorts of thyroid antibodies present, but because these are within the RR, no one ever payed attention. Only the nuclear physician who did the scintigram in Sept 2103 spoke of a "
not otherwise specified thyroiditis”..
I improved ferritin, mineral and vitamin levels, too, but nevertheless wasn’t able to increase the thyroid hormone intake due to tachycardias and arrhythmias.
Finally, because EVERY doctor stresses my T3 only medication and the “suppressed” TSH (but TSH is suppresses since years), I lately gave in and I’m changing to T4 with some T3 added. This month I take T4 37 mcg + T3 2x 6mcg.
Temp is low. Measured according to Dr. Rind (average of 3 values each) 97.8 – 97.6 – 97.9. The first two measurements are lowest, 96.6 or 97.1, the last is about 98.5.
There is definitively room for improvement regarding my thyroid: I really hope that this time I will be able to increase sufficiently to finally get improvement of symptoms.
It is really difficult to see through all this.
Should an insulin tolerance test (gold standard) be performed? This would be very difficult to enforce.
On April 2 I will have the MRI scan pituitary.
I would like to repeat that I was rather healthy until the cesarean delivery of my second child. Thereafter, I struggled with lack of energy and some hormonal problems. The final and permanent decline happened six weeks after a faulty amalgam removal. Today I know that I have difficulties detoxing heavy metals (23andMe).
Thank you very much for reading.
Pearl