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Autoimmune Polyendocrinopathy Syndrome

Discussion in 'Other Health News and Research' started by lizw118, Jun 5, 2013.

  1. lizw118

    lizw118 Senior Member

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    Hi Everyone
    I have been reading about Autoimmune Polyendocrinopathy Syndrome.
    http://som.ucdenver.edu/bdc/Book-Type1Diabetes/HTML/CH8/CH8.html
    The description fits a lot of my own stuff like hashimoto's thyroiditis, pernicious anemia (will be confirmed through endoscopy soon), adrenal fatigue (is this autoimmune?), etc.
    Chronic candida is a feature of this syndrome as well, which I also have.
    Does anyone know about this? Are there any treatments aside from steroids or anything like that?
    Thanks
    Liz
  2. lizw118

    lizw118 Senior Member

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  3. Ema

    Ema Senior Member

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    There is no such thing as adrenal fatigue. There is Addison's which is adrenal failure and this often is autoimmune in nature. You can test for the 21-OH autoantibodies. And there is HPA axis dysfunction where the brain does not give the adrenals the proper stimulation which causes cortisol dysregulation.

    I would think the treatments would depend on what you present with...if Addison's, physiological doses of hydrocortisone are an absolute must. Treatment for Hashi's is thyroid hormones. Pernicious anemia is treated with B12.

    Some people have been having success using IVIG to turn off autoantibody attacks but good luck getting insurance to cover that use.

    Ema
  4. Ema

    Ema Senior Member

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  5. lizw118

    lizw118 Senior Member

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    Hi Ema
    Is "IVIG" IV immunoglobulins? What kind of immunoglobulins? Wouldn't that make the immune reactions worse?
    I wonder if there is any holistic/eastern medicine way to turn off the antibody attacks. B12 injections and sublinguals hardly seem to help me. I don't know why. I am on cytomel and HC. I am trying to wean off HC bc my sex hormones went down on it and my adrenal gland stopped functioning. I have RT3 issues so I can only take a T3 med for the thyroiditis. I have consistently low immunoglobulins on blood tests, but I wonder if that is because of the HC?
    Thanks
    Liz
  6. Ema

    Ema Senior Member

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    Yes, IVIG is intravenous immunoglobulins.

    Have you tested total immuoglobulins and subclasses 1-4?

    HC does not cause low immunoglobulins. Deficiencies in the immune system do which can allow infections to proliferate and derail your endocrine system in particular. This can also cause high RT3 and unfortunately is not fixed by taking T3 only. It's fixed by stopping the infection and attacks.

    I did T3 only for more than a year and now I understand that T4 is very important to the metabolism. It's not just a storage hormone. I've been through the entire protocol and I'm sorry to say that I find it misguided. If the body is healed, RT3 will come down. It's just another sign of chronic illness.

    http://tiredthyroid.com/rt3.html

    What kind of testing have you had? Do you have Addison's? Can you post any of it?

    Ema
  7. Ema

    Ema Senior Member

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  8. lizw118

    lizw118 Senior Member

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    Hi Ema
    An ACTH stim test (urine) showed that I wasn't making enough of all of the cortisol metabolites, . The doctor told me those results meant I had adrenal fatigue. Additionally I had low morning cortisol on a saliva test (although imo it seems like everyone does). If I could go back in time I never would have started the HC to begin with, even though I do think the cytomel tired my adrenals. I felt much better on T3 only than T4/T3. Also the naturethroid caused my antibodies to go up. That said, I have lowered my cytomel down to only 5 mcg per day so that I am producing some of my own T4. That took a long time and a lot of acupuncture, trial and error. I am slowly trying to wean off the HC and it seems I am now stuck at around 12.5 mg per day. I can tell my hormones are shifting as I change these things because my breasts are tender and I am spotting. My SHBG was highish on cytomel so my free sex hormones went down. I also think the HC lowered my sex hormone levels.
    I tested positive for lyme disease. I don't know how long I have had it but probably a really long time. That is probably what sparked this whole thing. I have taken lots of ABX for that with some improvement.
    What I would really like to know, though, is how to improve my immune system. Why are my immunoglobulins low and why do I produce autoantibodies (aside from genetic factors)? Is there anything I can do to change that? I would like to get my system working better. I have tried taking colostrum for the IGs but had a bad reaction. I am very careful with diet, of course.
    Do you have autoimmune addison's and hashis?
    Liz
  9. Ema

    Ema Senior Member

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    Is it possible that you are confusing a 24 hour urine cortisol test with the ACTH stim test? A stim test is where you have blood taken, get an infusion of synthetic ACTH and then have your blood levels taken at 30, 60 and 90 minutes.
    A urinary free cortisol test is not good at determining low cortisol states unfortunately. It is really only good for determining excess cortisol such as found in Cushing's syndrome. I would not trust any diagnosis of low adrenal issues as a certainty with this test personally.

    Saliva tests are one of the most accurate measures of free cortisol. Did you have the 4x/day test or just the one measure?

    I would agree with you that many in the ME/CFS population have low AM cortisol but many also have swinging high/low patterns. Many people with ME/CFS have HPA axis dysfunction and problems with the circadian rhythm for sure though.

    I think using steroids appropriately after proper testing can be extremely valuable. However, it sounds like your practitioner may have missed some valuable testing.

    One must have strong adrenals to tolerate thyroid hormone, particularly T3. However, the body may be resistant to artificially inflating metabolism using thyroid meds during times of chronic illness.

    What are your current thyroid labs? TSH, FT4, FT3, RT3?

    How long were you on HC? How long have you been weaning?

    That's a big clue right there that your endocrine problems may actually be due to infections, both bacterial and viral. That is exactly what happened to me.

    Taking exogenous hormones can be an important part of recovery if that is the case but treating the pathogens cannot be ignored. Especially pathogens like Lyme which are well known to dysregulate the endocrine system.

    Who diagnosed you with Lyme? What testing did you have? How long and with what antibiotics did you treat? Why did you stop?

    That's the 20 million dollar question that we are all trying to address here!

    There are many theories and you can spend time reading about all the possible immune modulators and treatments on the forum. Treatment will depend on numerous factors including whether or not it seems that the immune system needs stimulating or suppressing.

    Have you had your total immunoglobulins including subclasses 1-4 tested? If not, I would do that first. If the total immunoglobulin level is low, there is a good chance that you could benefit from IVIG or Hizentra. This has helped me a lot.

    I would also think about testing for other pathogens, specifically viral including chronic EBV, CMV, and HHV6.

    You can research immune modulators such as Nexavir (which also kills viruses) and Equilabrant, Inosine/Immunovir.

    Have you tried a PRP spray instead of the full colostrum? What kind of reaction did you get?


    I have primary immunodeficiency (low immunoglobulins) which I believe led me to be susceptible to chronic infections. I have highly positive tests to EBV, CMV, HHV6, Parvo and Lyme. I believe these infections caused a dysregulation of my endocrine system which lead to a diagnosis of adrenal insufficiency.

    However, after 2.5 years on steroids and treating infections, I've just recently weaned off successfully and am not currently on steroids. I believe I did not have autoimmune Addison's (because I was able to wean successfully) but had either secondary adrenal insufficiency or HPA axis dysfunction. Time will tell though.

    I have some Hashi's antibodies but my hypothyroidism was also caused in my opinion by my body turning down my metabolism due to chronic infection and endocrine dysfunction. I'm now also off thyroid meds and my free hormone levels are optimal.

    Ema

    Ema
  10. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    Cornwall, UK
    I became very interested in ACTH, cortisol, etc., a few years ago when I had the Synacthen (synthetic ACTH to test for cortisol production) test in hospital after an emergency admission. It tested normal, yet many studies find that cortisol levels are low in ME and/or the diurnal secretion pattern is the opposite to what healthy people have.

    After looking at numerous scientific papers I realised that the Synacthen test will tend to come up normal for people with ME because our abnormal cortisol levels are due to not having the right amount of natural ACTH. Our response to ACTH may well be normal - but this is not helpful if we don't have enough ACTH!

    The following abstracts that I found then may be of interest - sorry I don't have links:

    • Several neuroendocrine studies have suggested hypoactivation of the hypothalamic-pituitary-adrenal axis in chronic fatigue syndrome. One possible determinant of this neuroendocrine abnormality, as well as the primary symptom of fatigue, is reduced hypothalamic secretion of corticotropin-releasing hormone (CRH). Because CRH and vasopressin secreted from the hypothalamus act synergistically at the pituitary to activate ACTH secretion, the ACTH response to peripheral infusion of vasopressin can provide an indirect measure of hypothalamic CRH secretion. We measured the ACTH and cortisol response to a one hour infusion of arginine vasopressin in 19 patients with chronic fatigue syndrome and 19 age and sex matched healthy volunteers. Patients with chronic fatigue syndrome had a reduced ACTH response to the vasopressin infusion and a more rapid cortisol response to the infusion. These results provide further evidence of reduced hypothalamic CRH secretion in patients with chronic fatigue syndrome.

      Altemus M, Dale JK, Michelson D, Demitrack MA, Gold PW, Straus SE. Abnormalities in response to vasopressin infusion in chronic fatigue syndrome. Psychoneuroendocrinology. 2001 Feb;26(2):175-88. Weill Medical College, Cornell University, Box 244, 1300 York Avenue, New York, NY 10021, USA.
    • BACKGROUND: Corticotropin-releasing hormone (CRH) and vasopressin (VP) are the two principal neuropeptide regulators of the hypothalamic-pituitary-adrenal axis in man, with VP serving to augment CRH-induced adrenocorticotropic hormone (ACTH) release. Unlike VP, desmopressin (DDAVP), which is a synthetic analogue of VP, when administered alone, has not been shown in healthy subjects to have consistent ACTH-releasing properties. It has been suggested that chronic fatigue syndrome (CFS), characterized by profound fatigue and a constellation of other symptoms, may be caused by a central deficiency of CRH. METHODS: We administered 100 micrograms ovine CRH (oCRH) and 10 micrograms DDAVP, both alone and in combination, to a group of subjects with CFS, and to a group of healthy volunteers. Our aim was to establish the effect of DDAVP on CRH-induced ACTH release in these two groups. RESULTS: The delta-ACTH responses to oCRH were attenuated in the CFS (21.0 +/- 4.5 ng/L) compared to the control subjects (57.8 +/- 11.0 ng/L; t = 3.2, df = 21, p < .005). The delta-cortisol responses were also reduced in the CFS (157.6 +/- 40.7 nmol/L) compared to the healthy subjects (303.5 +/- 20.9 nmol/L; t = 3.1, df = 21, p < .01). The delta-ACTH and delta-cortisol responses to DDAVP alone did not differ between the two groups. On administration of both CRH and DDAVP no response differences between the two groups for either ACTH (p = .3) or cortisol output (p = .87) were established. Comparing the ACTH and cortisol responses to CRH and CRH/DDAVP in only those individuals from each group who had both tests, the cortisol output to the combination was significantly greater in the CFS compared to the healthy group. The ACTH output was also increased in the former group, though this was not significant.
      CONCLUSIONS: DDAVP augments CRH-mediated pituitary-adrenal responsivity in healthy subjects and in patients with CFS. That DDAVP was capable of normalizing the pituitary-adrenal response to oCRH in the CFS group suggests there may be increased vasopressinergic responsivity of the anterior pituitary in CFS and/or that DDAVP may be exerting an effect at an adrenal level.

      Scott LV, Medbak S, Dinan TG. Desmopressin augments pituitary-adrenal responsivity to corticotropin-releasing hormone in subjects with chronic fatigue syndrome and in healthy volunteers. Biol Psychiatry 1999 Jun 1;45(11):1447-54. Department of Psychiatry, Trinity College Medical School, St. James' Hospital, Dublin, Ireland.
    • Hypofunctioning of the pituitary-adrenal axis has been suggested as the pathophysiological basis for chronic fatigue syndrome (CFS). Blunted adrenocorticotropin (ACTH) responses but normal cortisol responses to exogenous corticotropin-releasing hormone (CRH), the main regulator of this axis, have been previously demonstrated in CFS patients, some of whom had a comorbid psychiatric disorder. We wished to re-examine CRH activation of this axis in CFS patients free from concurrent psychiatric illness. A sample of 14 patients with CDC-diagnosed CFS were compared with 14 healthy volunteers. ACTH and cortisol responses were measured following the administration of 100 microg ovine CRH. Basal ACTH and cortisol values did not differ between the two groups. The release of ACTH was significantly attenuated in the CFS group (P < 0.005), as was the release of cortisol (P < 0.05). The blunted response of ACTH to exogenous CRH stimulation may be due to an abnormality in CRH levels with a resultant alteration in pituitary CRH receptor sensitivity, or it may reflect a dysregulation of vasopressin or other factors involved in HPA regulation. A diminished output of neurotrophic ACTH, causing a reduced adrenocortical secretory reserve, inadequately compensated for by adrenoceptor upregulation, may explain the reduced cortisol production demonstrated in this study.

      Scott LV, Medbak S, Dinan TG. Blunted adrenocorticotropin and cortisol responses to corticotropin-releasing hormone stimulation in chronic fatigue syndrome. Acta Psychiatr Scand 1998 Jun;97(6):450-7 Department of Psychological Medicine, St Bartholomew's and the Royal London School of Medicine, West Smithfield, UK.
    • The objective of this study was to evaluate and compare the basal circadian and pulsatile architecture of the HPA axis in groups of patients with FMS, CFS, or both syndromes with individually matched control groups. Forty patients with either FMS (n = 13), FMS and CFS (n = 12), or CFS (n = 15) were matched by age (18-65), sex, and menstrual status to healthy controls. Subjects were excluded if they met criteria for major Axis I psychiatric disorders by structured clinical interview (SCID). Subjects were admitted to the General Clinical Research Center where meals and activities were standardized. Blood was collected from an intravenous line every 10 min over 24 h for analysis of ACTH and cortisol. Samples were evaluable for ACTH in 36 subject pairs and for cortisol in 37 subject pairs. There was a significant delay in the rate of decline from acrophase to nadir for cortisol levels in patients with FMS (P <.01). Elevation of cortisol in the late evening quiescent period was evident in half of the FMS patients compared with their control group, while cortisol levels were numerically, but not significantly, lower in the overnight period in patients with CFS compared with their control group. Pulsatility analyses did not reveal statistically significant differences between patient and control groups. We conclude that the pattern of differences for basal circadian architecture of HPA axis hormones differs between patients with FMS and CFS compared to their matched control groups. The abnormalities in FMS patients are consistent with loss of HPA axis resiliency.

      Crofford LJ, Young EA, Engleberg NC, Korszun A, Brucksch CB, McClure LA, Brown MB, Demitrack MA. Basal circadian and pulsatile ACTH and cortisol secretion in patients with fibromyalgia and/or chronic fatigue syndrome. Brain Behav Immun. 2004 Jul;18(4):314-25.

      Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, MI, USA
    • Chronic Fatigue Syndrome (CFS) is a clinical condition characterized by a persistent or relapsing debilitating fatigue at rest, lasting more than 6 months, and made worse by exercise. At the present moment, there are three potential etiopathogenic factors: immunologic, viral and neuroendocrine. The purpose of our study was to evaluate possible alterations of the hypothalamic-pituitary-adrenal (HPA) axis in our CFS patients by studying the circadian rhythms of prolactin (PRL), thyrotropic hormone (TSH), adrenocorticotropic hormone (ACTH), and cortisol (CS). A total of 36 patients were enrolled according to the Centers for Disease Control and Prevention case-definition criteria. Twenty healthy subjects were included as controls. Blood samples were taken every 4 hours during a single 24-hour period. We performed a fluorometric enzyme immunoassay with serum PRL, cortisol and TSH, and an immunoradiometric assay with plasma ACTH. The circadian rhythms of PRL, TSH, ACTH and CS were statistically significant in both CFS and control groups. At 24:00 and 04:00 hrs the CFS patients showed lower ACTH levels than healthy subjects (p &#x003C; 0.001); the PRL levels were higher at 04.00 h in CFS patients than in healthy subjects.

      Racciatti D, Guagnano MT, Vecchiet J, De Remigis PL, Pizzigallo E, Della Vecchia R, Di Sciascio T, Merlitti D, Sensi S. Chronic fatigue syndrome: circadian rhythm and hypothalamic-pituitaryadrenal (HPA) axis impairment. Int J Immunopathol Pharmacol. 2001 Jan-Apr;14(1):11-15. Clinic of Infectious Diseases, University of Chieti, Chieti, Italy.
    • Previous studies have demonstrated concentrating neuroendocrinological disturbances in chronic fatigue syndrome (CFS) patients, concentrating in particular on low cortisol levels and a hypothalamic deficiency. In order to investigate the dynamic response of the adrenal glands, we measured dehydroepiandrosterone (DHEA) in serum after adreno-corticotropic hormone (ACTH) stimulation during 60 minutes in 22 CFS patients and 14 healthy controls. We found normal basal DHEA levels, but a blunted serum DHEA response curve to i.v. ACTH injection. This observation adds to the large amount of evidence of endocrinological abnormalities in CFS. Relative glucocorticoid deficiency might contribute to the overall clinical picture in CFS, and could explain some of the immunological disturbances observed in this syndrome.

      De Becker P, De Meirleir K, Joos E, Campine I, Van Steenberge E, Smitz J, Velkeniers B. Dehydroepiandrosterone (DHEA) response to i.v. ACTH in patients with chronic fatigue syndrome. Horm Metab Res 1999 Jan;31(1):18-21Comment in:
      Horm Metab Res. 1999 Jul;31(7):439

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