Sykdommen kan nemlig reverseres hvis oppdaget tidlig nok!
Dett gjelder autoimmun binyresvikt.
Dessuten fins antagelig en versjon som bare er slitne binyrer som følge
Binyrene må nemlig jobbe overtid for å holde stoffskiftet litt oppe når skjoldkjertelen svikter.
Sider av pasienter:
"Registrering i ROAS
Vi ønsker å registrere norske pasienter med primær binyrebarksvikt og polyendokriniske syndromer der binyrebarksvikt inngår. For å registrere pasienter må vi ha pasientinformasjon med samtykkeerklæring, et utfylt ROAS registreringsskjema og en blodprøve for lagring av serum og DNA. "
På www.addison.no sin gjestebok skriver professor Eystein Husebye om
det nye autoimmun-registeret. Haukeland sykehus driver og forsker på autoimmun
binyrebarksvikt for tiden.
http://www.haukeland.no/roas/forhelsepersonell/omaddisons.asp (gammel webside)(legges vel ned snart) Ny webside er http://www.helse-bergen.no/avd/roas/ Les på alle linker der på den siden, interessant. Du må ha Opera eller firefox nettleser og skalere ned utskriften hvis du ikke får printet dem ut.
Det ser ut som om de fant mange flere tilfeller av 21-OH hydroxylase svikt og autoimmunt polyendokrint syndrom enn antatt og at de derfor vil gjøre en større studie.
Se også APS I in Norway
Årsaken til ødeleggelse av binyrene kan være flere, før
var det tuberkulose som var vanligst, ellers kan det være at det skjer
en blødning eller at kjertelen bare går hen og dør, men
det som er vanligst nå er:
Så ROAS- prosjektet med APS I tar for seg den minste fraksjonen. Dessutenv il de ha register over alle andre primære addisonpasienter i Norge.
Hormonlabben har to prøver for binyreantistoffer.
Drøft dette med legen din, den ene (Anti-21-hydroxylase) er ny i juni i år. Man trenger ikke rekvirere den separat men den vil automatisk bli gjort når binyrebark antistoff blir rekvirert. Står på skjemaet.
Dessuten er antistoffer mot 17-alpha OH viktig.
Hello everyone...I just recently got tested for adrenal insufficiency and although i have not recieved any official diagnosis yet ( had blood drawn Aug 2nd) my question is..is it possible to have partial adrenal insufficiency and not be aware of it?..i also have Hashimotos Thyroiditis and have read that adrenal insufficiency is known to be linked with it. Also i have alot of physical stress invloved with my job which i heard can be damaging to your adrenal glands. If anyone who is knowledgable in this area can help..I'd greatly appreciate it thanks :)
From: kris Yes, you can have partial adrenal insufficiency. It's known as low adrenal reserve or mild adrenal insufficiency. Unfortunately, most mainstream physicians don't believe in this. For most of them, the term adrenal insufficiency means Addison's disease. Many people with hypothyroidism also have low adrenals but not enough to be considered Addison's. Some people do have both hypothryoidism and true Addison's disease but that doesn't seem to be as common as the hypo low reserve combo.Hypothyroidism itself can drain the adrenals so the big question is does one really have a true adrenal problem or is it the result of inadequate treatment of their thyroid problem.
For dette er den lange synacten-testen best. Den korte vil ikke vise noe(synacten=ACTH. hos den korte vil cortisol stige normalt. Hos den lange vil cortisol ikke stige normalt fordi den tester binyre-reserven. )
|Hva pasientene sier||
Det er relativt mye skriving i de amerikanske og engelske fora om "weak
adrenals" men ikke i Norge.
Hva pasientene i alle år har sagt
Mange pasienter har store problemer med å bli hørt av legene
siden legene bare har lest om addisonkrise på
www.tidsskriftet.no og legetidsskriftet har fortiet den langvarige
langsomme autoimmune varianten. Menn har typisk den plutselige varianten
med plutselig ødeleggelse av binyrene, mye omtalt i medidinsk litteratur,
mens kvinner har typisk den langsomme autoimmune varianten med lavt blodtrykk
og salthunger og vondt i nyrene og våkenhet om kvelden og trøtthet
om morgenen som hovedsymptomer.
Det som hypothyreosepasientene og andre har beskrevet i diverse fora som http://forums.about.com/ab-thyroid/start i folderen for "adrenal issues" og folderen for "Hormones/Diet/ Larrian" og http://forums.about.com/fatigue1/start og news:alt.support.thyroid (les hele arkivet som er søkbart på google groups), menopause diet forum etc presenterer som:
Bemerk at lavt Ferritin stresser binyrene og bør ligge over 70 og synkende østrogen til og med før overgangsalderen stresser binyrene veldig også. Kilde: Professor Larrien Gillespie.
til kontrast lister Haukeland kun opp :
Og pas. beretter vanligvis om vondt i ryggen ved nyrene, ikke magesmerter.
En pas. vil ikke nødvendigvis oppfatte at hun er våken om kvelden som søvnforstyrrelse.
|Årsaker||Før var det tuberkulose.
Dessuten kan det være HIV og fungus og blødninger av forskjellige årsaker, bl.a. stress. Dessuten metastaser. ALA etc.
" Disseminated fungal infections Several species of fungi can involve the adrenal glands and cause adrenal insufficiency. Histoplasmosis and paracoccidioidomycosis (South American blastomycosis) are important causes of adrenal insufficiency in endemic areas. In contrast, adrenal insufficiency is rare in patients with cryptococcosis, coccidioidomycosis, and North American blastomycosis. The adrenal glands are enlarged and may become calcified in all of these disorders. Recovery of adrenal function after prolonged anti-fungal treatment can occur
HIV infection Endocrine abnormalities are common in asymptomatic patients with human immunodeficiency virus (HIV) infection and those with the acquired immunodeficiency syndrome (AIDS) . The adrenal glands often show a necrotizing adrenalitis caused by cytomegalovirus infection, but infection with Mycobacterium avium-intracellulare or cryptococci and involvement by metastatic Kaposi's sarcoma can also occur
Medfødt, CAH etc. Det fins også LOCAH (late onset)
Sentral binyresvikt fra hypofysen/hypothalamus
De viktigste årsakene er nå autoimmunitet.
Fra Haukeland sykehus sine nettsider:
|"Autoimmunt betinget binyrebarkdestruksjon er årsaken
til Addisons sykdom i omlag 90 % av tilfellene i den industrialiserte verden.
Hos 60-70 % av pasientene kan det ved indirekte immunfluorescens påvises
autoantistoffer rettet mot alle tre soner av binyrebarken. Det viktigste
autoantigenet er 21-hydroksylase (21OH). Det er et av enzymene i kortisol-
og aldosteronsyntesen og uttrykkes utelukkende i binyrebarken hos mennesket
(Winqvist et al., 1992).
Hos omlag 50% av pasientene foreligger et såkalt polyendokrint syndrom, der mer enn et endokrint organ er affisert. (Neufeld et al., 1980). Også her er autoimmun destruksjon vanligst. Man skiller mellom to ulike typer autoimmune polyendokrine syndromer (APS) der binyrebarksvikt inngår. Det finnes også en rekke sykdommer der den polyendokrine svikten skyldes mutasjoner i enkeltgener. Eksempler på dette er adrenoleukodystrofi og kongenitt binyrebarksvikt med hypogonadisme assosisert med mutasjoner i transkripsjonsfaktoren DAX1.
Autoimmunt polyendokrint syndrom type 1 (APS I) APS I er en autosomal resessiv arvelig tilstand som vanligvis debuterer i barneårene. I tillegg til polyendokrin svikt, finner man typisk kronisk mukokutan candidiasis samt en rekke ektodermale manifestasjoner. De vanligste endokrine utfall er hypoparathyroidisme, binyrebarksvikt og ovarieinsuffisiens, fulgt av autoimmun diabetes mellitus type 1og autoimmun thyreoiditt i fallende frekvens (Ahonen et al., 1990).Pasientene kan også få gastrointestinale manifestasjoner som malabsorbsjon, perniciøs anemi og plateepitelkarsinom i munnhulen.
I tillegg til autoantistoffer mot 21OH har pasientene med APS I også autoantistoffer mot en rekke andre enzymer som side chain cleavage enzyme (SCC) (Winqvist et al., 1993), 17a-hydroksylase (17OH) (Krohn et al., 1992), aromatisk L-aminosyre dekarboksylase (AADC) (Rorsman et al., 1995, Husebye et al 1997) og tryptofan hydroxylase (TPH) (Ekwall et al, 1998). Analyse av autoantistoffer kan benyttes diagnostisk og ulike autoantistoffer er assosiert med visse manifestasjoner av sykdommen. For eksempel er antistoffer mot TPH som finnes i serotonin-produserende celler i tarmmukosa assosiert med malabsorbsjon (Ekwall et al, 1998).
Sykdomsgenet som nylig er karakterisert koder for et protein med ukjent funksjon kalt autoimmune regulator, (AIRE). (The Finnish-German APECED Consortium, 1997). "
|De forskjellige syndromer||
Fra http://jcem.endojournals.org/cgi/content/full/86/7/2909 og http://edrv.endojournals.org/cgi/content/abstract/23/3/327
Starter i barneårene
starter fra 30-årene
" APS-2/3 have strong female biases and can occur at any age, but
with adult peak onsets of about 30 yr. Whereas the order of appearance
of the clinical components of the disease can vary, the multiple prodromal
autoimmunities are often ongoing simultaneously. Autoimmune Addisons
disease can develop slowly over many years before symptoms appear, making
screening of patients with IMD and autoimmune thyroiditis for AAs valuable
for early identification of the disease. Some 1 in 200300 patients
with IMD will develop antibody-positive Addisons disease. Autoantibodies
to 21-OH occur in 2% of patients with IMD and 3% of patients with Graves
disease (26). Celiac disease, primary hypogonadism, chronic active hepatitis,
and myasthenia gravis infrequently occur in APS-2."
|APS III||dominant arveligt
" autoimmune thyroid disease in association with atrophic gastritis/pernicious anemia, vitiligo, and/or IMD, but not Addisons disease "
|APS IV||Autoimmunitet mot binyrene
|Isolated adrenal autoimmunity||Mest pga. 21-OH
Antas ikke å være pga. AIRE genet
|Første tegn, forløp|| "After the appearance of antibodies to the adrenal cortex
and/or to 21-hydroxylase (21-OHA), the first evidence of adrenal insufficiency
is usually an increase in PRA after patients have been recumbent for more
than 0.5 h. The raised renin level is due to a failing zona glomerulosa
with salt loss, with low-normal or low plasma aldosterone concentrations
(27). Zona fasciculata dysfunction can become evident months to years later,
first by raised afternoon serum ACTH levels, then by decreasing serum cortisol
responses to (ACTH) stimulation, and finally by decreasing basal serum cortisol
concentrations and the appearance of symptoms (Fig. 5). Thus, these autoantibodies
are useful markers for the prediction of the development of Addisons
disease, particularly so for children (28). There are two types of antibodies
detected by microscopic immunofluorescence: AAs reacting with only the adrenal
cortex and steroidal cell antibodies (SCAs) that react with all steroid
hormone-producing cells. One autoantigen is involved in reactions of AA
is the protein of P450 21-OH enzyme, with epitopes in the central segment
of the enzyme and the C-terminal portion (29, 30). Component antigens for
SCA have been recognized to be other P450 enzymes, 17--hydroxylase (17-OH)
(31) and SCC enzyme (32). Almost all patients with both Addisons disease
and gonadal failure have positive 17-OH and SCC antibodies and APS-1."
Langsomt progredierende forløp:
|Lavt blodsukker som symptom||
Et viktig symptom er lavt blodsukker og at man må spise noe søtt eller føler man seg dårlig.
Årsaken er at kroppen bruker lavt blodsukker til å stimulere
det sympatiske nervesystemet til å stimulere ACTH som trengs til
å sende binyrene beskjed om å sende ut mere mere cortisol
Vær obs. på at hvis man tar prøve av cortisol midt opp i denne lavt-blodsukker-stressituasjonen så kan blodprøvene på cortisol vise et høyt eller "normalt" øyeblikksbilde.
(Insulininjeksjon er en standard prøve for å teste om ACTH sendes ut på riktig måte, og også veksthormon)
En slags forklaring er på :http://www.hyperemesis.org/misc_reference_info.htm men de er ikke helt inne på den årsaksforklaringen jeg har gitt her .
(gammel: http://www.haukeland.no/roas/forside.asp) ROAS-prosjektet
||Cortison eller prednisolon, og om nødvendig florinef
Noen bruker kortere "kurer" med litt prednisolon istedenfor å ta medisin hele tiden. (en dose på 5 mg prednison alle 3 uker)
Se ellers om hvordan prednison kan brukes ved autoimmunitet:http://www.conceivingconcepts.com/medical/immune1.html
The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 7 2909-2922
Copyright © 2001 by The Endocrine Society Special Features
Addisons Disease 2001
Svetlana Ten, Maria New and Noel Maclaren
Department of Pediatrics, Weill Medical College of Cornell University, New York, New York 10021 Address correspondence and requests for reprints to: Noel K. Maclaren, M.D., Weill Medical College of Cornell University, 1300 York Avenue, Room LC-623, New York, New York 10021. E-mail: email@example.com.
" ADRENAL INSUFFICIENCY, OR Addisons disease, can present as a life-threatening crises, because it is frequently unrecognized in its early stages. A relatively uncommon disease in Western countries at an estimated prevalence rate near 120 per million (2), a survey of patients with Addisons disease who are members of the National Adrenal Disease Foundation revealed that 60% had sought medical attention from two or more physicians before the correct diagnosis was ever considered. No figures are available on the number of undiagnosed patients succumbing to adrenal insufficiency. Thus, physicians are advised to keep a high index of suspicion of adrenal insufficiency in unexplained illnesses. Adrenal insufficiency can present with ill-defined fatigue and weakness. It can mimic a gastrointestinal disorder or a psychiatric disease, especially depression. Adrenal insufficiency may cause persistent vomiting, anorexia, hypoglycemia, poor weight gain in a child, or unexplained weight loss in an adult, malaise, fatigue, muscular weakness, unexplained isotonic or hyponatremic dehydration, hyperkalemia, hypotension, hypoglycemia and especially generalized hyperpigmentation (Table 1). In our experience, the development of tiredness with muscular weakness, in particular, can be important clues as to the underlying diagnosis. The "muddy" hyperpigmentation in Addisons disease is due to the elevation of MSH and ACTH, caused by the compensatory activation of hypothalamic-pituitary axis. However, in rare cases, a defect of melanocyte response can result in the absence of hyperpigmentation (3). "
Autoimmune Addisons disease. Autoimmune Addisons disease is a major part of type-1 and -2 APS (APS-1 and APS-2). The definition of the type of APS is clinically important in predicting the potential occurrence of the other associated diseases both in patients and family members.
APS-1 is defined by the presence of three principle components of the disease: chronic mucocutaneous candidiasis or moniliasis, acquired hypoparathyroidism, and autoimmune [adrenal autoantibody (AA) positive] Addisons disease, albeit chronic active hepatitis, malabsorption/chronic diarrhea and alopecia universalis are common while girls are invariably hypogonadal by puberty. APS-1 affects males and females equally and often first manifests during infancy or early childhood. APS-1 is a rare recessive disease that has the highest incidences in genetically isolated populations, such as Iranian Jews (1 in 6009,000; Ref. 22), Finns (1 in 25,000; Ref. 23), and Sardinians (24), where founder effects are probable. Chronic mucocutaneous candidiasis caused by the infection of Candida albicans is usually the initial feature, almost always involving the mouth, and later the nails. Hypoparathyroidism usually occurs next, but hypocalcemia can be masked by untreated Addisons disease and only become declared by steroid replacement therapy (25). Juvenile onset pernicious anemia, vitiligo, anterior hypophysitis, celiac disease, and myositis can be additional features, with less frequent immune-mediated (type-1) diabetes (IMD), thyroid autoimmunity, and ectodermal dysplasias, especially among affected Finns.
APS-2 is defined by autoimmune Addisons disease together with autoimmune thyroid disease (Schmidts syndrome) and/or IMD (Carpenters syndrome). APS-3 is autoimmune thyroid disease in association with atrophic gastritis/pernicious anemia, vitiligo, and/or IMD, but not Addisons disease (25). APS-2/3 have strong female biases and can occur at any age, but with adult peak onsets of about 30 yr. Whereas the order of appearance of the clinical components of the disease can vary, the multiple prodromal autoimmunities are often ongoing simultaneously. Autoimmune Addisons disease can develop slowly over many years before symptoms appear, making screening of patients with IMD and autoimmune thyroiditis for AAs valuable for early identification of the disease. Some 1 in 200300 patients with IMD will develop antibody-positive Addisons disease. Autoantibodies to 21-OH occur in 2% of patients with IMD and 3% of patients with Graves disease (26). Celiac disease, primary hypogonadism, chronic active hepatitis, and myasthenia gravis infrequently occur in APS-2.
The presence of circulating autoantibodies to endocrine antigens is a serologic
characteristic of Addisons disease and other components of the APS "
" After the appearance of antibodies to the adrenal cortex and/or to 21-hydroxylase (21-OHA), the first evidence of adrenal insufficiency is usually an increase in PRA after patients have been recumbent for more than 0.5 h. The raised renin level is due to a failing zona glomerulosa with salt loss, with low-normal or low plasma aldosterone concentrations (27). Zona fasciculata dysfunction can become evident months to years later, first by raised afternoon serum ACTH levels, then by decreasing serum cortisol responses to (ACTH) stimulation, and finally by decreasing basal serum cortisol concentrations and the appearance of symptoms (Fig. 5). Thus, these autoantibodies are useful markers for the prediction of the development of Addisons disease, particularly so for children (28). There are two types of antibodies detected by microscopic immunofluorescence: AAs reacting with only the adrenal cortex and steroidal cell antibodies (SCAs) that react with all steroid hormone-producing cells. One autoantigen is involved in reactions of AA is the protein of P450 21-OH enzyme, with epitopes in the central segment of the enzyme and the C-terminal portion (29, 30). Component antigens for SCA have been recognized to be other P450 enzymes, 17--hydroxylase (17-OH) (31) and SCC enzyme (32). Almost all patients with both Addisons disease and gonadal failure have positive 17-OH and SCC antibodies and APS-1.
Cell-mediated immune processes are important autoimmune adrenal insufficiency.
Lymphocytic infiltrations of the adrenal glands are associated with follicle
formation and loss of adrenocortical cells with scarring. The cellular defect
in the APS may be associated with abnormal balances in cytokine production by
T cells. The subgroups of T helper (Th) cells Th1 and Th2, natural killer
cells (NK-T)produce a different profile of cytokines. Th1 cells secrete
interferon-, interleukin 2, and tumor necrosis factor , whereas Th2 cells secrete
interleukins 4, 5, and 10. A polarized Th2 response is associated with Graves
disease, and Th1 with IMD. APS-1 result from biased Th2 immune responses to
self-antigens and defective protective Th1 responses against invasion of yeast
C. albicans (26).
A major advance in understanding the genetic susceptibility of the APS was made evident when the gene responsible for APS-1 was independently isolated and described as the autoimmune regulator (AIRE) (33, 34). The AIRE gene consists of 14 exons spanning 11.9 kb of genomic DNA, which maps to the long arm of chromosome 21 (21q22.3). The AIRE gene is expressed as messenger RNA (mRNA) in thymus, lymph nodes, pancreas, adrenal cortex, and peripheral blood mononuclear cells. The AIRE protein contains two zinc finger (PHD-finger) and three LXXLL motifs that facilitate the interaction of different proteins with nuclear receptors, and a proline-rich region typical of a nuclear transcription factor. More than 20 different mutations in the AIRE gene have been detected in APS-1 patients with various ethnic backgrounds. R257X (exon 6) is the dominant mutation for Finnish and North Italian patients, whereas 1094del13 (exon 8) is a dominant mutation for British and American Caucasians and R139X (exon 3) is the dominant mutation in Sardinian patients with APS-1. There are no clear correlations between the mutations in the AIRE gene and APS-1 phenotypes reported. However, patients with the same AIRE mutation often present with different components of the diseases of the APS-1, suggesting roles for environmental factors and background (epistatic) genes. The gene encoding the cytotoxic T lymphocyte antigen-4 (CTLA-4) plays an important role in the down-regulation of T-cell activity whereas CTLA-4 polymorphisms have been associated with Addisons disease (35). The future research directions will be investigation of the role of AIRE protein in maintaining normal self-tolerance. It may be that the AIRE gene is involved in negative selection of self-reactive T-cell clones in the thymus and thereby in maintaining self-tolerance. Whatever its immunological functions, a recessive mutation of the AIRE gene inevitably results in widespread autoimmunities.
In our experience however, the AIRE gene is not involved in patients with isolated Addisons disease or APS-2, whereas obligatory heterozygote parents of children with APS-1 display neither the autoantibodies nor the component diseases of their offspring. Whereas APS-1 is not influenced by HLA phenotype, APS-2/3 pedigrees by contrast express an autosomal dominant-like pattern of inheritance with an incomplete penentrance, strongly influenced by HLA-DR/DQ phenotype. Thus, IMD and islet cell autoimmunity is related to the DRB1*0401 or 0405/DQA1*0301/DQB1*0302 and DRB1*03/DQA1*0501/DQB1*0201 haplotypes whereas DRB1*0403, DRB1*0406 and DQB1*0602 are dominantly protective. Hashimotos thyroiditis is associated with DQB1*0301 while Graves disease is associated with DRB3*0201 and DRB1*07 is protective (36). Addisons disease in the context of APS-2 is associated with DR3 haplotypes, whereas in unpublished studies of our own vitiligo seemed to be associated with DRB1*1301, albeit this needs confirmation. "
Four forms of Adrenal autoimmunity: fra http://edrv.endojournals.org/cgi/content/abstract/23/3/327
"Of Italian patients with primary AD (n = 317), 83% had autoimmune AD. At the onset, all patients with autoimmune AD (100%) had detectable adrenal cortex and/or steroid 21-hydroxylase autoantibodies. In the course of natural history of autoimmune AD, the presence of adrenal cortex and/or steroid 21-hydroxylase autoantibodies identified patients at risk to develop AD. Different risks of progression to clinical AD were found in children and adults, and three stages of subclinical hypoadrenalism have been defined. Normal or atrophic adrenal glands have been demonstrated by imaging in patients with clinical or subclinical AD.
Autoimmune AD presented in four forms: as APS type 1 (13% of the patients), APS type 2 (41%), APS type 4 (5%), and isolated AD (41%). There were differences in genetics, age at onset, prevalence of adrenal cortex/21-hydroxylase autoantibodies, and associated autoimmune diseases in these groups. "Incomplete" forms of APS have been identified demonstrating that APS are more prevalent than previously reported.
A varied prevalence of hypergonadotropic hypogonadism in patients with AD and value of steroid-producing cells autoantibodies reactive with steroid 17-hydroxylase or P450 side-chain cleavage enzyme as markers of this disease has been discussed. In addition, the prevalence, characteristic autoantigens, and autoantibodies of minor autoimmune diseases associated with AD have been described.
Imaging of adrenal glands, genetic tests, and biochemical analysis have been shown to contribute to early and correct diagnosis of primary non-autoimmune AD in the cases of hypoadrenalism with undetectable adrenal autoantibodies. An original flow chart for the diagnosis of AD has been proposed. "
|Type I||Type II|
Insulin-Dependent Diabetes Mellitus (IDDM)
Mucocutaneous Candidiasis (First Symptom)
Chronic aggressive Hepatitis
Autoimmune Thyroid Disease
Autosomal recessive transmitted
(60-65% have 3-5 symptoms)
Hyperthyroidism (Graves' Disease)
Associated with HLA-B8/DR-3
(beginning in 3. decade)
According to Betterle the course of an adrenal insufficiency can be classified into 4 stages with the help of endocrine parameters.
|Stage 0 normal adrenal function
Stage 1 raised plasma renin activity and normal to decreased serum aldosterone concentration
Stage 2 small or no increase of plasma cortisol after administration of ACTH (ACTH test)
Stage 3 elevated basal ACTH values
Stage 4 decreased basal plasma cortisol levels and appearance of typical symptoms of adrenal insufficiency
Her omtales også ovariesvikt som også professor Larrian Gillespie skriver om(omtalt på en annen side på siten her)
Fra Larrian på thyroid.about.com forum:Damage to the adrenals lowers the CBG, as does low estradiol....estradiol increases CBG 3 times which then shuts down adrenal hyperplasia as well as Addison's response...so that is why getting estradiol in place is so critical as it affects CBG by upregulating it, and downregulates TBG "
" From: Larrian Gillespie
When ferritin is low, a lot of thyroid/adrenal issues happen...now the rash from midcycle to day 3 is suggestive of an angiotensin problem, which is adrenal/ovarian...see where I am going? Yes, you need to be off the cortisol stuff to do testing and that means a month....and, why use glandular, which is a mixed compound when you can use regular cortef and not have all kinds of other elements that are foreign to the human body??? Really, please avoid all this glandular stuff on the market as it is NOT pharmaceutical grade and contains lots of contaminants, and is somewhat like Premarin...which has 17 different estrogens UNKNOWN to the human body which causes inflammation ....You are definitely WAAAAYYYY oversuppressed which leads to insulin resistance...and the low ferritin will prevent your getting proper balance in your thyroid/adrenal responses.....you may have "sick thyroid" syndrome, which means you have a polyglandular autoimmune disorder going on....so you need to check out those adrenal antibodies and perhaps ovarian antibodies too. "
Migrene kan også være involvert:
" From: Leslie
To: Larrian Gillespie
Hi Larrian, There is a strong connection between low cortisol levels and migraines and it is an amazing thing to witness everyday as I have with my DH's malady. He's had this condition since birth - allergies, digestive problems, nausea, panic attacks, high anxiety, insomnia, weakness, etc all his life. The headaches began around puberty and continued relentlessly all these years. "
Les selv om alt dette på http://forums.about.com/ab-thyroid/start
og innloggingssiden er http://thyroid.about.com/mpboards.htm
på folderen Hormones/Menopause /PCOs
Se ellers også http://www.conceivingconcepts.com/medical/immune1.html
Subclinical autoimmune Addisons disease, with or without metabolic signs of adrenal function failure, is characterized by the presence of adrenal cortex autoantibodies (ACA) and steroid 21-hydroxylase autoantibodies (21OHAb) (10). Several studies have shown that the presence of ACA and 21OHAb is not necessarily associated with the progression toward clinical Addisons disease (11). It has been reported that the presence of ACA and 21OHAb is a marker of rapid progression toward clinical adrenal insufficiency in children but not in adults with endocrine autoimmune diseases (12, 13). Recently, a prospective study of the levels of adrenal autoantibodies, in adult autoimmune patients without clinical signs of adrenal insufficiency showed that the levels of 21OHAb and ACA are strongly correlated with the degree of adrenal dysfunction and that the spontaneous remission of early stages of subclinical adrenal dysfunction along with the disappearance of 21OHAb and ACA can occur (14). In addition, high levels of ACA and 21OHAb were associated with an advanced stage of subclinical adrenal dysfunction and were predictive of the progression toward clinical Addisons disease (14). In a previous longitudinal study (15), some patients with subclinical adrenocortical failure (stage 2) showed a disappearance of ACA with recovery of normal adrenocortical function after a 6-month treatment with corticosteroids for Graves ophthalmopathy (GO). Furthermore, the remission of preclinical adrenal insufficiency persisted after discontinuation of corticosteroid treatment (15).
Adrenocortical functional studies
Adrenocortical function was evaluated by measuring basal plasma levels of ACTH, cortisol, aldosterone, and PRA as previously described (15). Plasma cortisol levels were also evaluated 60 min after iv infusion of 0.25 mg synthetic ACTH (normal peak response, >550 nmol/L). If adrenal antibodies were present, five stages (from 04) of subclinical adrenal dysfunction were recognized in accordance with previously reported criteria (15).
At the beginning of the study, the patient was positive for ACA in the presence of complement-fixing ACA, StCA, and 21OHAb (Fig. 1). A high PRA, low aldosterone levels, normal basal ACTH and cortisol levels, but impaired cortisol response to ACTH were observed in the absence of clinical signs and symptoms of Addisons disease (Table 1). These findings were consistent with the diagnosis of stage 2 subclinical adrenocortical failure (15).
The effect of short-term glucocorticoid therapy can be attributed to the well known immunosuppressive activity of steroids (21). Glucocorticoids could reduce B cell Ig production by decreasing the synthesis of IL-6 (21, 22). In preclinical Addisons disease, a short course of glucocorticoid therapy could prevent progressive adrenal failure by decreasing the B cell function and subsequently the production of adrenal autoantibodies. However, we observed not only the disappearance of 21OHAb, but also a complete remission of the metabolic signs of adrenal dysfunction in our patient with GO. Most likely, the corticosteroid therapy had a more general effect on the autoimmune process and also affected T cell-mediated pathways. It has been demonstrated that corticosteroids decrease both monocyte-macrophage function and T cell expansion (21, 22), which have been proposed as having a preponderant role in the pathogenesis of autoimmune Addisons disease (23). Destruction of adrenal cortical cells could be mediated by cytotoxic T lymphocytes. It is possible that a corticosteroid therapy, when carried out in an early stage of the subclinical adrenocortical failure, down-regulates cytotoxic T lymphocyte expansion and decreases the production of adrenal autoantibodies with the final result of a complete recovery of adrenal function.