Valvojat: MahaTar, Sienestäjä2
What it proves is that there is no such thing as a TSH range that is suitable for everyone, and that the range is different according to the effect of independent influences such as age, body mass, size of working thyroid volume and whether someone is on T4 or not. The T4 therapy range is very much lower than the "normal" untreated and sits around the 1 or lower mark. The 3-4 upper level that works for the normal person is not satisfactory and can indicate undertreatment. Also we're finding that people with no thyroid working at all cannot easily regain normal FT3 with T4 alone and that TSH suppression often has to happen, and in some people no amount of T4 will regain normal FT3 levels. Recent reviews by the gurus now admit that some people cannot handle T4 only and regain health. Just thought you'd like to know that the avalanche is beginning.
J Clin Endocrinol Metab. 2013 May;98(5):1982-90. doi: 10.1210/jc.2012-4107. Epub 2013 Mar 28.
Desiccated thyroid extract compared with levothyroxine in the treatment of hypothyroidism: a randomized, double-blind, crossover study.
Hoang TD1, Olsen CH, Mai VQ, Clyde PW, Shakir MK.
SAA JAKAA
Mietin, mitä tarvitaan, jotta saataisiin poliitikoiden ja terveydenhoidon huippu tajuamaan, että SUURI joukko ihmisiä elää kuin he olisivat vihanneksia!!!
1. Lähettäkää tuhat lääkäriä ulkomaille oppimaan uusinta tietoa kilpirauhasen vajaatoiminnasta! HETI!
2. Lähettäkää tuhat lääkäriä ulkomaille oppimaan miten parannetaan kilpirauhasen autoimmuunitulehdus eli Hashimoto, joka tuhoaa ihmisten elämän! HETI !
3. Lähettäkää tuhat lääkäriä ulkomaille oppimaan miten ihmisille lyhyessä ajassa, minulle vuodessa, voidaan antaa heidän elämänsä takaisinyhdistämällä vitamiinia, mineraaleja ja hormoneja! HETI!
4. Asettakaa vastuuseen sellaiset lääkärit, jotka eivät kuuntele potilaitaan, eivätkä sovella uusinta tiedettä potilaidensa saamiseksi pois invalidisoivasta tilastaan! HETI!
5. Asettakaa vastuuseen sellaiset organisaatiot ja poliitikot, jotka eivät tutki, miksi niin monet sairaat ihmiset ovat sosiaaliturvan varassa! HETI!
6. Lisätkää lääkärien koulutusohjelmaan kurssi joka keskittyy hormonipuutoksiin, niiden oireisiin ja niihin liittyviin sairauksiin! HETI!
7. Yhtieskunnalle / meillä ei ole varaa pitää ihmisiä sairaina, että ihmiset vuosikausia kulkevat lääkäriltä toiselle saamatta oikeaa hoitoa! HETI!
8. Auttakaa ihmisiä saamaan elämänsä takaisin! HETI!
Millions of people, largely women, all over the world suffer a seriously impaired quality of life and even early death because of undiagnosed, misdiagnosed or under-treated hypothyroidism. They are denied treatment, told they have chronic fatigue syndrome, which can't be treated, or not given enough hormone or the right type of hormone to make them better. This situation borders on an abuse of civil rights and gender discrimination. How many men would be told symptoms are all in your head?
It has been known how to treat hypothyroidism by replacing the missing hormone for around 120 years, but we cannot diagnose or indeed treat it properly because of the over reliance on a laboratory blood test and lack of knowledge by doctors of the complicated nature of the disease. They are not trained to treat it properly. An objective investigation into the nature of the disease and its treatment needs to be undertaken.
HS kirjoitti:Kilpirauhasen vajaatoiminta on Suomessa satojentuhansien ihmisten sairaus, mutta se tunnistetaan huonosti perusterveydenhoidossa, sanoo Suomen Kilpirauhasliiton toiminnanjohtaja Asta Tirronen
HESARI
Katja Bloigu kirjoitti:Hesari on käyttänyt sitä ainaista ja samaa asiantuntijaa, joka kuuluu koulukuntaan Thyroxinia kaikille riittävän suurilla annoksilla.
Tästä keinotekoisesta lääkkeestä on hyvin harvalle apua. Olisin suonut että Hesari olisi käsitellyt aihetta syvällisemmin ja kertonut kuinka ihmiset saavat avun. miten paljon se maksaa ja kuinka vähän kilpirauhasen ongelmiin erikoistuneita asiantuntijoita on Suomessa ja miten pitkät jonot niille on. Totuus on että kilppariongeliin ei saa mitään apua julkiselta puolelta, eikä perinteiseltä yksityiseltäkään, aivan muutamaa lääkäriä lukuun ottamatta. Jos haluaa todella hoitaa itseään, niin se maksaa. Ja henkilö jolla ei ole suht hyvä palkka, ei sitä pysty tekemään
Eltroxin® has for many years been the only levothyroxine-containing product sold in Denmark. On 28 December 2009, Euthyrox® entered the market in the strengths 25, 50 and 100 micrograms. Euthyrox® tablets have a scoreline so that they can be divided into equal parts.
Side effects
In the past two years and until 31 October 2009, inclusive, the Danish Medicines Agency has received a total of 846 reports of suspected adverse reactions from Eltroxin®. The reports were primarily submitted in the period March 2009 to October 2009. A single adverse reaction report may contain several adverse reactions, and altogether 4,643 suspected adverse reactions have thus been reported in the past two years up to and including 31 October 2009. The 10 most common adverse reactions reported during this period are displayed in the table below. These adverse reactions are all suggestive of overmedication or undermedication with Eltroxin®.
Side effect
Sleepiness 386
Headache 329
Dizziness 231
Nausea 187
Weight increase 153
Disturbance in attention 152
Impaired memory 134
Aching muscles 133
Arthralgia 130
Stomach pain 105
In the two-year period from 1 November 2007 to 31 October 2009, 112,216 persons were treated with Eltroxin®. In the three months from 1 August 2009 to 31 October 2009, 82,003 persons were treated with Eltroxin®.
The Danish Medicines Agency has recorded an increase in the number of reported side effects from Eltroxin®. The increase is observed after GlaxoSmithKline (GSK) has changed the excipients contained in Eltroxin®. The new excipients are commonly used in medicines.
Patients treated with a levothyroxine medicine – If levothyroxine and orlistat are taken simultaneously, they can interact to an extent that makes it difficult to control patients' hypothyroidism. It may be necessary to take orlistat and levothyroxine at different times of the day, and the levothyroxine dose may need adjustment.
8.6 Ved manglende effekt af antidepressiva
I flere danske og udenlandske behandlingsvejledninger anbefales det, at man ved manglende effekt
skifter til et antidepressivum med en anden farmakodynamisk virkningsprofil. SBU-rapporten konkluderer, at der er begrænset belæg for nytten ved at skifte mellem præparater med forskellig effekt på det noradrenerge og serotonerge system, men der er et presserende behov for flere studier.
I et netop publiceret systematisk review har man opgjort nytten af at skifte fra ét præparat til et andet
inden for SSRI-gruppen. Konklusionen er, at der ikke er videnskabelig dokumentation for nytten af
et sådant skift.
Der findes videnskabeligt belæg for potensering af behandlingen med lithium (evidensstyrke A).
En velgennemført metaanalyse af placebokontrollerede undersøgelser viser, at potensering af TCA,
fluoxetin og citalopram med lithium medfører effekt i løbet af 14 dage hos 50 % af patienterne mod
23 % ved potensering med placebo (NNT = 3,7).
En undersøgelse fra 2006 tyder på, at potensering med trijodthyronin (T3) har samme effekt som
potensering med lithium (evidensstyrke A) . Trijodthyronin er ikke et registreret lægemiddel i
Danmark, men thyroxin kan overvejes.
Main predictors of poor response to antidepressant treatment
• Somatic condition: Cushing’s disease
• Interaction between stressors and genes
(SERT,FKBP5,CRHR1) to predict response to
treatment
Thyrotropin releasing hormone
• Hypothyroidism; Polymorphism of the
deiodinase type1 gene
The relationship between thyroid function and MDD is well-
known. Indeed, hypothyroidism is associated with MDD,and
TRH levels correlate with symptom severity (Bauer et al., 2009).
Furthermore, MDD patients exhibit alterations in several mark-
ers of thyroid function, particularly of the thyroid hormone
triiodothyronine( T3)(see Hage and Azar, 2012 for a review).
Interestingly, T3 is widely used to improve the therapeutic out-
come of AD drugs in patients who exhibit poor response to
treatment (Aronson et al.,1996; Nierenberg et al.,2006), partic-
ularly in those treated with TCAs. Successful treatment with T3
alone has also been reported in some older studies (Feldmesser-
Reiss,1958; Flach et al.,1958; Wilson et al.,1974). These findings
are further supported by preclinical evidence. Indeed,T3 alone
elicited an AD-like effect in a bio-assay for AD response (Lifschytz
et al., 2006, 2011), whereas the combination of T3 with chronic
fluoxetine increased the effects of the SSRI (Brochet et al., 1987;
Eitan et al., 2010). This effect appears to be related to thy-
roid function because it has also been shown that the effects of
TCAs are reduced in rats in which hypothyroidism has been pro-
voked by the addition of propylthiouracil to their drinking water
(Martin et al.,1 987). The effects of T3 occur via an interaction
with nuclear thyroid hormone receptors (TRs). Four such recep-
tors have been described: α-1, α-2, β-1, and β-2. It would be of
interest to determine which of these receptors might mediate the
effects of T3. A recent study demonstrated that administration
of dronedarone, a specific TRα antagonist, prevented the AD-like
effects of T3, suggesting that the TRα receptor is responsible for
the effects of T3 (Lifschytz et al., 2011). This observation is con-
sistent with the finding that TRα receptors are the most highly
expressed TRs in the brain (Williams, 2008) as well as with the
observation that mice in which this receptor is mutated display
depressive-like behavior (Pilhatsch et al., 2010).
Few studies have investigated the association of polymor-
phisms of thyroid function-related genes with MDD and AD
response. However, the relationship of a polymorphism of the
deiodinase typeI (D1) gene (D1 converts inactive T4 to active
T3) with the ability of T3 to augment the effects of AD has been
investigated (Papakostas et al.,2009).
Interestingly, the effects of T3 in patients undergoing AD ther-
apy are particularly remarkable in some subcategories of patients,
particularly in women (Altshuler et al.,2001; Agid and Lerer,
2003) and in patients with a typical MDD.
Further progress could certainly be achieved in improving AD
response by (a) dosing pre-treatment T3 hormones in patients
and (b) studying polymorphisms of thyroid function related
genes. Such studies would enable the segregation of patients
according to their thyroid hormone status and the initiation of co-
therapy with T3 at the beginning of AD therapy in those patients
with the highest thyroid dysfunction.
Käyttäjiä lukemassa tätä aluetta: Ei rekisteröityneitä käyttäjiä ja 14 vierailijaa