RE: Further Info

[Guest guest]

Hi Pam, anyone take T3 will always have supressed TSH as you well know. As long as FT4 and FT3are in range then there is no problem. don't forget- don't take T3 containing meds for 24 hours before blood has been drawn or you will get a silly high result which will cause panic! Try to get referral to an endo from Sheila's list, rather than taking pot luck with the GP choice. See the forum files-' first visit to endo' Write your history, remember best as you can symptoms when taking T4 then list how you are now- point out the improvements, I find that docs like it all written out clearly- saves everybody time and effort. > thyroid treatment > From: doggy532001@...> Date: Wed, 9 Mar 2011 17:23:48 +0000> Subject: Further Info> > Sorry Sheila forget to add that one of the reasons I am likely to have a problem is that my TSH is always competely suppressed and therefore my GP says I am overactive. I have to have lots of blood tests done next week and I am sure this will be the case because it always has been.> > Pam> > > > ------------------------------------> > TPA is not medically qualified. Consult with a qualified medical practitioner before changing medication.> >

[Guest guest]

Thought you

might be interested in this Pam. http://www.thyroidmanager.org/Chapter4/ch01s03.html

Luv - Sheila

CLINICAL

APPLICATION OF TSH MEASUREMENTS AND SUMMARY

Table

4-4 lists conditions in which basal TSH values may be altered as practical

examples of the pathophysiology of the hypothalamic-pituitary thyroid axis.

This subject is also discussed in Chapter 6 from the standpoint of clinical

diagnosis. This section also serves as a summary of the clinically relevant

points in this chapter.

Table 4. Conditions

which may be associated with abnormal serum TSH concentrations

TSH reduced

Expected TSH

(mU/L)

Thyroid

Status

FT4

TSH

reduced

1.

Hyperthyroidism

<0.1

¢¬

¢¬,T3

2.

¡ÈEuthyroid¡É Graves¡Ç disease

0.2-0.5

N(¢¬)

N(T3¢¬)

3.

Autonomous nodules

0.2-0.5

N(¢¬)

N(T3¢¬)

4.

Excess thyroid hormone treatment

0.1-0.5

N,¢¬

N,¢¬

5.

Other forms of subclinical hyperthyroidism (including thyroiditis variants)

0.1-0.5

N,¢¬

N,¢¬

6.

Illness with or without dopamine

0.1-5.0

N

¢¬,N,¢­

7.

First trimester pregnancy

0.2-0.5

N(¢¬)

N(¢¬)

8.

Hyperemesis gravidarum

0.2-0.5

N(¢¬)

¢¬(N)

9.

Hydatiform mole

0.1-0.4

¢¬

¢¬

10.

Acute psychosis or depression (rare)

0.4-10

N

N(¢¬)

11.

Elderly (small fraction)

0.2-0.5

N

N

12.

Cushing¡Çs syndrome and glucocorticoids excess (inconsistent)

0.1-0.5

N

N

13.

Retinoid X receptor-selective ligands

0.01-0.2

¢­

¢­

14.

Hypothalamic-pituitary dysfunctions

<0.1-0.4

¢­

¢­

15.

Congenital TSH deficiency

a)

Pit-1 mutations

0

¢­

¢­

PROP 1 mutations

0

¢­

¢­

c)

TSH mutations of TSH b gene (CAGYC mutation)

0

¢­

¢­

d)

Skipping of TSH b gene exon 2

0

¢­

¢­

e)

Inactivating mutation of TRH receptor gene

1-2

TSH

Elevated

1.

Primary hypothyroidism

6-500

¢­

¢­

2.

Resistance to TSH

a)

with mutations of TSH receptor

without mutations of TSH receptor

6-100

N,¢­

N,¢­

3.

Recovery from severe illness

5-30

N

N,¢­

4.

Iodine deficiency

6-150

N,¢­

¢­

5.

Thyroid hormone resistance

1-15

N(¢­,¢¬)

¢¬

6.

Thyrotroph tumor

3-30

¢¬

¢¬

7.

Hypothalamic-(pituitary) dysfunctions

1-20

¢­

¢­

8.

Psychiatric illness (especially bipolar disorders)

0.4-10

N

N

9.

Test artifacts (endogenous anti-mouse g-globulin antibodies)

10-500

N

N

10.

¡Çs disease

5-30

N

N

Clinical

situations associated with subnormal TSH values

The

most common cause of a reduced TSH in a non-hospitalized patient is thyroid

hormone excess. This may be due to endogenous hyperthyroidism or excess

exogenous thyroid hormone. The degree of suppression of basal TSH is in

proportion to the degree and duration of the excess thyroid hormone. The

reduced TSH is the pathophysiological manifestation of the activation of the

negative feedback loop.

While

a low TSH in the presence of elevated thyroid hormones is logical, it results

from multiple causes. Prolonged excessive thyroid hormone causes physiological

" atrophy " of the thyroid stimulatory limb of the

hypothalamic-pituitary thyroid axis. Thus, TRH synthesis is reduced, TRH mRNA

in the PVN is absent, TRH receptors in the thyrotroph may be reduced; and the

concentration of TSH ¦Â and ¦Á subunits and both mRNAs in the thyrotroph are

virtually undetectable. Therefore, it is not surprising that several months are

usually required for the re-establishment of TSH secretion after the relief of

thyrotoxicosis. This is especially well seen in patients with Graves' disease

after surgery or radioactive iodine, in whom TSH remains suppressed despite a

rapid return to a euthyroid or even hypothyroid functional status. [360, 361]

Since TRH infusion will not increase TSH release in this situation, it is clear

that the thyrotroph is transiently dysfunctional. [362] A similar phenomenon

occurs after excess thyroid hormone treatment is terminated, and after the

transient hyperthyroidism associated with subacute or some variants of

autoimmune thyroiditis, though the period of suppression is shorter under the

latter circumstances. [363] This cause of reduced circulating thyroid hormones

and reduced or normal TSH should be distinguishable from central hypothyroidism

by the history.

Severe

illness is a common cause of TSH suppression although it is not often confused

with thyrotoxicosis. Quantitation of thyroid hormones will generally resolve

the issue. [294] Patients receiving high-dose glucocorticoids acutely may also

have suppressed TSH values although chronic glucocorticoid therapy does not

cause sufficient TSH suppression to produce hypothalamic-pituitary

hypothyroidism (see above).

Exogenous

dopamine suppresses TSH release. Infusion of 5-7.5 mg/Kg/min to normal

volunteers causes an approximately 50% reduction in the concentrations of TSH

and consequent small decreases in serum T4 and T3 concentrations. [327] In

critically ill patients, this effect of dopamine can be superimposed on the

suppressive effects of acute illness on thyroid function, reducing T4

production to even lower levels.331 Dopamine is sufficiently potent to suppress

TSH to normal levels in sick patients with primary hypothyroidism. [327] This

needs to be kept in mind when evaluating severely ill patients for this

condition. Dopamine antagonists such as metoclopramide or domperidone cause a

small increase in TSH in humans. However, somewhat surprisingly, patients

receiving the dopamine agonist bromergocryptine, do not become hypothyroid.

Although L-dopa causes a statistically significant reduction in the TSH

response to TRH, patients receiving this drug also remain euthyroid. [333]

Studies

in animals have suggested that pharmacological amounts of retinoids may

decrease serum TSH concentration (see also paragraph ¡ÈEffect of Thyroid Hormone

on TSH Secretion¡É). [78, 364] Recently, severe central hypothyroidism

associated with very low serum TSH concentration has been reported in patients

with cutaneous T-cell lymphoma treated with high-dose bexarotene, a retinoid X

receptor-selective ligand able to suppress TSH secretion. [365]

The

capacity of hCG to function as a thyroid stimulator is discussed in Chapter 14.

This may be manifested in patients with normal pregnancy as a slightly

subnormal TSH during the first trimester (0.2 - 0.4 mU/L) or by frank, though

mild, hyperthyroidism in patients with choriocarcinoma or molar pregnancy.

[366]

Patients

with acute psychosis or depression and those with agitated psychoses may have

high thyroid hormone levels and suppressed or elevated TSH values. The etiology

of the alterations in TSH are not known. Those receiving lithium for bipolar

illness may also have elevated TSH values due to impairment of thyroid hormone

release. Patients with underlying autoimmune thyroid disease or multi-nodular

goiter are especially susceptible. [367] A small fraction of elderly patients,

particularly males, have subnormal TSH levels with normal serum thyroid hormone

concentrations. It is likely that this reflects mild thyrotoxicosis if it is

found to be reduced on repeated determinations.

Congenital

central hypothyroidism with low serum TSH may result from mutations affecting

TSH ¦Â gene or the Pit-1 gene (see paragraphs ¡ÈThe Thyroid-Stimulating Hormone

Molecule¡É and ¡ÈRole of Pit-1 and its splicing variants in the regulation of TSH

¦Â gene expression¡É).

Causes

of an elevated TSH

Primary

hypothyroidism is the most common cause of an elevated serum TSH. The serum

free T4 is low normal or reduced in such patients but the serum free T3 values

remain normal until the level of thyroid function has markedly deteriorated.

[101] Another common cause of an elevated TSH in an iodine-sufficient

environment is the transient elevation which occurs during the recovery phase

after a severe illness. [305, 306] In such patients a " reawakening "

of the hypothalamic-pituitary thyroid axis occurs pari passu with the

improvement in their clinical state. In general, such patients do not have

underlying thyroid dysfunction. Iodine deficiency is not a cause of elevated

TSH in Central and North America but may be in certain areas of Western Europe,

South America, Africa and Asia.

The

remainder of the conditions associated with an elevated TSH are extremely rare.

Inherited (autosomal recessive) forms of partial (euthyroid

hyperthyrotropinemia) or complete (congenital hypothyroidism) TSH resistance

have been recently described associated to inactivating point mutations of the

TSH receptor gene. [368, 369] Interestingly, inherited dominant forms of

partial TSH resistance have also been described in the absence of TSH receptor

gene mutations. [370, 371]No TSH nor Gsa gene mutations were detected in these

excetpional cases. [370] and the underlying molecular defect(s) remain(s) to be

elucidated. More frequently, in a patient who has an elevated serum FT4, the

presence of TSH at normal or increased levels should lead to a search for

either resistance to thyroid hormone or a thyrotroph tumor. Hypothalamic-pituitary

dysfunction may be associated with normal or even modest increases in TSH are

explained by the lack of normal TSH glycosylation in the TRH-deficient patient.

The diagnosis is generally made by finding a serum free T4 index which is reduced

to a greater extent than expected from the coincident serum TSH. Psychiatric

illness may be associated with either elevated or suppressed TSH, but the

abnormal values are not usually in the range normally associated with

symptomatic thyroid dysfunction. The effect of glucocorticoids to suppress TSH

secretion has already been mentioned. This is of relevance in patients with

's disease in whom TSH may be slightly elevated in the absence of

primary thyroid disease.

Lastly,

while most of the artifacts have been eliminated from the immunometric TSH

assays, there remains the theoretical possibility of an elevated value due to

the presence of endogenous antimouse gamma globulin antibodies. [372, 373]

These antibodies, like TSH, can complex the two TSH antibodies resulting in

artificially elevated serum TSH assay results in euthyroid patients. Such

artifacts can usually be identified by finding non-linear results upon assay of

serial dilutions of the suspect serum with that from patients with a suppressed

TSH

Sheila

Sorry Sheila forget to add that one of the

reasons I am likely to have a problem is that my TSH is always competely

suppressed and therefore my GP says I am overactive. I have to have lots of

blood tests done next week and I am sure this will be the case because it

always has been.

Pam

[Guest guest]

>

>

> Hi Pam,

> anyone take T3 will always have supressed TSH as you well know.

As long as FT4 and FT3are in range then there is no problem. don't forget- don't

take T3 containing meds for 24 hours before blood has been drawn or you will get

a silly high result which will cause panic!

> Try to get referral to an endo from Sheila's list, rather than taking pot

luck with the GP choice. See the forum files-' first visit to endo'

> Write your history, remember best as you can symptoms when taking T4 then

list how you are now- point out the improvements, I find that docs like it all

written out clearly- saves everybody time and effort.

>

>

Hi

Thanks for the advice, I will follow this up. I am not at all confident about

seeing an Endo at all but I guess some of them have to be better than others!

Good idea re writing out symptoms but all I can remember when I took all T4 was

that I felt terrible really toxic all the time and that was on just 50 mcg

thyroxine.

BW

Pam

[Guest guest]

Pam,

I've NEVER in the last 12 years managed to have a TSH of more than 0.1 and

usually it is 0.01.

I've heard all this rubbish about me being hyperthyroid, or thyro toxic several

times....

What you need to do, is learn the signs of hyperthyroidism, and then the next

time there is a comment about the low TSH just say, My t4 and T3 are in range

and I don't have any of the signs of hyperthyroidism, such as: * Palpitations

* Heat intolerance

* Nervousness

* Insomnia

* Breathlessness

* Increased bowel movements

* Light or absent menstrual periods

* Fatigue

* Fast heart rate

* Trembling hands

* Weight loss

* Muscle weakness

* Warm moist skin

* Hair loss

Look who ever it is in the eye and say, that when you have some of these signs

and if your T4 or T3 go out of range, then you will consider changing the

meds....

Works for me

x

>

> Sorry Sheila forget to add that one of the reasons I am likely to have a

problem is that my TSH is always competely suppressed and therefore my GP says I

am overactive.

>