help needed for battle with NHS

[Guest guest]

Hi,

I have an ongoing fight with the QE in Birmingham. The NHS are basically forcing

me to go the ombudsman about it - they have already forced me down their own

complaints procedure, but I want to reply to some of their comments with hard

evidence, but I am having problems locating what I need. My brain is not at it's

best at the moment - and I'm just getting frustrated.

If you know of hard evidence from well respected (in the NHS's eyes) sources

that contradicts or if anyone wants to comment on the following please feel free

to rip what they have said to shreds and send me a link if you can - I'd really

appreciate it!

1. There is a large body of evidence, and associated local, national and

international guidelines indicating that a rise in serum TSH is an essential

prerequisite for the diagnosis of primary hypothyroidism.

2. Dr F has tried to explain the potential long term consequences of treatment

with exogenous thyroid hormones, especially as you have indicated that thyroid

function testing whilst on treatment has

revealed suppression of TSH, which is a biochemical marker of thyroid

hormone excess. Areas of clinical concern associated with long term TSH

suppression from exogenous thyroid hormone treatment would be

augmentation of risk of atrial fibrillation and osteoporosis.

3. You had a short synacthen test to assess adrenocortical reserve (a test to

see if you are producing sufficient adrenal steroid hormones) in May 2010 and

this was found to be more than adequate, with a peak serum cortisol value of

901nmol/l (Le. a response to the injection showing very healthy adrenal steroid

production).

4. You were again found to have entirely normal test of

thyroid function. A check of serum prolactin, gonadotrophins, random

oestradiol and IGF- 1 (various pituitary and other hormones) were all normal.

5. In the absence of a rise in TSH (and in the absence of a fall in serum free

T4 and T3 (the main hormones produced by the thyroid gland) there is no

biochemical evidence of primary hypothyroidism in your case. Consequently there

is no established indication for thyroxine replacement therapy. Furthermore, in

the absence of a diagnosis of primary hypothyroidism it is not logical, or good

practice, to

ascribe a patient's symptoms to that diagnosis.

6. you request further information regarding the diagnosis and management of

hypothyroidism with University Hospitals Birmingham Foundation Trust. The

practice of the large and expert team in endocrinololoy is indeed in accord with

the British and American Thyroid Associations and readily available on their

websites.

7. There is considerable peer reviewed and published information in the medical

literature on the potential risks associated with thyroxine treatment in doses

causing suppression of serum TSH.

I think that's the main ones - hope everyone's blood pressure is ok after

reading it!!

From a very cross and irritated

Dawn

[Guest guest]

Hi Dawn - I have also been down the complaints process as far as the ombudsman .

I did not have the problem of disputing tests as there were no tests except some

old TSH tests to consider. I most definitely think that the ombudsman is a good

idea however there are a few things to bear in mind . I had ICAS at the

complaints meeting as an independant witness and after that I kept her informed

and she was helpful in getting replies from the hospital . As far as the

ombudsman goes they have certain criteria to work to [it is worth printing them

off the internet ] They will tell you that they are lay not medical people and

hence use a medical adviser . You are entitled to see this medical report-I

found some important items missing and responded where I found gaps . If you

provide evidence [i did some ] any medical evidence should be considered and

commented on by this advisor .If not why not!!!!! Studies like the HUNT STUDIES

from Norway about colesterol and heart disease would have been useful. What you

are not allowed to see is what is said by the hospital so try not to leave

anything out. It is difficult with brain fog and I could have prepared better if

it happened now and I have improved greatly with Dr P's help -yes we are at a

disadvantage because of this brain fog but it is no reason not to try as the

more complaints about this the better . Good luck

[Guest guest]

>> Hi,> > I have an ongoing fight with the QE in Birmingham. The NHS are basically forcing me to go the ombudsman about it - they have already forced me down their own complaints procedure, but I want to reply to some of their comments with hard evidence, but I am having problems locating what I need. My brain is not at it's best at the moment - and I'm just getting frustrated. > > If you know of hard evidence from well respected (in the NHS's eyes) sources that contradicts or if anyone wants to comment on the following please feel free to rip what they have said to shreds and send me a link if you can - I'd really appreciate it!> > 1. There is a large body of evidence, and associated local, national and international guidelines indicating that a rise in serum TSH is an essential prerequisite for the diagnosis of primary hypothyroidism.

NOT TRUE> > 2. Dr F has tried to explain the potential long term consequences of treatment with exogenous thyroid hormones, especially as you have indicated that thyroid function testing whilst on treatment has> revealed suppression of TSH, which is a biochemical marker of thyroid> hormone excess. NOT TRUE

Areas of clinical concern associated with long term TSH suppression from exogenous thyroid hormone treatment would be> augmentation of risk of atrial fibrillation and osteoporosis.> NOT TRUE - there are many more dangers with not having enough thyroxine

> 3. You had a short synacthen test to assess adrenocortical reserve (a test to see if you are producing sufficient adrenal steroid hormones) in May 2010 and this was found to be more than adequate, with a peak serum cortisol value of 901nmol/l (Le. a response to the injection showing very healthy adrenal steroid production).

What time of day? And do these people not read the information that comes with Levothyroxine?> > 4. You were again found to have entirely normal test of> thyroid function. A check of serum prolactin, gonadotrophins, random> oestradiol and IGF- 1 (various pituitary and other hormones) were all normal.

By whose measures?> > 5. In the absence of a rise in TSH (and in the absence of a fall in serum free T4 and T3 (the main hormones produced by the thyroid gland) there is no biochemical evidence of primary hypothyroidism in your case. Consequently there is no established indication for thyroxine replacement therapy. Furthermore, in the absence of a diagnosis of primary hypothyroidism it is not logical, or good practice, to> ascribe a patient's symptoms to that diagnosis.

Again NOT TRUE> > 6. you request further information regarding the diagnosis and management of hypothyroidism with University Hospitals Birmingham Foundation Trust. The practice of the large and expert team in endocrinololoy is indeed in accord with the British and American Thyroid Associations and readily available on their websites.

NHS guidelines state that thyroid diagnosis and management should not rely on blood tests alone.

> > 7. There is considerable peer reviewed and published information in the medical literature on the potential risks associated with thyroxine treatment in doses causing suppression of serum TSH.

There's way more that show that this is rubbish!!

> > I think that's the main ones - hope everyone's blood pressure is ok after reading it!!> > From a very cross and irritated > Dawn>

[Guest guest]

Hi Dawn

" If you know of

hard evidence from well respected (in the NHS's eyes) sources that contradicts

or if anyone wants to comment on the following please feel free to rip what

they have said to shreds and send me a link if you can - I'd really appreciate

it! "

OK - so you DID ask. Keep scrolling. This is long. The biggest problem here appears to centre around the

level of TSH as the be all and end all of reaching a diagnosis.

Problem is Dawn, that no

matter what studies you show the NHS medical practitioners, the majority refuse

to acknowledge it if it goes against what they have been brought up to believe.

They take their lead about thyroid disease from the British Thyroid

Association who have prepared

NO guidelines on the diagnosis and management of those with symptoms of

hypothyroidism.

Neither have NICE prepared

any guidelines on the diagnosis and management of hypothyroidism. All the BTA

have done is,

under the umbrella of the RCP

written a statement on the diagnosis and management of PRIMARY hypothyroidism

and nothing else. Primary

hypothyroidism, means the THYROID GLAND doesn't produce an adequate amount of

thyroxine (T4). W (** - SEE BELOW) - or

- peripheral resistance to thyroid hormones at the cellular level. It is not

due to a lack of thyroid

hormones. Normal amounts of

thyroid hormones and TSH are usually detected by blood tests; therefore blood

tests

do NOT detect euthyroid

hypometabolism. This is usually inherited. However environmental toxins may

also cause or

exacerbate the problem. The

pervasiveness of euthyroid hypometabolism has yet to be recognised by the

majority

of mainstream medicine but

already is in epidemic proportions. Euthyroid hypometabolism produces the same

sort of

symptoms that primary,

secondary, tertiary or other type of hypothyroidism does, and needs treatment

using the

active thyroid hormone T3 -

but doctors cannot diagnose this by using TSH, free T4 or free T3 blood tests.

Two papers stand out as

demonstrations of the limits of the customary thyroid practice. First, Drs.

Baisier, Hertoghe, and Eeckhaut (Thyroid Insufficiency? Is Thyroxine the Only

Valuable Drug?) studied the failures of the customary practice of endocrinology

and found that these subjects had the same collection of symptoms as patients

with deficient thyroid gland secretion (the proper definition of

hypothyroidism). They found an evaluation of eight nonspecific symptoms is a

good clinical diagnostic. They also found diagnostic information in the

subjects urine that correlated better with the symptoms. And finally, in a

follow-up

study, they treated these failed subjects with desiccated thyroid successfully.

[1] Second, Dr. Marshall Goldberg, discovered euthyroid hypometabolism in 6% of

his 500 subjects. They had the list of symptoms of hypothyroidism but were not

found to have any deficiency of the secretion by the thyroid gland. [2,3] Thus,

Dr. Goldberg explained the existence of symptoms in spite of a thyroid gland

function test (a.k.a. TFT) within reference ranges.

1.

Baisier, W V, Herto ghe, J., Bee khaut, W ., Thyroid I nsufficiency? Is T

hyroxine the O nly Valuab le Drug, J Nutr and Environ Med, September 2001,

11(3):159-166

2. Goldb

erg M, T he Case F or Euthyro id Hypo metabolism , Am J Med Sc October, 1960

pgs 479-493

3.

Goldberg M, Dagnosis of Euthyroid Hypometabolism, Am J Obst & Gynec, 81(5):

1053-1058, 1961

You will note that the BTA

have failed to back up any single statement with references to scientific

evidence to any research or studies - which makes that particular document

their OPINION only. Go to our web site and read through some of the

responses/rebuttals to this misleading (and in parts, incorrect) statement that

is on their web site http://www.tpa-uk.org.uk/rcp_campaign09.php

.Through reading these you will find a lot of references to show that

what the University Hospitals Birmingham Foundation Trust are recommending, is

actually wrong and there is much research and studies that have been done to

show this.

You can give them lots of

references from these docuoments, but you must INSIST that they also give you

references to all the research and studies to back up their own statements. It

is NOT enough that they quote to you the American and British Thyroid

Association web sites. Don't they even question whether any of what they read

is their opinion or a statement of fact?

" 1. There is a large

body of evidence, and associated local, national and international guidelines

indicating that a rise in serum TSH is an essential prerequisite for the

diagnosis of primary hypothyroidism. "

There is also a large body of

evidence and associated local, national and international guidelines indicating

that the results of a TSH ONLY should not be a pre-requisite in isolation to

other thyroid function tests. See below:

DISCUSSIONS ON THYROID

DIAGNOSIS

SERUM TSH: IS THE TSH SERUM

MEASUREMENT ALONE SUFFICIENT FOR DIAGNOSIS AND FOLLOW-UP OF THYROID DEFICIENCY?

Claim: TSH

is the first line test to do. It is sufficient to diagnose all forms of eu-,

hypo- and hyperthyroidism. No other test is necessary for the diagnosis.

Facts: TSH

is often insufficient on its own to diagnose between eu-, hypo- and

hyperthyroidism, particularly to diagnose milder, borderline states of

hypothyroidism. Other tests are necessary, as is a complete clinical evaluation

(medical history, actual complaints, physical examination) of the patient.

Doubts on the usefulness of

the serum TSH test alone for diagnosis. Overreliance on laboratory tests

without clinical evaluation may lead to considerable diagnostic errors

2. Nicoloff JT, Spencer CA.

The use and misuse of the sensitive thyrotropin assay. J Clin Endocrinol

Metab. 1990;71:553-8.

3. De Los Santos ET,

Mazzaferri EL. Sensitive thyroid-stimulating hormone assays: Clinical

applications

and limitations. Compr Ther.

1988; 14(9): 26-33.

4. Becker DV, Bigos ST,

Gaitan E, JCrd, rallison ML, Spencer CA, Sugarawa M, Van

Middlesworth L, Wartofsky L.

Optimal use of blood tests for assessment of thyroid function. JAMA

1993 Jun 2; 269: 273

(“the decision to initiate therapy shoul be based on both clinical and

laboratory

findings and not solely on

the results of a single laboratory test”)

5. Rippere V. Biochemical

victims: False negative diagnosis through overreliance on laboratory

results—a personal

report. Med Hypotheses. 1983; 10(2): 113.

Discussions and controversy

in medical associations and journals on the TSH reference range

6. Surks MI, Ortiz E, s

GH, Sawin CT, Col NF, Cobin RH, lyn JA, Hershman JM, Burman

KD, Denke MA, Gorman C,

RS, Weissman NJ. Subclinical thyroid disease: scientific review

and guidelines for diagnosis

and management. JAMA. 2004;291:228–38 (conclusions of a consensus

panel of the Endocrine

Society, the American Thyroid Association,and American Association of

Clinical Endocrinology.

Although the panel concluded that there was good data that patients with

slight elevations of TSH

above 4.5 may progress to overt hypothyroidism, and that levothyroxine

therapy would prevent

symptoms, they did not agree that early treatment provided any benefit!)

7. Dickey RA, Wartofsky L,

Feld S. Optimal thyrotropin level: normal ranges and reference intervals are

not equivalent. Thyroid. 2005

Sep;15(9):1035-9

8. Wartofsky L, Dickey RA.

The evidence for a narrower thyrotropin reference range is compelling. J

Clin Endocrinol Metab. 2005

Sep;90(9):5483-8 (remarkable article of which a lot of the following

information is extracted)

9. Gharib H, Tuttle RM,

Baskin HJ, Fish LH, Singer PA, McDermott MT. Subclinical thyroid dysfunction:

a joint statement on

management from the American Association of Clinical Endocrinologists, the

American Thyroid Association,

and The Endocrine Society. J Clin Endocrinol Metab. 2005;90:581–5

10. Surks MI. Commentary:

subclinical thyroid dysfunction: a joint statement on management from the

American Association of

Clinical Endocrinologists, the American Thyroid Association, and The

Endocrine Society. J Clin

Endocrinol Metab. 2005;90:586–7

11. Ringel MD, Mazzaferri EL.

Editorial: subclinical thyroid dysfunction: can there be a consensus about

the consensus? J Clin

Endocrinol Metab. 2005;90:588–90

12. Pinchera A. Subclinical

thyroid disease: to treat or not to treat? Thyroid. 2005;15:1–2

18

Studies that show that

the serum TSH reference range of 0.1-5.1 mU/liter for a POPULATION is too

large. Studies indicating a population mean value of 1.5 mU/liter for an

iodine-sufficient population

13. Vanderpump MPJ, Tunbridge

WMG, French JM, Appleton D, Bates D, F, Grimley J,

Hasan DM, Rodgers H,

Tunbridge F. The incidence of thyroid disorders in the community: a twentyyear

follow-up of the Whickham

Survey. Clin Endocrinol (Oxf). 1995;43:55–68

14. Hollowell JG, Staehling

NW, Flanders WD, Gunter EW, Spencer CA, Braverman LE. Serum TSH, T4,

and thyroid antibodies in the

United States population (1988 to 1994): National Health and Nutrition

Examination Survey (NHANES

III). J Clin Endocrinol Metab. 2002; 87:489–99

15. Andersen S, sen KM,

Brunn NH, Laurberg P. Narrow individual variations in serum T4 and T3 in

normal subjects: a clue to

the understanding of subclinical thyroid disease. J Clin Endocrinol Metab.

2002;87:1068–72

16. Demers LM, Spencer CA.

Laboratory medicine practice guidelines: laboratory support for the

diagnosis and monitoring of

thyroid disease. Clin Endocrinol (Oxf). 2003;58:138–40

17. Baloch Z, Carayon P,

Conte-Devolx B, Demers LM, Feldt-Rasmussen U, Henry JF, LiVosli VA,

Niccoli-Sire P, R, Ruj

J, Smyth PP, Spencer CA, Stockigt JR, Guidelines Committee, National

Academy of Clinical

Biochemistry 2003 Laboratory medicine practice guidelines. Laboratory support

for the diagnosis and

monitoring of thyroid disease. Thyroid. 2003 Jan;13(1):3-126

A longitudinal study in

diabetics where a baseline TSH levels above the 1.53 mU/liter predicted

subsequent thyroid dysfunction, whereas no thyroid

dysfunction if TSH levels < 1.53 mU/liter, the reference range for

diabetics should then be 0.4-1.52 mU/liter

18. Warren RE, Perros P,

Nyirenda MJ, Frier BM. Serum thyrotropin is a better predictor of future

thyroid

dysfunction than thyroid

autoantibody status in biochemically euthyroid patients with diabetes:

implications for screening.

Thyroid. 2004;14:853–7

If the serum TSH reference

range would be based upon a cohort of truly normal individuals with no

personal or family history of thyroid dysfunction, no visible or palpable

goiter, not taking any medication, who are seronegative for

thyroid preoxidase antibodies, and whose blood samples are

drawn fasting in the morning

hours (06–10 h), the TSH reference range would become 0.4–2.5

mU/L (Demers & co, Baloch & co.)

19. Demers LM, Spencer CA.

Laboratory medicine practice guidelines: laboratory support for the

diagnosis and monitoring of

thyroid disease. Clin Endocrinol (Oxf). 2003;58:138–40

20. Hollowell JG, Staehling

NW, Flanders WD, Gunter EW, Spencer CA, Braverman LE. Serum TSH, T4,

and thyroid antibodies in the

United States population (1988 to 1994): National Health and Nutrition

Examination Survey (NHANES

III). J Clin Endocrinol Metab. 2002; 87:489–99

21. Baloch Z, Carayon P,

Conte-Devolx B, Demers LM, Feldt-Rasmussen U, Henry JF, LiVosli VA,

Niccoli-Sire P, R, Ruj

J, Smyth PP, Spencer CA, Stockigt JR, Guidelines Committee, National

Academy of Clinical

Biochemistry 2003 Laboratory medicine practice guidelines. Thyroid. 2003

Jan;13(1):3-126

When data for subjects

with positive TPOAb or a family history of autoimmune thyroid disease are

excluded, the normal reference interval becomes much tighter, i.e.

0.4–2.0 mU/liter. This tighter reference

range may certainly be more applicable to African-Americans, who have a lower

mean TSH

22. Hollowell JG, Staehling

NW, Flanders WD, Gunter EW, Spencer CA, Braverman LE. Serum TSH,

T4, and thyroid antibodies in

the United States population (1988 to 1994): National Health and

Nutrition Examination Survey

(NHANES III). J Clin Endocrinol Metab. 2002; 87:489–99

23. Demers LM, Spencer CA.

Laboratory medicine practice guidelines: laboratory support for the

diagnosis and monitoring of

thyroid disease. Clin Endocrinol (Oxf). 2003;58:138–40

19

Publications with data

to support a more narrow reference range for serum TSH that would be obtained

when persons with diffuse hypoechogenicity of the thyroid on ultrasound, a

condition that precedes thyroid peroxidase antibody positivity in

autoimmune thyroid disease, would be excluded

24. Pedersen OM, Aardal NP,

Larssen TB, Varhaug JE, Myking O, Vik-Mo H. The value of

ultrasonography in predicting

autoimmune thyroid disease. Thyroid. 2000;10:251–9

For the American

Association of Clinical Endocrinologists the revised reference TSH range is

0.3– 3.0 mU/L

25. American Association of

Clinical Endocrinologists. American Association of Clinical Endocrinologists

medical guidelines for clinical

practice for the evaluation and treatment of hyperthyroidism and

hypothyroidism. Endocr Pract.

2002;8:457–69

A study, which suggests

that the serum TSH cut-off point between hypo- and euthyroidism is 2, not 4 or

5.5

27. Michalopoulou G,

Alevizaki M, Piperingos G, Mitsibounas D, Mantzos E, Adampoulos P, Koutras DA.

High serum cholesterol levels

in persons with 'high-normal' TSH levels: Should one extend the

definition of subclinical

hypothyroidism? Eur J Endocrinol. 1998 Feb;138(2):141-5(Treating TPO

antibody-positive

hypercholesterolemic patients with TSH levels between 2-4 mU/L with low dose

levothyroxine normalizes TSH

levels and improves the lipid profile)

In 2003, the National

Academy of Clinical Biochemistry (NACB) has reduced the upper limit of the

reference range from 5.5 to 4.1 mU/L, but stating also that " greater

than 95% of healthy, euthyroid subjects have a serum TSH concentration between

0.4 - 2.5 mU/L " . " .. patients with a serum TSH >2.5 mU/L, when

confirmed by repeat TSH measurement made after 3 to 4 weeks, may be in the

early stages of thyroid failure, especially if thyroid peroxidise antibodies

are detected”

28. Baloch Z, Carayon P,

Conte-Devolx B, Demers LM, Feldt-Rasmussen U, Henry JF, LiVosli VA,

Niccoli-Sire P, R, Ruj

J, Smyth PP, Spencer CA, Stockigt JR, Guidelines Committee, National

Academy of Clinical

Biochemistry 2003 Laboratory medicine practice guidelines. Thyroid. 2003

Jan;13(1):3-126

Supporters of the

recommendations of the consensus panel (Endocrine Society, American Association

of Clinical Endocrinologists, American Thyroid Association) promote a target

TSH range of 1.0–1.5 mU/liter in patients already receiving T4 therapy

29. Baloch Z, Carayon P,

Conte-Devolx B, Demers LM, Feldt-Rasmussen U, Henry JF, LiVosli VA,

Niccoli-Sire P, R, Ruj

J, Smyth PP, Spencer CA, Stockigt JR, Guidelines Committee, National

Academy of Clinical

Biochemistry 2003 Laboratory medicine practice guidelines. Thyroid. 2003

Jan;13(1):3-126

The lower end of the normal

or reference range for TSH lies between 0.2 and 0.4 mU/liter, as indicated by a

number of clinical studies

30. Baloch Z, Carayon P,

Conte-Devolx B, Demers LM, Feldt-Rasmussen U, Henry JF, LiVosli VA,

Niccoli-Sire P, R, Ruj

J, Smyth PP, Spencer CA, Stockigt JR, Guidelines Committee, National

20

Academy of Clinical

Biochemistry 2003 Laboratory medicine practice guidelines. Thyroid. 2003

Jan;13(1):3-126

31. Parle JV, lyn JA,

Cross KW, SC, Sheppard MC. Prevalence and follow-up of abnormal

thyrotrophin (TSH)

concentrations in the elderly in the United Kingdom. Clin Endocrinol (Oxf).

1991;34:77-83

32. Warren RE, Perros P,

Nyirenda MJ, Frier BM. Serum thyrotropin is a better predictor of future

thyroid

dysfunction than thyroid

autoantibody status in biochemically euthyroid patients with diabetes:

implications for screening.

Thyroid. 2004;14:853–7

33. Canaris GJ, Manowitz NR,

Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study.

Arch Intern Med.

2000;160:526–34

34. Sawin CT, Geller A,

Kaplan MM, Bacharach P, PW, Hershman JM. Low serum thyrotropin

(thyroid stimulating hormone)

in older persons without hyperthyroidism. Arch Intern Med.

1991;151:165–8

35. Hershman JM, Pekary AE,

Berg L, DH, Sawin CT Serum thyrotropin and thyroid hormone

levels in elderly and

middle-aged euthyroid persons. J Am Geriatr Soc. 1993;41:823–8

36. Parle JV, Maisonneuve P,

Sheppare MC, Boyle P, lyn JA. Prediction of all-cause and

cardiovascular mortality in

elderly people from one low serum thyrotropin result: a 10-year cohort

study. Lancet.

2001;358:861–5

The TSH reference range

for an INDIVIDUAL is narrower than the reference range for a population. The

value of a population-based reference range is limited when the individual

patient-based reference range (i.e. his personal reference

range) is narrow

37. Fraser CG, EK.

Generation and application of data on biological variation in clinical

chemistry.

Crit Rev Clin Lab Sci.

1989;27:409–37

38. EK. Effects of

intra- and interindividual variation on the appropriate use of normal ranges.

Clin

Chem. 1974;20:1535–42

The individual TSH

reference ranges are remarkably narrow within a relatively small segment of the

population reference range, i.e. confined to only 25% of a range of 0.3–5.0

mU/liter. A shift in the TSH value of the individual outside of his or her

individual reference range, but still within the population reference

range, would not be normal for that individual. For example, an individual (as

in ’s series) with a personal range of 0.5–1.0

mU/liter would be at subphysiological thyroid hormone levels at the

population mean TSH of 1.5 mU/liter (as explained by Wartofsky 2005)

39. Andersen S, sen KM,

Brunn NH, Laurberg P. Narrow individual variations in serum T4 and T3

in normal subjects: a clue to

the understanding of subclinical thyroid disease. J Clin Endocrinol

Metab. 2002;87:1068–72

Studies of twins have

data to support that each of us has a genetically determined optimal free T4

(FT4)-TSH set point or relationship

40. Demers LM, Spencer CA.

Laboratory medicine practice guidelines: laboratory support for the

diagnosis and monitoring of

thyroid disease. Clin Endocrinol (Oxf). 2003;58:138–40

41. Meikle AW, Stringham JD,

Woodward MG, JC. Hereditary and environmental influences on

the variation of thyroid

hormones in normal male twins. J Clin Endocrinol Metab. 1988 ; 66:588–92

A measured TSH

difference of 0.75 mU/liter can already be significant in a patient. The

NACB guideline 8 states that " the magnitude of difference in ...TSH values

that would be clinically significant when monitoring a patient’s response

to therapy... is 0.75 mU/liter.” Greater TSH fluctuations in a specific

patient may mean that s/he

becomes hypothyroid or hyperthyroid.

42. Baloch Z, Carayon P,

Conte-Devolx B, Demers LM, Feldt-Rasmussen U, Henry JF, LiVosli VA,

Niccoli-Sire P, R, Ruj

J, Smyth PP, Spencer CA, Stockigt JR, Guidelines Committee, National

21

Academy of Clinical

Biochemistry 2003 Laboratory medicine practice guidelines. Thyroid. 2003

Jan;13(1):3-126

A serum TSH that rises

in a given individual from a set point of 1.0 to 3.5 is likely to be abnormally

elevated and imply early thyroid failure. A minor change in serum free T4

results in an amplified change in TSH to outside of the usual

population-based reference range, although the free T4 is still within

its own population-based reference range, because of the the log-linear

relationship between TSH and free T4. In the case of subclinical

hypothyroidism, for example, a slight drop in free T4 results in an

amplified and inverse response in TSH secretion (as explained by Wartofsky

2005)

43. DS. Subclinical

hypothyroidism. N Engl J Med. 2001;345:260–5

44. Ayala A, Wartofsky L.

Minimally symptomatic (subclinical) hypothyroidism. Endocrinologist.

1997;7:44–50

There is a 3-fold

difference between the average daily maximal TSH (3) and minimal TSH (1 mIU/ml)

89. Brabant G, Prank K, Ranft

U, Schuermeyer T, Wagner TO, Hauser H, Kummer B,

45. Feistner H, Hesch RD, von

zur Muhlen A. Physiological regulation of circadian and pulsatile

thyrotropin secretion in

normal man and woman. J Clin Endocrinol Metab. 1990 Feb;70(2):403-9

Conclusion: TSH

reference range is too large => need for narrower ranges

46. Pain RW. Simple

modifications of three routine in vitro tests of thyroid function. Clin Chem.

1976;

22(10): 1715-8.

47. Dickey RA, Wartofsky L,

Feld S. Optimal thyrotropin level: normal ranges and reference intervals are

not equivalent. Thyroid. 2005

Sep;15(9):1035-9

48. Wartofsky L, Dickey RA.

The evidence for a narrower thyrotropin reference range is compelling. J

Clin Endocrinol Metab. 2005

Sep;90(9):5483-8

Other arguments that

may explain why the TSH test alone is not the only test. The TSH

test is insufficient to diagnose all forms of hypothyroidism, including the

borderline forms. The frequency of abnormal TSH values

49. Canaris GJ, Manowitz NR,

Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study.

Arch Intern Med. 2000;160:526–34

50. Warren RE, Perros P,

Nyirenda MJ, Frier BM. Serum thyrotropin is a better predictor of future

thyroid

dysfunction than thyroid

autoantibody status in biochemically euthyroid patients with diabetes:

implications for screening.

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Interlaboratory/intermethod

differences in functional sensitivity of immunometric assays of

thyrotropin (TSH) and impact

on reliability of measurement of subnormal concentrations of TSH.

Clin Chem. 1995

Mar;41(3):367-74

154. Faber J, Gam A,

Siersbaek Nielsen K. Improved sensitivity of serum thyrotropin measurements:

Studies on serum sex

hormone-binding globulin in patients with reduced serum thyrotropin. Acta

Endocrinol Copenh 1990;

123(5): 535-40

155. Laurberg P. Persistent

problems with the specificity of immunometric TSH assays. Thyroid. 1993

Winter;3(4):279-83

156. Schlienger JL, Sapin R,

Grunenberger F, Gasser F, Pradignac A. Thyrotropin assay by

chemiluminescence in the

diagnosis of dysthyroidism with low thyrotropin and normal thyroid

hormones levels. Pathol Biol

Paris. 1993; 41(5): 463-8

157. Spencer C, Eigen A, Shen

D, Duda M, Qualls S, Weiss S, Nicoloff J. Specificity of sensitive assays

of thyrotropin (TSH) used to

screen for thyroid disease in hospitalized patients. Clin Chem. 1987

Aug;33(8):1391-6

158. Spencer CA, Challand GS.

Interference in a radioimmunoassay for human thyrotropin. Clin Chem

1977;23(3): 584-8

159. Kahn BB, Weintraub BD,

Csako G, Zweig MH. Factitious elevation of thyrotropin in a new ultrasensitive

assay: Implications for the

use of monoclonal antibodies in 'sandwich' immuno-assay. J

Clin Endocrinol Metab. 1988

Mar;66(3):526-33

160. Kourides IA, Weintraub

BD, Martorana MAL, Maloof F. Alpha subunit contamination of human

albumin preparations:

Interference in radioimmunoassay. J Clin Endocrinol Metab. 1976; 43(4):

919-23

161. Bartlett WA, Browning MC,

Jung RT. Artefactual increase in serum thyrotropin concentration

caused by heterophilic

antibodies with specificity for IgG of the family Bouidea. Clin Chem. 1986;

32(12): 22(4-9)

162. Csako G, Weintraub BD,

Zweig MH. The potency of immunoglobulin antibodies in a monoclonal

immunoradiometric assay for

thyrotropin. Clin Chem. 1988 Jul;34(7):1481-3

163. Seghers J, Schruers F,

De Nayer P, Beckers C. Interference in thyrotropin (TSH) determination:

Falsely elevated TSH values

in a transplanted patient. Eur J Nucl Med. 1989; 15(4): 194-6

164. Spencer C, Eigen A, Shen

D, Duda M, Quails S, Weiss S, Nicoloff J. Specificity of sensitive assays

of thyrotropin (TSH) used to

screen for thyroid disease in hospitalized patients. Clin Chem.

1987;33(8):1391-6

165. Ealey PA, Marshall NJ,

Ekins RP. Time-related thyroid stimulation by thyrotropin and

thyroidstimulating

antibodies, as measured by

the cytochemical section bioassay. J Clin Endocrinol

Metab. 1981;52(3): 483-7

Doubts on the

adequateness of measuring the serum TSH as a help to monitor a thyroid

treatment ( follow-up). The serum TSH test for follow-up: The risk of

misinterpretation increases when monitoring the treatment of hyper- or

hypothyroidism

166. Talbot JN, Duron F,

Feron R. Aubert P, Milhaud G. Thyroglobulin, thyrotropin and thyrotropin

binding inhibiting

immunoglobulins assayed at the withdrawal of antithyroid drug therapy as

predictors of relapse of

Graves' disease within one year. J Endocrinol Invest. 1989; 12(9): 589-95

In 36-47 % of cinically

euthyroid patients receiving adequate long-term thyroid therapy for

hypothyroidism, an undetectable serum TSH is found

167. lyn JA, Black EG,

Betteridge J, Sheppard MC. Comparison of second and third generation

methods for measurement of

serum thyrotropin in patients with overt hyperthyroidism, patients

receiving thyroxine therapy,

and those with nonthyroidal illness. J Clin Endocrinol Metab 1994;

78(6): 1368-71

168. Gow SM, Caldwell G, Toft

AD, Seth J, Hussey AJ, Sweeting VM, Beckett GJ. Relationship between

pituitary and other target

organ responsiveness in hypothyroid patients receiving thyroxine

replacement. J Clin

Endocrinol Metab. 1987; 64(2): 364-70

After intake of

thyroidhormones, the serum TSH is transitorily depressed within 60 minutes and

remains low for up to 9 hours after intake

169. Chopra U, Carlson HE,

DH. Comparison of inhibitory effects of 3,5,3'-triiodothyronine

(T3), thyroxine (T4),

3,3,',5'-triiodothyronine (rT3,), and 3,3'-diiodothyronine (T2) on

thyrotropinreleasing

hormone-induced release of

thyrotropin in the rat in vitro. Endocrinology.

1978;103(2):393-402

Some patents who

exhibit reversion of an initially high TSH level back into the reference range,

are found to subsequently develop mild thyroid failure

170. Calaciura F, Motta RM,

Miscio G, Fichera G, Leonardi D, Carta A, Trichitta V, Tassi V, Sava L,

Vigneri R. Subclinical

hypothyroidism in early childhood: a frequent outcome of transient neonatal

hyperthyrotropinemia. J Clin

Endocrinol Metab. 2002;87:3209–14

Supporters of the

recommendations of the consensus panel promote a target TSH range of 1.0–

1.5 mU/liter in patients already receiving T4 therapy, whereas they refuse to

accept TSH levels of 3–10 mU/liter as abnormal in patients not receiving

T4 therapy.

171. Baloch Z, Carayon P,

Conte-Devolx B, Demers LM, Feldt-Rasmussen U, Henry JF, LiVosli VA,

Niccoli-Sire P, R, Ruj

J, Smyth PP, Spencer CA, Stockigt JR, Guidelines Committee, National

Academy of Clinical

Biochemistry 2003 Laboratory medicine practice guidelines. Thyroid. 2003

Jan;13(1):3-126

The lower end of the

normal or reference range for TSH lies between 0.2 and 0.4 mU/liter, as

indicated by a number of clinical studies

172. Baloch Z, Carayon P,

Conte-Devolx B, Demers LM, Feldt-Rasmussen U, Henry JF, LiVosli VA,

Niccoli-Sire P, R, Ruj

J, Smyth PP, Spencer CA, Stockigt JR, Guidelines Committee, National

Academy of Clinical

Biochemistry 2003 Laboratory medicine practice guidelines. Thyroid. 2003

Jan;13(1):3-126

173. Parle JV, lyn JA,

Cross KW, SC, Sheppard MC. Prevalence and follow-up of abnormal

thyrotrophin (TSH)

concentrations in the elderly in the United Kingdom. Clin Endocrinol (Oxf).

1991;34:77-83

174. Warren RE, Perros P,

Nyirenda MJ, Frier BM. Serum thyrotropin is a better predictor of future

thyroid dysfunction than

thyroid autoantibody status in biochemically euthyroid patients with

diabetes: implications for

screening. Thyroid. 2004;14:853–7

30

175. Canaris GJ, Manowitz NR,

Mayor G, Ridgway EC. The Colorado thyroid disease prevalence study.

Arch Intern Med.

2000;160:526–34

176. Sawin CT, Geller A,

Kaplan MM, Bacharach P, PW, Hershman JM. Low serum thyrotropin

(thyroid stimulating hormone)

in older persons without hyperthyroidism. Arch Intern Med.

1991;151:165–8

177. Hershman JM, Pekary AE,

Berg L, DH, Sawin CT Serum thyrotropin and thyroid

hormone levels in elderly and

middle-aged euthyroid persons. J Am Geriatr Soc. 1993;41:823–8

178. Parle JV, Maisonneuve P,

Sheppare MC, Boyle P, lyn JA. Prediction of all-cause and

cardiovascular mortality in

elderly people from one low serum thyrotropin result: a 10-year cohort

study. Lancet.

2001;358:861–5

TSH testing only is a hugely

controversial area and one that has been around forever. I would point out to

the Birmingham University Hospital that the BTA stand alone in their above statement: They

take no account of the patients history, symptoms, signs or results of an

appropriate examination, which goes against the recommendations laid down by

the GMC, the DoH and their own 'sister' organisation the BTF. On the BTA

web site, they state:

The BTA state: " The Clinical Committee of the Society

for Endocrinology and the British Thyroid Association recommend the use of

sensitive and specific blood tests as the only method for the precise diagnosis

of thyroid dysfunction and for the monitoring of treatment with approved

medications... " - also " Currently the BTA does

not hold the view that treatment for thyroid disease, either under- or

over-active, should be commenced if patients have thyroid function test results

within the normal laboratory reference range " .

.....the BTF state: " The biochemical results have to be considered

alongside clinical symptoms, and together they determine the point at which the

physician will introduce Thyroxine therapy " .

....the GMC state: " Good clinical care must include: an adequate

assessment of the patient's conditions, based on the history and symptoms and,

if necessary, an appropriate examination; "

....the DOH state: " Blood tests are useful in helping diagnose

hypothyroidism but should not be used in isolation and other factors must be

taken into account such as the absence or presence of symptoms. This is why at

present it is considered good medical practice to rely upon clinical history

and examination, in addition to blood tests, in the diagnosis of this

condition.

" 2. Dr F has tried to

explain the potential long term consequences of treatment with exogenous thyroid

hormones, especially as you have indicated that thyroid function testing whilst

on treatment has revealed suppression of TSH, which is a biochemical marker of

thyroid hormone excess. Areas of clinical concern associated with long term TSH

suppression from exogenous thyroid hormone treatment would be augmentation of

risk of atrial fibrillation and osteoporosis. "

Any good doctor who knows how

the thyroid system function will be aware that TSH is naturally suppressed when

the pituitary recognises the body has sufficient thyoxine in the blood so it

stops secreting TSH. Why would the pituitary want to do otherwise? TSH is also a

biochemical marker of a lack of deficient thyroid hormone in the blood. Also,

it has been shown that osteoporisis improves with thyroid treatment [1]

1.

Svanberg E, Healey J, Mascarenhas D. Anabolic effects of rhIGF-I/IGFBP-3 in

vivo are influenced by thyroid status. Eur J Clin Invest. 2001

Apr;31(4):329-36.

THYROID TREATMENT AND

THE HEART

Claim: Thyroid hormone treatment is

dangerous for the heart as it can cause side effects such as atrial

fibrillation.

Facts: Euthyroidism (normal thyroid

function) is essential for the heart; both hypothyroidism as well as

hyperthyroidism impair the working of the heart and may facilitate atrial fibrillation.

Arguments

contra thyroid treatment: because of possible

cardiac side effects, especially in cardiac patients

Hyperthyroidism:

causes tachycardia (critic: tachycardia is the

result of hyperthyroidism, hypocorticism, or drinking of caffeinated beverages;

avoiding these conditions by adequate treatment or abstention will prevent many

cases of tachycardia)

1. Maciel

BC, Gallo L Jr, Marin Neto JA, Maciel LM, Alves ML, Paccola GM, Iazigi N. The

role of the autonomic nervous system in the resting tachycardia of human

hyperthyroidism. Clin Sci (Lond). 1987 Feb;72(2):239-44

2. Abadie

E, Leclercq JF, Fisch A, Babalis D, Blanche PM, Passa P, Coumel P. Pathogenesis

of tachycardia in hyperthyroidism. Value of Holter monitoring and the use of a

beta-blocker. Presse Med. 1985 Feb 2;14(4):197-9

Hyperthyroidism

(high serum thyroid hormones) is associated with an increased risk of atrial

fibrillation

3. Parmar

MS. Thyrotoxic atrial fibrillation. Med Gen Med. 2005 Jan

4;7(1):74 (atrial fibrillation was seen in 15 % of hyperthyroid patients)

4. Dorr

M, Volzke H. Cardiovascular morbidity and mortality in thyroid dysfunction.

Minerva Endocrinol. 2005 Dec;30(4):199-216 (5.2 times more risk of atrial

fibrillation in hyperthyroidism)

5. Frost L, Vestergaard P, Mosekilde L. Hyperthyroidism and risk of atrial fibrillation or flutter: a population-based study. Arch Intern Med. 2004 Aug 9-23;164(15):1675 (atrial fibrillation was observed in 8.3 % of hyperthyroid patients)

Hyperthyroidism

is associated with an increased risk of angina pectoris

6. Gitlin MJ. L-triiodothyronine-precipitated angina and clinical response. Biol Psychiatry. 1986 May;21(5-6):543-5Possibility to administer a betablocker together with thyroid medication to hypothyroid patients with angina pectoris7. Ellyin F, Fuh CY, Singh SP, Kumar Y. Hypothyroidism with angina pectoris. A clinical dilemma. Postgrad Med. 1986 May 15;79(7):93-8

Patients

aged 40 years or older at emergency admission who present a high serum free and

total T3, have an increased risk of of angina pectoris and mycocardial infarct at admission and 3 years later (critic: possibly due to

hypocorticism that increases (the conversion of T4 into)T3??)

8.

s A, Ehlers M, Blank B,

Exler D, Falk C, Kohlmann T, Fruehwald-Schultes B, Wellhoener P, Kerner W, Fehm

HL. Excess triiodothyronine as a risk factor of coronary events. Arch Intern

Med. 2000 Jul 10;160(13):1993-9

A high

serum T4 is found in patients with coronary heart disease (critic: possibly accompanied by a low serum T3, which reflects

a clinical more hypothyroid state, because of the decrease in conversion of T4

to T3 that is generally observed in the disease state)

9. Sidorenko BA, Begliarov MI, Titov VN, Masenko VP, Parkhimovich RM. Blood thyroid hormones in ischemic heart disease (a comparison with coronary angiographic data, severity of stenocardia and blood lipid level)] Kardiologiia. 1981 Dec;21(12):96-101

10. Selivonenko

VG, Zaika IV. The function of the thyroid and thyrotropic function in patients

with chronic ischemic heart disease and rhythm disorders. Lik Sprava. 1998

Jan-Feb;(1):81-3

Arguments

pro thyroid treatment: the

heart needs to have thyroid hormones or heart disease appears; also the case

for cardiac patients (but they must be treated with great caution and should

receive lower thyroid doses)

Associations between thyroid hormone levels and heart healthThyroid hormone levels are positively correlated with the heart rhythm11. Tseng KH, Walfish PG, Persaud JA, Gilbert BW. Concurrent aortic and mitral valve echocardiography permits measurement of systolic time intervals as an index of peripheral tissue thyroid functional status. J Clin Endocrinol Metab. 1989 Sep;69(3):633-8

A

lower serum T3 (and higher serum T4) is found in heart patients with arrhythmia

12. Selivonenko

VG, Zaika IV. The function of the thyroid and thyrotropic function in patients

with chronic ischemic heart disease and rhythm disorders. Lik Sprava. 1998

Jan-Feb;(1):81-3

13. Inama G, Furlanello F, Fiorentini F, Braito G, Vergara G, Casana P. Arrhythmogenic implications of non-iatrogenic thyroid dysfunction. G Ital Cardiol. 1989 Apr;19(4):303-10 (Hypothyroidism in patients with hyperkinetic ventricular arrhythmias (25%), atrial fibrillation (37.5%) and atrio-ventricular block (37.5%))14. Vanin LN, Smetnev AS, Sokolov SF, Kotova GA, Masenko VP. Thyroid function in patients with ventricular arrhythmia. Kardiologiia. 1989 Feb;29(2):64-7 (Hyperthyroidism was diagnosed in 4.8% of 21 patients with persistent ventricular arrhythmias, and latent hypothyroidism was diagnosed in 38.1%)15. Vanin LN, Smetnev AS, Sokolov SF, Kotova GA, Masenko VP. Study of thyroid function in patients with paroxysmal supraventricular tachycardia. Kardiologiia. 1989 Jan;29(1):71-416. Nesher G, Zion MM. Recurrent ventricular tachycardia in hypothyroidism--report of a case and review of the literature. Cardiology. 1988;75(4):301-617. Fredlund BO, Olsson SB. Long QT interval and ventricular tachycardia of " torsade de pointe " type in hypothyroidism. Acta Med Scand. 1983;213(3):231-5

Low

serum T3 and T4 levels are found in patients with coronary

heart disease

18. Miura

S, Iitaka M, Suzuki S, Fukasawa N, Kitahama S, Kawakami Y, Sakatsume Y,

Yamanaka K, Kawasaki S, Kinoshita S, Katayama S, Shibosawa T, Ishii J. Decrease

in serum levels of thyroid hormone in patients with coronary heart disease.

Endocr J. 1996 Dec;43(6):657-63

A low

serum free T3 in patients with coronary bypass increases the risk of

postoperative atrial fibrillation

(higher risk than that of not taking a beta-blocker)

19. Cerillo AG, Bevilacqua S, Storti S, ni M, Kallushi E,

Ripoli A, Clerico A, Glauber M. Free triiodothyronine: a

novel predictor of postoperative atrial fibrillation. Eur J Cardiothorac Surg.

2003 Oct;24(4):487-92

Progressively lower serum T3 levels are found in patients with ischemic heart disease form coronary stenosis to mycocardial infarct20. Telkova IL, Tepliakov AT. Changes of thyroid hormone levels in the progression of coronary artery disease. Arteriosclerosis. Klin Med (Mosk). 2004;82(4):29-3421. Pavlou HN, Kliridis PA, Panagiotopoulos AA, Goritsas CP, Vassilakos PJ. Euthyroid sick syndrome in acute ischemic syndromes. Angiology. 2002 Nov-Dec;53(6):699-707 22. Pimenov LT, Leshchinskii LA. Thyroid hormone changes (iodothyroninemia) in patients with acute myocardial infarction, and their clinical significance. Kardiologiia. 1984 Oct;24(10):74-7Low serum free and total T3 (and low free T4 and high TSH) levels are found in patients suffering from acute mycocardial infarct with poor outcome23. Satar S, Seydaoglu G, Avci A, Sebe A, Karcioglu O, Topal M. Prognostic value of thyroid hormone levels in acute myocardial infarction: just an epiphenomenon? Am Heart Hosp J. 2005 Fall;3(4):227-33

Auto-immune thyroidiits

is associated with poorer heart indices

24. Zoncu S, Pigliaru F, Putzu C, Pisano L, Vargiu S, Deidda M, tti S, Mercuro G. Cardiac function in borderline hypothyroidism: a study by pulsed wave tissue Doppler imaging. Eur J Endocrinol. 2005 Apr;152(4):527-33 (namely “impairment of systolic ejection, a delay in diastolic relaxation and a decrease in the compliance to the ventricular filling. Several significant correlations were found between the parameters and serum-free T(3) and T(4) and TSH concentrations. Data strongly support the concept of a continuum spectrum of a slight thyroid failure in autoimmune thyroiditis”)

Increased incidence of

auto-immune thyroiditis and overt hypothyroidism in men with acute mycocardial

infarct, which may have contributed to the

development of the disease.

25. Cerillo

AG, Bevilacqua S, Storti S, ni M, Kallushi E, Ripoli A, Clerico A, Glauber

M. Free triiodothyronine: a novel predictor of postoperative atrial

fibrillation. Eur J Cardiothorac Surg. 2003 Oct;24(4):487-92

A low

serum T3 or T4 (hypothyroidism) is found in cardiac failure:

26. Khaleeli AA, Memon N. Factors affecting resolution of pericardial effusions in primary hypothyroidism: a clinical, biochemical and echocardiographic study. Postgrad Med J. 1982 Aug;58(682):473-627. Reza MJ, Abbasi AS. Congestive cardiomyopathy in hypothyroidism. West J Med. 1975 Sep;123(3):228-3028. Rays J, Wajngarten M, Gebara OC, Nussbacher A, Telles RM, Pierri H, no G, Serro-Azul JB. Long-term prognostic value of triiodothyronine concentration in elderly patients with heart failure. Am J Geriatr Cardiol. 2003 Sep-Oct;12(5):293-7 (“Lower serum T3 in cardiac failure: the odds ratio for events was 9.8 (95% confidence interval,2.2-43, p=0.004) for patients in the lowest tertile of triiodothyronine, that is, lower than 80 ng/dL, compared with patients with levels above 80 ng/dL”)29. Pingitore A, Landi P, Taddei MC, Ripoli A, L'Abbate A, Iervasi G. Triiodothyronine levels for risk stratification of patients with chronic heart failure. Am J Med. 2005 Feb;118(2):132-6

30. Klein I, Ojama K. In: Werner & Ingbar’s The

Thyroid, ed. Braverman LE & Utiger RD, Lippincott-Raven Publishers,

Philadelphia, 1996, 62: 799-804

A low serum free T3

index/reverse T3 ratio in chronic heart failure patients is a highly

significant predictor of poor outcome

31. Cerillo

AG, Bevilacqua S, Storti S, ni M, Kallushi E, Ripoli A, Clerico A, Glauber

M. Free triiodothyronine: a novel predictor of postoperative atrial

fibrillation. Eur J Cardiothorac Surg. 2003

32. Hamilton MA, son LW, Luu M, Walden JA. Altered thyroid hormone metabolism in advanced heart failure. J Am Coll Cardiol. 1990 Jul;16(1):91-5

33. Kozdag

G, Ural D, Vural A, Agacdiken A, Kahraman G, Sahin T, Ural E, Komsuoglu B.

Relation between free triiodothyronine/free thyroxine ratio, echocardiographic

parameters and mortality in dilated cardiomyopathy. Eur J Heart Fail. 2005

Jan;7(1):113-8

A low

serum T3 or T4 in heart patients is associated with an increased risk of

cardiac arrest/death

34. Wortsman J, Premachandra BN, Chopra IJ, JE.

Hypothyroxinemia in cardiac arrest. Arch Intern Med. 1987 Feb;147(2):245-8

35. Iervasi G, Pingitore A, Landi P, Raciti M, Ripoli A, Scarlattini M, L'Abbate A, Donato L. Low-T3 syndrome: a strong prognostic predictor of death in patients with heart disease. Circulation. 2003 Feb 11;107(5):708-13

Cardiovascular disease

and mortality is increased in hypothyroidism (+ 70

% for both)

36. Dorr

M, Volzke H. Cardiovascular morbidity and mortality in thyroid dysfunction.

Minerva Endocrinol. 2005 Dec;30(4):199-216

Thyroid therapy of cardiac patientsCorrective thyroid therapy is safe in hypothyroid patients with common benign cardiac arrhythmias at the condition that thyroid treatment is started at low doses and then gradually and prudently increased to the adequate dose. The treatment does not trigger an increase in arrhythmia frequency except in rare patients with baseline atrial premature beats. It is, however, associated with an increase in basal, average and maximal heart rates.37. Polikar R, Feld GK, Dittrich HC, J, Nicod P. Effect of thyroid replacement therapy on the frequency of benign atrial and ventricular arrhythmias. J Am Coll Cardiol. 1989 Oct;14(4):999-1002Thyroid therapy corrects the bradycardia of hypothyroidism38. Yamauchi K, Takasu N, Ichikawa K, Yamada T, Aizawa T. Effects of long-term treatment with thyroxine on pituitary TSH secretion and heart action in patients with hypothyroidism. Acta Endocrinol (Copenh). 1984 Oct;107(2):218-24 (“T4 doses should be adjusted to maintain normal ET/PEP (systolic time intervals) rather than normal serum TSH levels”)Thyroid therapy corrects the ventricular arrhythmia39. Vanin LN, Smetnev AS, Sokolov SF, Kotova GA, Masenko VP. Thyroid function in patients with ventricular arrhythmia. Kardiologiia. 1989 Feb;29(2):64-7 (“Thyroid therapy for hypothyroidism led to the disappearance of paroxysms of ventricular tachycardia and reduced the total number and grades of ventricular extra-systoles in patients with ventricular arrhythmias; moreover, sensitivity to antiarrhythmic agents developed to replace an earlier resistance”)

Coronary heart disease

in humans: the improvement with thyroid treatment

40.

BO. Prophylaxis of ischaemic heart-disease by thyroid therapy. Lancet. 1959 Aug

22;2:149-52

41. Holland

FW 2nd, Brown PS Jr, RE. Acute severe postischemic myocardial depression

reversed by triiodothyronine. Ann Thorac Surg. 1992 Aug;54(2):301-5

42. Israel

M. An effective therapeutic approach to the control of atherosclerosis

illustrating harmlessness of prolonged use of thyroid hormone in coronary

disease. Am J Dig Dis. 1955 June;161-8

43. Yokoyama

Y, Novitzky D, Deal MT, Snow TR. Facilitated recovery of cardiac performance by

triiodothyronine following a transient ischemic insult. Cardiology. 1992;81(1):34-45

Adequate thyroxine

replacement in hypothyroidism prevents coronary artery disease progression

44. Perk

M, O’Neill BJ; The effect of thyroid therapy on angiographic artery

disease progression . Can J Card. 1997;13(3):273-6

Desiccated

thyroid therapy improves cardiac failure refractory to digitalis in humans

45. Zondek H. Myxedema Heart. Munch Med Wochenschr.

1918, 65: 1180-3

46. Khaleeli AA, Memon N. Factors affecting resolution of pericardial effusions in primary hypothyroidism: a clinical, biochemical and echocardiographic study. Postgrad Med J. 1982 Aug;58(682):473-6

T3-therapy

improves the outcome of open heart sugery, especially heart transplants

47. Novitzky D, Fontanet H, Snyder M, Coblio N, D, Parsonnet V. Impact of triiodothyronine on the survival of high-risk patients undergoing open heart surgery. Cardiology. 1996 Nov-Dec;87(6):509-15. 48. Novitzky D, DK, Chaffin JS, Greer AE, DeBault LE, Zuhdi N. Improved cardiac allograft function following triiodothyronine therapy to both donor and recipient. Transplantation. 1990 Feb;49(2):311-6

Thyroid

hormone therapy greatly reduces the lesions of experimental myocardial infarct

in rats

49. Holland

FW, Brown PS, RE. Acute severe postischemic myocardial depression reversed by

triiodothyronine. Ann Thorac Surg 1992 54: 301-305

Thyroid therapy reduces coronary artery disease and cardiac fibrosis in mice50. Yao J, Eghbali M. Decreased collagen mRNA and regression of cardiac fibrosis in the ventricular myocardium of the tight skin mouse following thyroid hormone treatment. Cardiovasc Res. 1992 Jun;26(6):603-7Thyroid therapy reduced the lesions of experimental cardiac arrest in dogs51. Facktor MA, Mayor GH, Nachreiner RF, D'Alecy LG. Thyroid hormone loss and replacement during resuscitation from cardiac arrest in dogs. Resuscitation. 1993 Oct;26(2):141-62

Thyroid therapy reduced

the complications of hemorrhagic shock in dogs

52. Shigematsu

H, Shatney CH. The effect of triiodothyronine (T3) and reverse triiodothyronine

(rT3) on canine hemorrhagic shock. Nippon Geka Gakkai Zasshi. 1988

Oct;89(10):1587-93.

*********************************************

THYROID THERAPY AND

BONE DENSITY

Studies

with association between thyroid therapy and increased loss of bone density

Bone loss during thyroid treatment mainly occurs in HRT untreated postmenopausal women and who have a suppressed TSH, possibly being overtreated with thyroid hormones 4. Taelman P, Kaufman JM, Janssens X, Vandecauter H, Vermeulen A. Reduced forearm bone mineral content and biochemical evidence of increased bone turnover in women with euthyroid goitre treated with thyroid hormone. Clin Endocrinol (Oxf). 1990 Jul;33(1):107-175. Stall GM, S, Sokoll LJ, Dawson- B. Accelerated bone loss in hypothyroid patients overtreated with L-thyroxine. Ann Intern Med. 1990 Aug 15;113(4):265-96. Adlin EV, Maurer AH, Marks AD, Channick BJ. Bone mineral density in postmenopausal women treated with L-thyroxine. Am J Med. 1991 Mar;90(3):360-6

7.

TL, Kerrigan J, AM, Braverman

LE, Baran DT. Long-term L-thyroxine therapy is associated with decreased hip

bone density in premenopausal women. JAMA. 1988;259:3137-41

Bone loss is mainly transitory only during the first year with no increased fracture incidence8. Tremollieres F, Pouilles JM, Louvet JP, Ribot C. Transitory bone loss during substitution treatment for hypothyroidism. Results of a two year prospective study. Rev Rhum Mal Osteoartic. 1991 Dec;58(12):869-759. Ribot C, Tremollieres F, Pouilles JM, Louvet JP. Bone mineral density and thyroid hormone therapy. Clin Endocrinol (Oxf). 1990 Aug;33(2):143-53

Oestrogen therapy neutralizes, prevents bone loss induced by

corrective thyroid therapy

10. Schneider

DL, Barrett-Connor EL, Morton DJ. Thyroid hormone use and bone mineral density

in elderly women. JAMA 1994;271:1245-9

Studies where thyroid therapy does not cause or increase loss of

bone density

11. Greenspan

SL, Greenspan FS, Resnick NM, Block JE, Friedlander AL, Genant HK. Skeletal

integrity in premenopausal and postmenopausal women receiving long-term

L-thyroxine therapy Am J Med. 1991;91:5-14

12. lyn

JA, Betteridge J, Daykin J, Holder R, Oates GD, Parle JV, Lilley J, Heath DA,

Sheppard MC. Long-term thyroxine treatment and bone mineral density. Lancet. 1992

Jul 4;340(8810):9-13

13. Eulry F, Bauduceau B, Lechevalier D, Magnin J, Crozes P, Flageat J, Gautier D. Bone density in differentiated cancer of the thyroid gland treated by hormone-suppressive therapy. Study based on 51 cases. Rev Rhum Mal Osteoartic. 1992 Apr;59(4):247-5214. Grant DJ, McMurdo ME, Mole PA, Paterson CR, Davies RR. Suppressed TSH levels secondary to thyroxine replacement therapy are not associated with osteoporosis. Clin Endocrinol (Oxf). 1993 Nov;39(5):529-33.

Studies where thyroid therapy improves bone formation

15. Svanberg E, Healey J, Mascarenhas D. Anabolic effects of rhIGF-I/IGFBP-3 in vivo are influenced by thyroid status. Eur J Clin Invest. 2001 Apr;31(4):329-36

" 3. You had a short

synacthen test to assess adrenocortical reserve (a test to see if you are

producing sufficient adrenal steroid hormones) in May 2010 and this was found

to be more than adequate, with a peak serum cortisol value of 901nmol/l (Le. a

response to the injection showing very healthy adrenal steroid

production). "

This test is ONLY done to see

whether the patient has either 's disease (too little to no cortisol

production) or Cushing's Syndrome (too high a level of cortisol secretion). It

does not show whether the patient has 'adrenal fatigue' or 'low

adrenal reserve' which are the STAGES leading up to 's disease. In fact,

because doctors do not recognise any of these stages, they are allowing the

patient to reach complete adrenal insufficiency ('s disease) which is

quite appalling. Cortisol production has a diurnal rhythm and should be tested

at four specifric times during the day, i.e. 8.00a.m. - 12 noon, - 4.00p.m. and

again at midnight. Taking a 'snapshot' of this in the morning only does not

give a total picture.

" 4. You were again

found to have entirely normal test of thyroid function. A check of serum

prolactin, gonadotrophins, random oestradiol and IGF- 1 (various pituitary and

other hormones) were all normal.

Did you get the actual

results given for these Dawn together with the reference range for each test

done? If not, get these and post them on the forum? "

5. In the absence of a rise in TSH (and in the absence of a fall in serum free T4 and T3 (the main hormones produced by the thyroid gland) there is no biochemical evidence of primary hypothyroidism in your case. Consequently there is no established indication for thyroxine replacement therapy. Furthermore, in the absence of a diagnosis of primary hypothyroidism it is not logical, or good practice, to ascribe a patient's symptoms to that diagnosis.**Please see above. The thyroid function blood test results DO NOT INDICATE EUTHYROID HYPOMETABOLISM which over 250,000 people in the UK suffer from. DOES THYROID TREATMENT DEFINITELY SUPPRESS THE THYROID GLAND?No, after stopping thyroid medications, the thyroid axis recovers its initial condition in 2 to 3 weeks on the average1. Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN. Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy. J Clin Endocrinol Metab. 1975 Jul;41(1):70-80 (full recoveryback to initial serum T3, T4, TSH levels is obtained after a mean of 16 to 22 days, even after 28 years of treatment)

2. Vagenakis

AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH. Recovery of pituitary

thyrotropic function after withdrawal of prolonged thyroid-suppression therapy.

N Engl J Med. 1975 Oct 2;293(14):681-4 (“During exogenous hormone

administration, 131l uptake was suppressed, and serum thyrotropin

concentrations before and after administration of thyrotropin-releasing hormone

were undetectable. …. After withdrawal of long-term thyroid hormone,

decreased thyrotropin reserve persisted for two to five weeks. Detectable

values of serum thyrotropin (less than 1.2 muU per milliliter) and a normal

131l uptake usually occurred concurrently in two to three weeks. Serum

thyroxine concentration returned to normal at least four weeks after hormone

withdrawal.”)

3. Greer

MA. The effect on endogenous thyroid activity of feeding desiccated thyroid to

normal human subjects. N Engl J Med. 1951 Mar 15;244(11):385-90 (“After

withdrawal of thyroid therapy, thyroid function returned to normal in most

subjects within 2 weeks, although a few were depressed ofr 6-11 weeks. Thyroid

function returned as rapidly in those whose glands had been depressed by

several years of thyroid medication as it did for those whose glands had been

depressed for only a few days.”)

4. Mosier

HD, DeGolia RC. Effect of prolonged administration of thyroid hormone on

thyroid gland function of euthyroid children. J Clin Endocrinol Metab. 1960

Sep;20:1296-301. (“In all of the echildren and adolescents included in

this study, thyroid function returned to normal (as judged by clinical signs

ans by laboratory measurements) within four months after discontinuing thyroid

hormone,in spite of previous administration of suppressive doses for periods of

20 too 125 months during years of somatic growth”).

5. Farquharson RF, Squires AH. Inhibition of the secretion of the thyroid gland by continued ingestion of thyroid substance. Tr A Am Physicians. 1941;56:876. ston MW, Squires AH, Farquharson RF. The effect of prolonged administration of thyroid. Ann Intern Med. 1951 Nov;35(5):1008-22 7. Riggs DS, Man EB, Winkler AW. Serum iodine of euthyroid subjects treated with desiccated thyroid. J Clin Invest. 1945;24:722-31

8. Stein

RB, Nicoloff JT. Triiodothyronine withdrawal test -a test of thyroid-pituitary

adequacy. J Clin Endocrinol Metab. 1971 Feb;32(2):127-9

If the thyroid treatment is stopped because it is judged not necessary, recovery takes place9. Rubinoff H, Fireman BH. Testing for recovery of thyroid function after withdrawal of long-term suppression therapy. J Clin Epidemiol. 1989;42(5):417-20 (At 8 weeks, 30 of the 45 patients whose chart reviews did not demonstrate a clear need for thyroid replacement., were normal)

6. you request further

information regarding the diagnosis and management of hypothyroidism with

University Hospitals Birmingham Foundation Trust. The practice of the large and

expert team in endocrinololoy is indeed in accord with the British and American

Thyroid Associations and readily available on their websites.

You need to ask WHY they are

in accordance with the BTA and ATA when the BTA have produced NO hypothyroid

guidelines whatsoever. Doctors are allowed to use whatever

guidelines/guidance/statements on the diagnosing and treatment of hypothyroidism

that they wish, even if these have been produced in another country so long as

they can back up their reasons for picking a particular guideline to follow.

All statements in guidelines, guidance, statements must be backed up with the

scientific evidence to research and studies

to show that all statements are correct when

dealing with the lives of those suffering.

7. There is considerable peer

reviewed and published information in the medical literature on the potential

risks associated with thyroxine treatment in doses causing suppression of serum

TSH.

Agreed - See references

above.

I think that's the main ones - hope everyone's blood

pressure is ok after reading it!!

From a very cross and irritated

Dawn

___

[Guest guest]

Hi Dawn this is probably a bit late for a reply but I should have mentioned that

somebody from ICAS told me that the Ombudsman was sending back complaints to be

solved locally in quite a few cases . Hence your idea of continuing locally is

probably the best -you can say you followed all avenues . Make sure you have ALL

your records Its funny what the other side can come up with . Don't get out

of time on this as there are time limits -get replies back as quickly as

possible . I gave the hospital too long but in the end it was all considered as

issues were linked . Good luck

[Guest guest]

> Hi Shelia>> That's brilliant - thank you so much - I let you know how it goes!>> Dawn x>>>> ________________________________> Keep scrolling. This is long.