Thyroid function tests and hypothyroidism
BMJ 2003; 326 doi: https://doi.org/10.1136/bmj.326.7384.295 (Published 08 February 2003) Cite this as: BMJ 2003;326:295All rapid responses
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High dosage thyroid replacement should be considered in
'refractory' hypothyroidism
Dear Sir,
There has been correspondence in the British Medical Journal
(8th February 2003) discussing tangentially risk assessment in patients
receiving high dosage thyroid replacement. As my practice is mainly
concerned with problems of thyroid function, I seek advice from colleagues
on the advisability of long term high dosage thyroid replacement in
patients with refractory hypothyroidism.
Hypothyroid patients who do not respond to thyroid treatment comprise
two groups namely patients who show no improvement but become clinically
thyrotoxic and patients who show no improvement nor adverse effect. The
latter creates a frustrating and difficult situation for both patient and
doctor which is often compounded by FT4 or FT3 levels above the upper
limit of the 95% reference interval and TSH levels approaching zero.
During the last decade I have treated at least fifty patients who had
irresolvable or refractory hypothyroidism with sodium thyroxine at dosages
over 350µg per day or natural Armour Thyroid extract at over 4 Grains per
day or a combination of the two medications at equivalent dosage. These
patients have been returned to optimal or near optimal health with no
evidence of adverse effect.
The critical question concerns possible long term adverse effects. A
priori, it is unlikely that restoration of a patient to health where she
is up and about and living a full life will be detrimental or associated
with long term pathological sequelae. Perceived complications are
unproven. Cardiac irregularity is a well recognised feature of
hypothyroidism and usually disappears on thyroid replacement and (in my
experience) asymptomatic thyroxine induced irregularity is rare but is
easily detected by physical examination and is reversible within 1-2 days.
Evidence of osteoporosis is insecure and may have arisen from the
purported association of osteoporosis with chronic hyperthyroidism where
there may also be accompanying hyperparathyroidism with bone
demineralisation but this is speculation. The author has never encountered
significant adverse effects in patients restored to euthyroidism by high
dosage thyroid replacement.
There is a second more philosophic consideration; many patients
unequivocally state that they would rather run the gauntlet of putative
and unproven pathological sequelae than continue a wretched hypothyroid
existence. This raises an ethical question on the degree of self
determination or self selection of medical care which is desirable,
acceptable or indeed is a patient¹s right in a society based on consensual
rather than dictatorial principles.
However it remains an unpalatable fact that many patients are
receiving inadequate and ineffective thyroid replacement from unfounded
fears that return of a patient to euthyroidism will be accompanied by
crumbling bones or undiagnosable cardiac pathology. It is suggested that
the efficacy and safety of higher dosage thyroid replacement be subjected
to the scrutiny of formal clinical trial.
Yours sincerely,
Gordon R B Skinner MD, DSc, FRCOG, FRCPath
Competing interests:
None declared
Competing interests: No competing interests
Dear Sirs,
I have no training or clinical experience of endocrinology, so I will not
attempt to present any evidence which would contradict your views. (
Although my wife developed a hoarse voice with all the other symptoms, the
ENT hospital department have suggested hypothyroidism, but of course they
cannot prescribe thyroxine.)
However as the husband of one of the people you condemm as having "psycho-
social problems" I feel at least I am entitled to ask some very basic
questions.
1) The reference level for TSH for "healthy patients" is 0.5 to 5.0.
Can you explain why certain patients function normally at 0.5 and others
at 5.0 ? If you could accurately predict a healthy patient's TSH from some
other factors, this would remove any doubt about an individual patient's
reference level. If you have no idea, doesn't this suggest some lack of
certainty concerning TSH and the other hormones ?
2) Without knowing a reference level, would you agree there will be
cases where 2 patients both present to an endocronologist with TSH levels,
say 5x their normal level; one patient is diagnosed and treated, the other
patient is told their problems are all due to over-eating, clinical
depression, and the many other symptoms are due to an unfortunate
coincidence or just unexplained.
The reason for this of course is patient A had a reference level of 0.5,
the other had nearer to 5. Patient A despite their 5x increase is still in
the "normal" range, patient B is above the range. Would you agree this is
a thyroid lottery, those lucky enough to be born with a higher level are
more likely to be treated ? If the exact range from 0.5 to 5 is as
irrelevant as you say, why are patients with 5.1 diagnosed hypothyroid,
while 4.9 are hypochondriac ?
3) Reducing the method to its basics:-
All healthy patients have a TSH level of 0.5 to 5.0.
Therefore all patients with a TSH of 0.5 to 5.0 are healthy.
Does it not occur to you there may be a slight flaw in this logic ? In
most fields of science, we would also test the contrary, i.e. do all
unhealthy patients have a TSH range outside 0.5 to 5.0 ? If this test had
been done in 1973, when the hormone test was first introduced, we know the
answer would have been no, many patients present with numerous specific
clinical symptoms (not just overweight and tired) but have TSH in the
normal range. How different the diagnosis of hypothyroidism might been,
if this had been done before taking the TSH range as gospel and throwing
out all the symptoms.
4) Do you or indeed any endocrinologists have any psychiatric
training ? What are your qualifications to diagnose all these patients
with depression ? If you could take the time to read all the patients'
accounts published, you would find that all patients sent to psychiatrists
from endocrinology are diagnosed as mentally normal, the only thing making
them depressed is all the symptoms that the doctor cannot explain. Your
absolute certain diagnosis of every symptom, from hoarse voice, dry skin
and deafness to severe fluid retention as due to "psycho-social problems"
is a very confident diagnosis outside your field, something you deplore in
those outside the endocrine speciality.
5) Would you at least agree that some patients are in-appropriately
treated, after the thyroid cause has been eliminated ? For instance Diana
Holmes was treated for 6 severe conditions such as Myasthenia Gravis,
coeliac disease, etc, treated with massive doses of steroids, antibiotics,
Mestinon, etc (Tears Behind
Closed Doors, Normandi Publishing
2002). None of these had any effect, and she was only cured and
back to full health after being treatd with thyroxine. Of course your
diagnosis would be that all her disabilities were due to some
psychological reason and the thyroxine had the "magic" placebo effect that
can explain everything (but why didn't the previous 6 treatments have this
effect ?). Therefore none of the previous treatments were appropriate.
So why are you so opposed to patients trying a short-term test of a low
dose of thyroxine, to try to cure these symptoms that leave doctors
baffled ? ( A simple medical waiver form would remove any risk of patient
litigation if anything went wrong). The alternatives can be also be
drastic. The antidepressents that you and collegues hand out like sweets
are also not without side effects.
6) If you have seen the patient-oriented websites, you will know that
many patients are having to dose themselves with thyroxine with no medical
supervision, since they cannot find a GP who will consider the symptoms.
Would you not agree that GPs should at least be allowed to monitor and
advise patients even though they are not prescribing the hormone ?
I would be very interested to hear your replies.
You state it is only a vociferous minority who claim that throxine
has cured them ( so obviously they must be wrong). Of course the rest, the
majority of patients diagnosed as normal by the GP and endocrinologist
simply accept the diagnosis, because they are never told that some medical
staff do have doubts. Of this minority who do decide to and have the
resources to research deeper, a much smaller minority actually manage to
find a GP who will try out thyroxine on them. So it is even more
surprising that so many hundreds of people have mananged to find a way
through this process and found a cure.
I have a nagging suspicion that the medical profession have seized on
these hormone levels as an OBJECTIVE method to decide the course of
treatment, without having to make any clinical judgement which they fear
might result in litigation. But gentlemen I must point out that litigation
can work both ways. If one day a high court judge finally decides that
hundreds, thousands of patients have suffered crippling illness and
disability due to medical neglect, the litigation will be severe indeed
against those who so "vociferously" blocked any patient choice.
So once again, are you still totally opposed to seriously disabled
patients being give a small test of thyroxine if all else has failed ?
Your banning policy may not quite be as risk-free as you think.
Competing interests:
None declared
Competing interests: No competing interests
Whilst beginning with a strong backlash against the 'rogue medical
professionals' and almost certainly the self-diagnosing internet browsing
patients, the article makes a strong case for TSH testing as a basis of
diagnosis. However...
Medical professionals must have guidelines in which to work, and base
their decisions upon. Patients, such as myself, understand this. Problems
quickly arise when a patient feels unwell, yet often has just a few
minutes of their GPs time in which to voice their concerns. A check of the
most recent blood works on their computer screen, and the GP
assures/dismisses (depending on which side of the desk you sit) based upon
the numbers being within the regarded range. The internet savy or just
plain unconvinced patient search the internet and finds.... widely
differing suggested ranges!
Several UK sources suggest a TSH reference range of 0.4 - 4.5 whilst
my GP insists it should be 0.3 - 5.5
This may not seem a huge difference, but it's highly significant to
me as I'm currently 4.6, feeling unwell but my GP will not increase my T4
dosage. (my current T4 being 13.6 in a stated range of 10 - 23)
Now it appears that the USA have amended their range to peak at 3.0 !
With UK GP's working to differing ranges, and most unable or
unwilling to consider supplementing T4 with T3 for patients who are still
feeling unwell, patients comments and 'gut feelings' MUST take a higher
significance than mere numbers.
Medical professionals need to look beyond the figures to the quality
of life of their patient. It is us, after all, that have to live with our
widely differing blood results long after our three-minute consultation
with you has ended.
Competing interests:
None declared
Competing interests: No competing interests
Biochemists have known for some time that the Thyroid and Parathyroid are
both profoundly affected by the secosteroid hormone 1,25-dihydroxyvitamin-D
(1,25-D) [1].
There is an excellent drawing illustrating the systemic
effects of this steroid available online from University of California,
Riverside, Dept of Biochemistry (click here to view it).
Unfortunately, clinical medicine has been slow to use this knowledge, and
this secosteroid is rarely measured, even today.
I have some 1,25-D data which demonstrates that between 20% and
50% of euthyroid patients are suffering from undiagnosed
inflammation, most probably as the result of an undiagnosed immune condition.
This data would indicate that a significant percentage of the population could be at
risk.
The 1,25-D secosteroid is formed in large quantities in inflamed tissue. It
is a component of the immune system's Th1 inflammatory response.
Angiotensin II is also involved.
We have recently proposed a working description of the Th1 endocrine
biochemistry [2]
The Th1 inflammatory cycle is mounted in response to infection.
It has been shown, in-vitro, that gram-negative bacteria release
lipopolysaccharides and lipopeptides [3]. Most folks'
immune systems seem to neutralize the infective agent and recover, but a proportion
of the population does not manage to immediately kill all the bacteria, and
those which remain continue to
secrete lipopolysaccharide and lipopetides. Consequently, the body's immune reaction is
sustained for long periods, sometimes for life. A small proportion of these
continuing immune reactions are severe
enough to cause the most chronic immune disease, Sarcoidosis [4]. We have
found that measuring the elevated
production of 1,25-D steroid gives a reliable indication of the
degree of immune
dysfunction.
We have achieved excellent results using antibiotics to induce remission in
chronic sarcoidosis, but, at this point, have been unable to get our
results through peer-review. Give it time... maybe another decade or two...
Half a
century ago, Thomas McPherson Brown reported
positive results with antibiotics in Rheumatoid Arthritis [5],
but, despite significant popular acclaim [6]
his discovery has still not been acknowleged by the mainstream clinical community.
'Therapeutic probe' with some older antibiotics is now reliably curing
'autoimmune' disease, and this has given reasonable confirmation that the so-called
'autoimmune' diseases are actually due to Cell Wall Deficient
bacteria [7,8].
These are species of resistant bacteria (including strep species) which have developed resistance to the antibiotics
whose mode of attack on the organism is destruction
of the cell walls (such as the
penicillins). I would therefore caution against using the "auto"-immune
word, as the immune system is clearly reacting to a simulus, not to itself.
Unfortunately I suspect it may take a very long time for this pathogenesis to be
recognized, and fully adopted into clinical practice.
It is becoming clear that recognition of the (relatively simple) biochemistry whereby
bacteria affect the thyroid and parathyroid via Th1 and 1,25-D will take equally as long to
transition from the realm of Molecular Biochemistry into clinical
practice.
Guy Scadding first noted the links between
this secosteroid's metabolism and Immune Disease in the BMJ back in 1950 [9].
I agree with
Dr. Flachsbart, "we only have to look into the old books to find the new
things". Unfortunately, most of these old books were
burned during the 'wonder-drug' and 'Evidence Based
Medicine' revolutions...
1. Norman AW, Adams D, Collins ED, Okamura WH, Fletterick RJ: Three-dimensional model of the ligand binding domain of the nuclear receptor
for 1alpha,25-dihydroxy-vitamin D. J Cell Biochem 1999 Sep 1;
74(3):323-33 [PubMed Abstract]
Note: There is an excellent
colored image of this Thyroid 1,25-D receptor at URL
http://biochemistry.ucr.edu/faculty/norman.html
2. Marshall TG, Marshall FE: New Treatments Emerge as Sarcoidosis
Yields Up its Secrets. Clinmed 2003 Jan 27;2003010001.
clinmed.netprints.org/cgi/content/full/2003010001
(accessed 27 Jan 2003) [Full Text]
3. Mühlradt PF, Kiess M, Meyer H,Süssmuth R, Jung G. Structure and
Specific Activity of Macrophage-Stimulating Lipopeptides
from Mycoplasma hyorhinis. Infect Immun 1998 Oct; 6(10): 804-10 [Full Text]
4. Marshall TG, Marshall FE: Brown, et al, ACCESS Study finds Bacterial
Pathogens in Sarcoidosis Patients. [Electronic Letter] Chest 2003: Feb
12. Available from URL http://www.chestjournal.org/cgi/eletters/123/2/413#96
5. Brown TMcP, Wichelhausen RH, Robinson LB, Merchant WR: The in-vivo
action of aureomycin on pleuropneumonia-like organisms associated with
various rheumatic diseases. J Lab Clin Med 1949; 34: 1304-1410
6. The Road Back Foundation: Rheumatic Treatment and Research.
Available from URL http://www.roadback.org
7. Cantwell AR Jr: Variably acid-fast bacteria in a case of systemic sarcoidosis and
hypodermitis sclerodermiformis. Dermatologica 1981; 163(3):239-48 [PubMed Abstract]
8. Almenoff PL, Johnson A, Lesser M, Mattman LH: Growth of acid fast L
forms from the blood of patients with sarcoidosis. Thorax 1996 May; 51(5):530-3 [PubMed Abstract]
9. Scadding JG: Sarcoidosis, with special reference to lung
changes. BR
Med J 1950; 1: 745-753
Competing interests:
None declared
Competing interests: No competing interests
Dear Sir,
the connections between acute respiratory infections,
acute rheumatic fever and hyperthyreoidism were first described by v.
Basedow, 28. March 1840.
The connections between acute respiratory infections,
acute rheumatic fever and diabetes mellitus were first
described by Ebstein, 1876.
And Veil again focussed these lines of evidence to
the central point: Induction by streptococcal infection.
We only have to look into the old books to find the new things.
W. H. Veil: Der Rheumatismus und die streptomykotische Symbiose.
Enke, Stuttgart, 1939.
All the best to You
Yours
Friedrich Flachsbart
Competing interests:
None declared
Competing interests: No competing interests
Editor- Toft and Beckett finish their review of thyroid function
tests in hypothyroidism with the intriguing statement that residual
symptoms in treated patients might relate to the underlying chronic
inflammatory disorder rather than subtle abnormalities of thyroid hormone
status.(1) This struck a cord with us since we have noted a striking
excess of cases of treated hypothyroidism amongst a population of
idiopathic chronic cough(2) and in non-smokers with fixed airflow
obstruction(3) and have shown that idiopathic chronic cough is associated
with a bronchoalveolar lavage lymphocytosis.(2) We have suggested that
this may be due to homing of activated lymphocytes from the primary site
of autoimmune inflammation to embryologically related structures such as
the airways.(2-4)
The mechanism of airway inflammation and damage in autoimmune thyroid
disease may be analogous to that thought to be responsible for airway
complications of inflammatory bowel disease. The concept that inflammatory
bowel disease and autoimmune thyroid disease are associated with airway
disease and that the pathogenesis is similar and not related to thyroid
hormone status is supported by a recent study showing a 2-3 fold excess of
cough, sputum production and breathlessness, and a remarkably similar
profile of respiratory symptoms, amongst a cohort of patients with
inflammatory bowel disease and another with treated autoimmune thyroid
disease.4 Further evidence for a link between thyroid disease and
respiratory disease independent of thyroid hormone status has been
reported in a study showed a 2-3 fold increase in death from respiratory
disease in a large cohort of patients with normal thyroxine but suppressed
thyrotropin.(5)
These findings would be consistent with the view of thyroid disease
as a generalised, rather than organ-specific autoimmune disease. It is
tempting to speculate that other non-specific symptoms as well as
recognised complications of hypothyroidism such as ischaemic heart disease
are related to similar inflammatory mechanisms.
References
1. Toft AD,.Beckett GJ. Thyroid function tests and hypothyroidism.
BMJ 2003;326:295-6.
2. Birring S.S., Brightling, C. E., Symon, F. A., Barlow, S.,
Wardlaw, A. J., and Pavord ID. Lymphocytic bronchoalveolitis in idiopathic
chronic cough. Thorax 57, iii1. 2002.
3. Birring SS, Brightling CE, Bradding P, Entwisle JJ, Vara DD, Grigg
J et al. Clinical, radiologic, and induced sputum features of chronic
obstructive pulmonary disease in nonsmokers: a descriptive study.
Am.J.Respir.Crit Care Med. 2002;166:1078-83.
4. Birring S.S., Morgan A.J., Prudon B, McKeever T.M., Lewis S.A.,
Falconer Smith J.F., Robinson R.J., Britton J.R., and Pavord ID.
Respiratory symptoms in patients with treated hypothyroidism and
inflammatory bowel disease. Thorax in press. 2003.
5. Parle JV, Maisonneuve P, Sheppard MC, Boyle P, Franklyn 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.
Competing interests:
None declared
Competing interests: No competing interests
William Silen, formerly Johnson and Johnson Professor of Surgery at
Harvard and Chief of the Surgical Services at the Beth Israel in Boston,
used to speak of the pooped-out syndrome that developed in patients after
major surgery. Depression is a common feature in these patients. He
ascribed the syndrome to hypothyroidism.
It is now appreciated that many patients develop haemodynamically
compensated shock, or an inadequacy of mitochondrial oxidative
phosphorylation, during or immediately after major surgery. Organ
dysfunctions and failures tend to occur almost exclusively in these
patients. If persistent this might lead to a depletion in adenine
nucleotide stores and hence in the capacity to replenish ATP stores after
the demand for energy release by ATP hydrolysis. ATP depletion is a
serious biochemical abnormality for I may take as long as 300 days to
replenish (1). It may take much longer and might not even be possible if a
significant degree of impairment of mitochondrial oxidative
phosphorylation persists.
Any impairment of ATP resynthesis is likely to compromise the
replenishment of endocrine pools and the electrohemical gradients needed
to release them in a timely and appropriate manner (2). Thyroid hormones
open the permeability transition pores on mitochondrial membranes and
thereby decrease the magnitude of the protonmotive force driving ATP
resynthesis. Oxidative phosphorylation is thus uncoupled and the
generation of heat increased. An increase in metabolic rate is required to
accommodate these changes. This effect appears to be beneficial for in
hypothyroidism it is deficient. If increased to to excessive degrees,
however, opening the permeability transition pores may induce apoptosis
and even cellular necrosis (3,4).
ATP turnover would seem to be a far more sensitive measure of the
adequacy of ATP resynthesis than measures of ATP, ADP, adenine nucleotide
energy charge, or phosphorylation potential (1). I suspect the same
applies to the assessment of thyroid function, hormonal turnover rates
being likely to be far more sensitive than the conventional measurements.
But what of the ATP pools upon which thyroid hormonal function would
appear to depend? Should ATP turnover rates be included in the assessment
of thyroid function (5)?
1. Ingwall JS. ATP synthesis in the normal and failing heart. In:
Heart failure, Poole-Wilson PA, Colucci WS, Massie BM, Eds, Churchill
Livingston, New York, 1997
2.Treating dementia with light and near infrared waves
Richard G Fiddian-Green bmj.com/cgi/eletters/325/7376/1312#29607, 12 Feb
2003
3. Madness, hyperhomocysteinemia, metabolic rate and body temperature
Richard G Fiddian-Green
bmj.com/cgi/eletters/325/7378/1433#28469, 6 Jan 2003
4. Coronary revascularisation: treatment or prevention? Richard G Fiddian-
Green bmj.com/cgi/eletters/326/7381/134#29010, 22 Jan 2003
5. Thyroid function tests and hypothyroidism Anthony D Toft and Geoffrey J
Beckett
BMJ 2003; 326: 295-296
Competing interests:
None declared
Competing interests: No competing interests
DEAR EDITOR - In their recent editorial on thyroid function tests and
hypothyroidism, Toft and Beckett discuss the target TSH (thyroid
stimulating hormone) concentration for patients receiving thyroxine
replacement therapy for primary hypothyroidism.[1] They suggest that
patients with continuing non-specific symptoms (despite a TSH within the
laboratory reference range) are ‘under-replaced’. They conclude that
simply satisfying the recommendations of the American Thyroid Association
and restoring TSH concentrations to normal is inadequate. They state that
“some patients only achieve a sense of well-being if their TSH is low or
undetectable” and that “most patients feel well only with a low normal TSH
concentration”.[1]
Primary care physicians in the UK provide sole continuing clinical
care for majority of patients (82%) with primary hypothyroidism.[2] Before
considering changing their clinical practice, physicians should know that
almost no empirical evidence exists to support the assertion that
hypothyroid patients feel better with a TSH concentration that is ‘low
normal’, undetectable or suppressed.[1] By comparison, two systematic
reviews with meta-analysis have found that reducing TSH levels with
thyroxine therapy increases the risk of osteoporosis - particularly in
post-menopausal women.[3,4] An issue of considerable clinical importance
as women over the age of 50 years comprise 84% of patients prescribed
thyroxine replacement therapy in primary care.[2] TSH suppression also
increases the risk of atrial fibrillation.[5]
Existing levels of TSH suppression in the community already pose a
threat to women’s health. Many hypothyroid patients are currently over-
replaced with thyroxine in the UK. The proportion of patients with
suppressed levels of TSH is over 20% [2,6] in primary care, whilst
undetectable TSH levels (on ultra-sensitive assay) are 12%.[2] A change in
routine clinical practice which further reduces women’s TSH on thyroxine
replacement therapy is likely to increase both osteoporosis and atrial
fibrillation - without any good evidence that these women will feel any
better.
Dr Mike Crilly
MRCGP, MFPHM, MPH.
Senior Lecturer in Clinical Epidemiology
& Public Health Medicine.
Aberdeen University Medical School, Department of Public Health, Polwarth Building at Foresterhill, Aberdeen AB25 2ZD
Conflicts of interest: None
References
[1] Toft AD, Beckett GH. Thyroid function tests and hypothyroidism
Measurement of serum TSH alone may not always reflect thyroid status. BMJ
2003;326:295-296 (8 February)
[2] Crilly,M. Thyroid adherence study. Impact of an educational
booklet on thyroxine adherence inpatients with primary hypothyroidism: a
randomised controlled clinical trial in primary care. [MD Thesis:
submitted University of Manchester UK, 2002]
[3] Faber J, Galloe AM. Changes in bone mass during prolonged
subclinical hyperthyroidism due to L-thyroxine treatment: a meta-analysis.
Eur J Endocrinol 1994;130(4):350-6.
[4] Uzzan B, Campos J, Cucherat M, Nony P, Boissel JP, Perret GY.
Effects on bone mass of long term treatment with thyroid hormones: a meta-
analysis. J Clin Endocrinol Metab 1996;81(12):4278-89.
[5] Sawin CT, Geller A, Wolf PA, Belanger AJ, Baker E, Bacharach P,
et al. Low serum thyrotropin concentrations as a risk factor for atrial
fibrillation in older persons. N Engl J Med 1994;331(19):1249-52.
[6] De Whalley P. Do abnormal thyroid stimulating hormone level
values result in treatment changes? A study of patients on thyroxine in
one general practice. Br J Gen Pract 1995;45(391):93-5
Competing interests:
None declared
Competing interests: No competing interests
Dear Sir
The editorial in the BMJ 2003, 8th February, by Toft and Beckett is
disappointing in a number of regards. The opening paragraph encapsulates
the generalised and arrogant approach taken by Dr Toft together with so
many of his colleagues. His suggestion that patients with symptoms of
hypothyroidism, but normal blood tests, are a “vociferous minority” who
have psychosocial problems, is entirely misleading and quite insulting to
a great many patients. If he could be persuaded to take the trouble to
undertake a full clinical appraisal, including the invaluable basal
temperature test, suggested by Barnes as long ago as 1945 in the Lancet,
he would doubtless be able to make a diagnosis of hypothyroidism on
clinical grounds, and learn for himself the pitfalls of an uncritical
reliance on blood tests.
His second paragraph, concerning “misguided medical practitioners”
who in their alleged unwisdom actually try to solve their patients’
problems by using T3 as well as T4, or natural desiccated thyroid, is
again gratuitously insulting. These practitioners do not attempt to hit
some desired T4 or TSH level, but actually titrate the dosage to their
patients’ needs. A process called listening to the patient. Reliance on
the “sensitivity” of the TSH, expressly disregarding the clinical
response, is misplaced; the test approach must have a sensitivity of at
least 0.02 mu/l, which is difficult to reliably achieve and thus affords a
frequently seen cause for error.
He raises again the spectre of iatrogenic hyperthyroidism as a cause
of osteoporosis and atrial fibrillation. Although a theoretical
possibility, there is no evidence for this and I have never seen it in
many thousands of patients. It is particularly unlikely when patients
have been taught the value of self-monitoring.
Dr Toft refers to Pollock et al, who purported to demonstrate, in a
much criticised paper, that thyroxine helped a little in patients with
incontrovertible hypothyroidism but didn’t at all if they hadn’t. As with
the authors, Dr Toft confuses symptoms with a full clinical appraisal
providing a consequent diagnosis, which it is perfectly proper for an
experienced physician to make despite a normal TSH and T4. Neither this
paper nor Dr Toft’s comments have furthered understanding in any way.
Again, he refers to “the exquisite” sensitivity of the TSH which
leads him and his colleagues astray. He is right to point out that
pituitary or hypothalamic weakness, very much more common than he
believes, will provide a false low TSH; he would do well to remember that
a hypometabolic pituitary/hypothalamic axis is a commonly met cause of
unreliable TSH estimations.
However his observation that a replacement providing a higher than
normal T4 and suppressed TSH allows for greater patient well-being is to
be welcomed. Further is to be welcomed his consideration concerning the
addition of T3 to T4, if somewhat rather late in the day. Perhaps he
might in due course be persuaded that the use of T2 as well, as with
desiccated thyroid, confers additional advantage.
Yours faithfully
Dr Barry Durrant-Peatfield M.B., B.S., L.R.C.P, M.R.C.S.
Competing interests:
None declared
Competing interests: No competing interests
Severe Hypothyroid symptoms with normal TSH
I read with interest your article which at first seemed to state that
TSH is the "gold standard " in the first line of diagnosing Hypothyroidism
and your early statements about patients insisting they have hypothyrodism
when the TSH is los even though they have symptoms is egged on by some
clinicians.Well what I found odd was your article then gave proof at the
end that people can and do have normal TSH and Hypothyroid disease and
should be checked for it with symptoms...I don;t get the point of your
article...
I myself had a rapid weight gain after a lifetime of being a very
thin person even after four children..I was an ER nurse at the time and
was also getting weaker and weaker,,I also had asthma and fibromyalgia and
undiagnosed Rheumatoid arthritis..By the time I left my primary doctor to
find another I had gained 80 lbs!!! One particular time I remember was
when I had come home from a camping trip with my husband where we had
been hiking 20 miles every day this is while I was around the 40lb
overweight stage and I had gained 7 lbs,,,the doctor was not
concerned,.,,As a nurse I realized that it was impossible to hike like
this and gain weight without a serious metabolic disorder...but since my
TSH was normal..still nothing was done..
Worse still I have a mother with Hashimotos and a sister with Graves
...this did not phase them..
I was still working and going to other docs for my other troubles so
having little time to search for new docs but when my GYN saw me for my
routine visit he ordered a T4 and T3 resin uptake and these were abnormal
but really not that awful but sent me to an endocrinologist...I had
brittle hair,nails that bent in half and peeled,my legs had three plus
pitting edema by this point ,my heels of my feet were so dry a thick layer
of skin fell right of of both heels...I was now so tired I could no longer
drive,,,,My eyes were puffy and I had a sed rate of 54 my cholesterol was
and is high at 250 I am now on Synthroid and very slowly getting better
Competing interests:
None declared
Competing interests: No competing interests