Thyroid
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see also http://www.tpa-uk.org.uk/thyroid_adrenal_dysfunction.pdf
SUGGESTIONS FOR AN APPROACH TO THE MANAGEMENT OF THYROID
DEFICIENCY
by Dr Barry J Durrant-Peat field
M.B., B.S., L.R.C.P., M.R.C.S.
Approved Civil Aviation Medical Examiner
The clinical syndrome of thyroid deficiency is very much more
common than is
generally realised; Barnes, in several publications, drew
attention to this in
the last two decades, as has the present writer more recently.
One reason for
this, is a tendency to think of hypothyroidism and rnyxoedema as
one of the same
thing, when this is quite wrong. Myxoedema, as doctors were
taught in medical
school, is the end result of a progressive disease process
resulting in more or
less total absence of thyroid hormone; whose symptoms and signs
are no doubt
perfectly familiar. But this state of deficiency has to start
somewhere, winding
down over a variable period to the terminal state of myxoedema.
Symptoms and
signs will naturally vary according to the extent of the level of
deficiency
reached. Clearly, a 10% loss may have little to show for it;
whereas a 25% loss
may have several very definite symptoms and signs; and a 40% loss
even more so.
Furthermore, patients show very individual response to any given
level of
dysfunction; while one may complain of excessive fatigue and
weight gain,
another may be more troubled by depression and menstrual problems.
That the diagnosis is all too frequently missed, is an inevitable
result of
this fundamental misunderstanding, and is commonly the result of
an incomplete
clinical appraisal in favour of the standard thyroid function
tests. These tests
are the real problem in diagnostic failure since there are
inherent problems in
interpreting blood levels of thyroxine and/or thyroid stimulating
hormone (TSH)
when blood levels may differ widely from tissue blood levels.
Since the
diagnosis may very properly, and easily, be made clinically,
unreliable blood
levels should NOT take precedence over clinical judgment.
Equally unsatisfactory is the acceptance by doctors and patients
alike of
poor response to thyroid replacement.
The present writer has been constantly alarmed and dismayed by
hypothyroid
patients who for years, all too often, have been obliged to
accept a much less
than satisfactory amelioration of their illness, being taught to
expect no more
than some improvement. It is perfectly possible that complete and
long lasting
remission should be obtained, and neither doctor nor patient
should accept
anything less. Further, the response should be monitored, not
just by the
doctor, but by the patients themselves. Since there often is a
dynamic
situation, the patients should be educated and taught to monitor
themselves,
making their own adjustments to dosage. In this connection,
frequent monitoring
by blood tests may be quite misleading and unhelpful. Surely it
must be more
satisfactory for the physician to ask the patients how they feel;
and guide the
informed patient in establishing the right dosage levels of
replacement therapy.
One of the most taxing problems in diagnosis is the multiplicity
of
symptoms, which need not be rehearsed here. It is all too easy to
pigeonhole the
polysymptomatic patient as one of the heart sink variety, and
much too often,
for example, inappropriately exhibit, perhaps, Prozac. Thyroid
deficiency may
cause all sorts of major and minor symptoms; and their very
frequency should
raise an index of suspicion for thyroid deficiency. The simple
Basal Temperature
Test, (see below), wrongly derided by many authorities, can
provide valuable
clinical backup. Finally, there is nothing wrong with a thought-fully
planned
trial of treatment with an informed and co-operative patient.
Hypothyroidism is due either to:-
A. Deficiency of thyroid hormone production;
B. Failure of thyroid hormone to reach the tissues.
Both may operate together in varying degrees.
Deficiency of hormone production is due to:-
1. Environmental Toxins/ deficiencies
2. Genetic thyroid failure
3. Thyroid failure secondary to pituitary insufficiency
4. Thyroid surgery
5. Treatment of previous overactivity
6. Major surgery
7. Tonsillectomy
8. Major trauma
9. Glandular fever
Failure of hormone to reach the tissues results from:-
1. Receptor resistance, or failure
2. Dysfunction of T4T3 conversion
3. Adrenal insufficiency
Dealing in turn with the therapeutic management of these
problems, we may turn
first to (A) Thyroid hormone production failure. This will be due
to:-
1. Environmental toxins and deficiency
(A) Toxins
A number of chemical agents tend to interfere with the
manufacture of thyroid
hormone. Notables among these are:
Poly chlorinated Biphenyls (Paints and wood preservatives)
Resorcinol (Millet)
Phthylate Esters (Plastics)
Thiouracil (Cabbages, Turnips, Cassava.)
Anthracin
Bromoform
Cyanides (Barbiturates)
Fluorides
Thiocyanates (Smoking)
Caffeine
Aspirin
Lithium
Amiodarones
The elimination of these from the diet may be desirable, if not
always
practical.
(B) Nutritional Deficiencies
(i) Iodine. Endemically absent in certain inland areas e.g. (Peak
District)
(ii) Minerals in particular: Selenium
Iron
Magnesium
Zinc
(iii) Vitamins.
Vit A - Conversion of Carotene to Vit A is inhibited by low
thyroid states, and
may cause yellow pigmentation.
It controls uptake of Iodine into the thyroid gland.
Deficiency also reduces T.S.H
Vit B Riboflavin, Niacin, Pyridoxine play a role in thyroid
hormone manufacture.
Vit C & Vit E
Deficiency has been shown to cause hyperplasia at cellular level
in the thyroid.
Clearly, part of the management of hypothyroidism requires some
dietary
advice; the provision of iron and vitamins and other minerals is
simple and
obvious.
2. Genetic Thyroid Failure.
This will have become apparent soon after birth; but may not be
obvious
cretinism. A sickly child, with poor weight gain, frequent
infections, lethargy,
or oddly enough, hyper kinesia, and is a candidate for genetic
poor thyroid
function. Thyroid replacement is mandatory as early as possible.
3. Pituitary Failure.
This is a more common problem than is recognised, and apart from
its
specific clinical features, it may be a cause of secondary
hypothyroidism. The
pituitary may have a genetic deficiency, when it will have been
probably
recognised early. Not uncommon is Sheehans Syndrome,
resulting from major
trauma from accidents or surgery. Adenomas of the pituitary may
cause pressure
atrophy and / or abnormal hormone outputs. But the pituitary may
be involved in
the general multiple deficiency state, and more specifically in
low thyroid
states. This partial failure in hypothyroidism may well be a
cause of low T.S.H,
so that a vicious spiral may slip into being. The danger of a low
or normal
T.S.H in this situation being mis-interpreted when thyroid
function tests are
carried out is quite clear. In this situation, correction of the
thyroid state
will bring benefits to the pituitary; and may explain why some
patients on
thyroid replacement therapy begin to need lesser doses as time
passes.
Correction of the thyroid deficiency is clearly necessary; but
adrenal
insufficiency, considered in more detail later, as a consequence
of lowered ACTH
output, may require cortisone and Dehydroepiandrosterone (DHEA)
in addition.
4. Thyroid Surgery.
This is undertaken as a treatment for pathology of the thyroid
itself, or as
a treatment for overactivity, discussed below. Thyroid cysts,
Adenomas or
Carcinomas are necessarily removed by surgery; and it is
sometimes necessary to
remove goitres where the size is causing respiratory or
oesophageal
embarrassment. Hashimotos disease may come into this
category.
Replacement by thyroid hormone is an obvious consequence.
5. Treatment of previous thyroid overactivity, by surgery or 1131
ablation.
Graves disease is widely treated, where medical methods are
deemed
unsatisfactory, by partial thyroidectomy, or Radioactive Iodine
ablation. This
is often unsatisfactory, since it is very difficult to get it
right. Either too
much is removed or destroyed; (in which case replacement therapy
is a permanent
necessity) or too little, and it may have to be done again.
For such patient's replacement therapy is an obvious no option
requirement.
6. Major Surgery,
Most particularly in this context comes cholecystectomy and
hysterectomy.
Many doctors are aware that women may suffer weight gain and loss
of well being
after this surgery; and this will be found to be due to early
loss of thyroid
function. Replacement therapy is required.
7. Tonsillectomy.
Quite why in adults tonsillectomy may result in slow running down
of thyroid
function, is not clear, but may be the result of interruption of
the blood
supply. The present writer has noted a number of cases of young
adults
misdiagnosed as M.E sufferers in this situation. Replacement
therapy provides a
most satisfactory return to normal.
8. Major Trauma,
Major road traffic accidents, and surgical accidents are known to
precipitate thyroid and/ or pituitary insufficiency. In this
category have been
noted the major psychic trauma of certain life events.
Replacement indicated,
with regard given to pituitary - adrenal function.
9. Glandular Fever.
This is an often met with cause of failure of the thyroid/
adrenal axis.
Evidence has pointed to pituitary damage causing secondary
hypothyroidism; But
progressive loss of thyroid producing cells within the thyroid
has been noted.
In either event, replacement is required. Discussion of failure
of uptake at
tissue level may be conveniently dealt with in the section below
on therapeutic
options. Consideration should now be given to the aims of
replacement therapy.
The overall purpose is to restore metabolism to normal, so as to
eliminate
all hypothyroid symptoms, and to secure a sense of normal well
being. This
implies that thyroid hormone levels in each and every cell are
nominal; that all
the exchange reactions are taking place, as they should be.
Sadly, this ideal is
at least as often as not, simply not reached, often by a long way.
Residual
tiredness, lack of drive, depression is frequently admitted to.
Menstrual
dysfunction may remain a feature. Skin problems, fluid retention,
digestive
problems, arthralgia, may remain in some degree. Many patients
will continue to
com-plain of weight gain, or great difficulty in losing it, and
receive scant
sympathy.
In this situation, the physician may estimate thyroid function by
Free
Thyroxine Index (FTI), or Thyroid Stimulating Hormone (TSH); and
be confronted
by normal readings. It is the present writer's view that these
estimations may
be seriously flawed, and their value fundamentally limited. The
most popular, at
the moment, is the TSH. This may be much affected by poor
pituitary function
itself due to hypothyroidism; it may be low or normal, rather
than raised. The
FTI is subject to several errors. Poor tissue uptake is probably
the most
telling. If the actual use by the tissues is reduced by poor
conversion of T4 to
T3 (see below) and/or receptor block, then high or normal blood
tests will
result. Haemoconcentration may be an additional factor.
There can be no substitute for proper clinical appraisal. If the
patient
sounds and looks hypothyroid, then probably that is the problem -
irrespective
of pathological testing.
The net result very much too often in clinical practice is to
underdose. To
provide full remission of symptoms, the level in the tissues of
thyroid hormone
should be as high as possible, short of too much. (The patient/doctor
monitoring
to achieve this is described later). The situation is worsened by
a tightly held
misapprehension in many quarters that there are grave risks
associated with
overdose. These are largely apocryphal and must be corrected.
Probably most
widely held, is that thyroid overdose is bad for the heart. The
risk is there if
coronary artery insufficiency, previous M.I or incipient failure
already
compromises the heart; the risk of over working a damaged heart
is obviously
undesirable. The healthy heart will not be damaged by minor
degrees of overdose,
whether by accident or design; and is rarely much affected even
by high levels
of thyroid hormone, as in Graves Disease.
Another anxiety is osteoporosis. There is a risk in sustained
overdose, and
untreated hypothyroidism, but this is still not certain. There is
NO risk of
osteoporosis in thyroid supplementation in correct, physiological
doses
obviously; and in any inadvertent minor overdose is rapidly
detected by
monitoring, and therefore of no consequence either.
Suppression of the thyroid gland as a result of treatment is
another
frequently expressed anxiety. There is a sensitive negative
feedback operating
through the hypothalamus and the pituitary Overdose will suppress
the thyroid;
but this will come back to normal at once when the dose is
adjusted. Not
treating a patient with an under active thyroid for fear of
promoting further
depression is quite unrealistic.
Vague fears that thyroid is like "speed"; that any
deliberate or accidental
overrunning of the metabolism will result in early "burn out";
have been
expressed. All that can be said is that is simply not true.
The correct management of thyroid replacement requires a flexible
approach;
full explanation to the patient, and monitoring, relying as much
on the patients
assessment as the physicians own clinical impression. One may
often be obliged
to deal with partial response to replacement therapy, with
failure to respond to
an increase of dose; and more wrongly, some symptoms of overdose
on small levels
of treatment. These will include raised pulse rate, tremor,
breathlessness,
headaches. Sometimes an encouraging response levels off and drops
back.
To understand what is happening, it should be clear that five
matters have
to be considered in planning replacement therapy:
1. Dose
2. Vehicle
3. Conversion T4 - T3
4. Receptor resistance or deficiency
5. Adrenal insufficiency
1. Dose. This has to be infinitely variable. It starts low and
will be
increased progressively and incrementally, until full response is
obtained.
Neither doctor nor patient should be satisfied with 60% response;
or 80%; 100%
is the target. The patient will be asked to monitor their
response to treatment.
This is satisfactorily done by three simple exercises.
1. Basal Temperature, this is the temperature (10 ins Axillary,
or 3 ins in
mouth) immediately on waking. It is low in hypo metabolic states,
but will rise,
albeit slowly, in response to treatment, (as reported elsewhere
this is valuable
diagnostically). A sudden rise may indicate, all things being
equal, the start
of overdose.
2. Basal Pulse. This may be taken at the same time as
temperature; overdose
will result in a rise of the resting pulse. 8O bpm will usually
signify
overdose.
3. "Feel good factor". It is possible to ask the
patients to make a
subjective assessment, say, one out of ten, on the same days as
temperature or
pulse. Since improvement in thyroid replacement may be quite
slow, placebo
effect does not occur; if the patient feels better, then they are
better.
Considerations will be given to actual dosage shortly.
4. Vehicle. There are three options to choose from.
1. Thyroxin (T4)
2. Tertroxin (T3)
3. Dried, natural thyroid U.S.P
1. In this country Thyroxin (marketed usually as Eitroxin (Glaxo),
is almost
invariably used. Of the naturally occur-ring thyroid hormones it
is the chief.
The thyroid hormone in the natural state is made up of around 80%
Thyroxine (T4)
15% Trilodothyronine (Tertroxin T3)
residual 5% Diiodothyronine
Mono idothyronine
Thyronine
Thyroxine works quite well for the more simple, uncomplicated,
early, not
too severe, hypothyroid patient. But note should be made that
this is not how
thyroid hormone is naturally produced. There is a body of
opinion,
sympathetically supported by the writer, that if natural thyroid
is not to be
used, then at least T4 should be combined with T3 for a more
satisfactory and
more logical replacement.
2. Trilodothyronine - Tertroxin (T3). This is quite considerably
more potent
than T4, four or five times so, but unlike T4, with an 8 day half
life, the half
lifes about 8 hours. It is also fifteen times as expensive.
3. Dried Natural Thyroid. Used from about 1900, desiccated
thyroid fell into
disfavour in this country and availability ceased in 1985. The
synthetic
Thyroxine was considered to be a better, purer preparation.
Though, of course,
it is purer - not containing the other thyronines - this may be
its weakness;
and ignores the fact that thyroid replacement need not be exact.
The amount
required varies from day to day, even hourly; and this dynamic
variation may be
compensated for by the patients own thyroid - which
although deficient, may
still be taking most of the load. It is widely used in USA, as
Natural Thyroid
U.S.P., but in the U.K has to be specifically imported. It almost
invariably
works better than the synthetic Eitroxin, and is generally
preferred by patient.
About half of patients in the writers practice are
maintained on this
preparation. (Gold Line Laboratories, Fort Lauderdale; or Armour
thyroid, from
The Bames Foundation, Trumbull, Connecticut).
4. Conversion. Thyroxine has a low biologic activity, and is
transported, linked
to a binding globulin in a non-active state. The removal of one
of the four
Iodine atoms, from the Thyronine molecule, converts it to the
biologically most
active Trilodothyronine (T3) - available as Tertroxin. This is
achieved by the
(largely liver produced), 5 Diodase enzyme. In this form, it will
be passed, via
receptors, into the cell, where passage of protein and sugars
across cell
membranes is encouraged, and mitochrondrial activity stimulated.
It is now clear
10 that prolonged and/or severe hypothyroidism may be associated
with partial
failure of the 5-Diodase enzyme. Although suspected, this
situation may be
diagnosed in default when failure of response in thyroid
replacement occurs. The
effect of Thyroxine in this situation is to cause an overload of
unused T4 due
to conversion failure. This will cause some symptoms of thyroid
excess, high
pulse, tremor, headache for example, while the hyperthyroid
symptoms remain (It
is of remark that on occasions, high T4 levels in this situation
have resulted
in inappropriate hypothyroid medication, or thyroid ablation).
Thyroid function
tests will show high FTI and low TSH; resulting in thyroid
supplementation
actually being withdrawn by the physician.
Management, where this problem is believed to be present,
consists in
discontinuing some or all T4 and substituting with T3, preferably
in divided
doses. Since poor conversion may be associated with a raised sex
hormone binding
globulin (SHBG) and high levels of exogenous oestrogen, re-appraisal
of any HRT
may need to be considered. Ensuring correct levels of vitamins A
& B, Iron and
Magnesium (as above), is also mandatory.
5. Receptor resistance or deficiency.
Resistance to the passage of T3 via the receptors has been seen
in a number
of cases. Why this occurs is not clear, but long periods of
thyroid dysfunction
are associated. The replacement dose of the chosen thyroid
hormone has to be
much larger than usual, which may cause some heart searching.
Deficiency results
from a protracted low thyroid state; prolonged low level
desensitises the
receptors. This will improve with time, and treatment of any
Adrenal
insufficiency present.
Adrenal Insufficiency
This might be more properly described as low adrenal reserve.
Since
hypothyroidism adversely affects every cell, every tissue, every
gland, in the
body it is clear that the endocrine system as a whole will be
also similarly
affected. The adrenals will be subject firstly to lowered
efficiency resulting
from a lowered vitality primary to hypothyroidism, and
secondarily, to reduced
ACTH stimulation from the pituitary. As a result, in general,
patients with a
protracted and / or severe hypothyroid state will have some
degree of adrenal
insufficiency. A significant level of this will be suspected in
these
situations:
1. Longstanding and severe hypothyroidism.
2. Episodes of extreme exhaustion, or collapse.
3. Bad response to minor illness.
4. Multiple allergies.
5. Digestive problems - Diarrhoea
Flatulence
Weight loss
6. Increasing arthralgia and morning stiffness.
7. Pallor, yellow pigmentation (due to poorly metabolised
carotene)
8. Fainting, dizziness
These patients often present with dark rings under their eyes,
looking quite
ill. Blood pressure is low, with a positive Raglans sign. (Pressure
fails to
rise on standing). These symptoms and signs, it will be
appreciated, are those
of the early phases of Addions Disease.
Estimation of blood Cortisol is usually unhelpful, but
De-hydroepiandrosterone sulphate (DHEA), the main hormone output
from the
adrenals will be found to be low. Depressed levels in the
endocrine system as a
whole are likely to be found. The low adrenal reserve means
patients are more or
less well, until challenged by the stress of illness, (or life
events) and the
replacement therapy itself initially, of thyroid hormone. And
this partial
failure will affect adversely T4-T3 conversion; and the integrity
of the thyroid
receptors.
It is essential to manage this insufficiency where present, or
where
suspected. Remarkably, patients with symptoms, signs and blood
pathology of low
thyroid, may improve completely on management and correction of
the adrenal
problems alone; as conversion and receptor efficiency improves,
the thyroid
hormone circulating - partly unused - is brought into play.
Adrenal insufficiency is dealt with by the provision of the two
hormones
most likely to be lacking; Cortisone/hydrocortisone, and DHEA.; (as
pointed out
above, low DHEA may be used to infer low cortisone output). The
treatment
therefore, is the exhibition of, ideally, Hydrocortisone. This
should be given
in divided doses initially of 5mgm qds; after a week, lO mgm qds
may be used.
This remains a physiological dose, not challenging or suppressing
the adrenal
function, but supplementing it. In these doses all of the usual
anxieties
associated with cortisone do not apply; since restoration of
normality is being
aimed at.
This may need to be explained to patients long subject to media
induced
fears of the horrors of corticosteroids. (Their physicians may
share these
anxieties, unnecessarily,). Dr McCormack Jeffries papers on
the subject are
most worthy of study. DHEA has reached prominence in recent times
as a hormone
of multiple, and magic properties. Certain it is that the
adrenals secrete more
DHEA than anything else, and the amount is inversly proportional
to age. It is
metabolised to oestrogen and/or testosterone; but also has been
shown to play a
role in reducing obesity; in reducing atherosclerosis and
cholesterol; it
inhibits the glucose -6- dehydrogenase enzyme in cancer; it
improves immune
response, and, possibly, acts as a neural facilitator. In
physiological doses,
there seems to be no problem in its long-term use. If levels are
demonstrably
low, it is reasonable to provide replacement therapy.
Treatment Protocol
1. General consideration. Correction of Nutritional deficiencies,
and
elimination of environmental challenges and toxins, has been
noted above.
2. Simple, early hypothyroidism. Readily available tablets of
Eitroxin 50mg may
be used. Initial dose is low (in the elderly as low as 25mg daily)
and will
usually start at 50mg daily. This may be increased 25mg daily
every two or three
weeks. The ceiling is reached at the judgement of the physician
with feedback
from the patient. It is unusual to go higher than 300mg.
3. Moderate hypothyroidism. If the synthetic products are to be
used, many
patients will benefit if, when a dose of lOOmg or more is used,
Tertroxin (T3)
is added. lOmg for each lOOmg of T4 is to be preferred, although
this means
halving the standard 20mg tablet. The dose may be increased
incrementally at the
physician (and patients) discretion.
If natural thyroid is to be used a start may be made with 1/2;
grain.
(Commensurate with its 100 years of use by the medical
profession, natural
thyroid is still measured in grains). Dosage is increased by 72
gr. every two
weeks; usually by six the dose will level off. Improvement on any
given dose
continues for weeks and weeks; and the temptation, scenting
victory, to increase
the dose too soon, should be resisted. (One grain equivalent 65mg
of natural
thyroid is equivalent to 38mg T4 and 9mg T3). The definitive dose
may remain
unchanged for months or years; but the patients should be allowed
to make small
adjustments themselves, depending on activity, ambient
temperature, for example.
4. Severe hypothyroidism. As indicated above, simple replacement
is unlikely to
be sufficient. Receptor block and adrenal insufficiency require
adrenal support;
preferably initiated a week before thyroid supplementation is
started. A
satisfactory protocol is to, start with 5mgm hydrocortisone qds,
and after a
week, double the dose. Alternatively Prednisolone 2.5 mgm (or the
enteric-coated
Deltacortril) may be used, doubling after a week. Clinical
judgment, based on
the patients condition being normal - perhaps after about
three months - will
enable the dose then to be halved, and then discontinued. It will
be a matter of
clinical judgment and preference to use T4 and T3 or natural
thyroid.
Some patients already on thyroxine, but far from well, have to be
considered
separately. If the condition is really quite severe, and
increasing thyroxine
makes matters worse, it should 14 be stopped for a short while
and cortisone
exhibited. The sudden improvement in thyroid uptake brought about
by the
cortisone may actually result in overdose symptoms if exogenous
thyroid is
continued. The treatment of choice is to restart thyroid hormone,
using instead
T3, after a 7 day interim period; lO mg for a few days, then 20
mg and so on.
After the improvement is seen to be full, and sustained, Eltroxin
(or natural
thyroid) can be re introduced. The general improvement may,
secondarily, improve
endogenous thyroid production, which can result in the overall
exogenous dose
being reduced.
As regards DHEA, its significance in the management of adrenal
insufficiency
is unsure, but where low levels have been found, it seems proper
and logical to
restore them to normality. In women 25mgm daily, and men 50mgm
daily sometimes
produces significant benefit. In this practice, its use has
always been an
advantage.
The management of hypothyroidism in children requires fine
clinical
judgement; but one quarter to one half of the adult dose seems to
be a
satisfactory starting point. Reliance on blood testing should be
modified by
clinical appraisal of the child and its parents
observations. The diagnosis is
often missed in children; and should be considered in any child
often ill. The
basal temperature test may prove a helpful pointer.
Thyroid insufficiency may have a number of different causes and
its symptoms
may masquerade as a number of different illnesses. It should
always be
considered in patient's with pro-longed ill health, and the
diagnosis rely on
history and examination; the reliance of the profession on the
pathological
tests in favour of thoughtful appraisal is to be deplored. The
treatment is
inexpensive and low tech, requiring a few simple guidelines and a
listening
approach by the physician. Rarely is consultant advice necessary;
the family
physician is well able to initiate and monitor the treatment even
in quite
severe cases. The rewards are invariable; with no fuss, and with
delight, the
patients always get better. This common condition is one of few
where simple
measures can transform patient's lives.
REFERENCES
1. The Unsuspected Illness. Bames. Harper and Row. 1976
2. Jackson. A.S. Hypothyroidism. J.A.M.A. 165: 121: 1957
3. B. Durrant-Peatfield. Aspects Of A Common Missed Diagnosis.
Journal
Of Nutrition And Environmental Medicine. 6: 4: Dee 1996
ORD W.M, On Myxoedema, a term proposed to be applied to
anessential condition
in the critinoid infection observed in middle aged women.
Transactions Of The
Medical - Chirurgical Society Of London
57:6(~611877
5. E. Hertzogue. Treatment Of Myxoedema International Clinic Week.
New York 4: 14: 1915
6. The Fallacy Of Thyroid Function Tests. The Riddle Of Heart
Attacks.
Barnes & Barnes 1976. ROBINSON PRESS. ISSN 0-913730-27-0
7. Interindividual Differences In The Pituitary-Thyroid Axis
Influence
The Interpretation Of Thyroid Function Tests. Clinical
Endocrinology.
39:101-107:1993
8. Staub et al. Spectrum Of Sub Clinical And Overt Hypothyroidism.
American Journal Of Medicine 92: June 1992 pp 631
9. Barnes. Temperature v Basal Metabolism. Journal Of American
Medical Association. 119: 1072, 1942
10. Klause Wenzel. Osteoporosis. Lancet 340 15. 8. 92 pp 435-6
11. Franhyn et al. Long-term Thyroxine treatment and bone mineral
density. Lancet 340 4.7.92
12. Jeffries. W.M. Safe Uses Of Cortisone. Charles C. Thomas.
1981
13. Klinefelter et al. Single Dose Prednisone Therapy. J.A.M.A.
241 No 25
22.6.79
14. Barnes. Etiology And Treatment Of Lowered Resistance To U.R.I.s
Federation Proceedings 12 No I March 1953
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