[ Home ] [ HYPOTHYROIDISM ] [Low Adrenals]

see also

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.)
Cyanides (Barbiturates)
Thiocyanates (Smoking)
The elimination of these from the diet may be desirable, if not always

(B) Nutritional Deficiencies
(i) Iodine. Endemically absent in certain inland areas e.g. (Peak District)
(ii) Minerals in particular: Selenium
(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
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 Sheehan’s 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. Hashimoto’s 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.
Grave’s 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
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 Grave’s 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
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
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
life’s 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 patient’s 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 writer’s 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
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
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 Raglan’s 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
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 patient’s) 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 patient’s 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
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 it’s 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.

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
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.
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
14. Barnes. Etiology And Treatment Of Lowered Resistance To U.R.I.’s
Federation Proceedings 12 No I March 1953

86 Foxley Lane,
Surrey CR8 3EE
Tel: 44 020 8660 0905

Copyright All rights reserved