RE: Re: Deb's experience with needing adrenal support-- comments

[Guest guest]

I know some out here think Tish is over exagerating the adrenal issue but,

join the 's group and you will see why. They will tell you it can

kill you and will warn you to be extremely careful with any kind of steroid

treatment. Not to mention nearly everyone on the board has osteo due to the

steroids robbing their body of calcium. You have pretty severe muscle

waisting that occurs also when taking steroids. If it were not for me

spending time listening to other patients on the board, I would not

have realized just how dangerous it can get. A couple have seriously nearly

died from not getting enough Cortisone. Like Tish said, it is rare but does

happen. If you look at 's disease as a whole it is labeled a rare

disease and there are not that many diagnosed with it vs. thyroid patients.

I also have been on treatment for adrenal fatigue for a year and I can say

there were a few times that I thought I would have to go to the hospital

from it. If you go interview some of the folks on the board they

will inform you that they will not give you adrenal dosage information...the

first thing they will emphasize is to get a doctor who KNOWS how to treat

the adrenals first due to how dangerous it can be. I think Meg on the yahoo

addisons board can tell you first hand how many times she has nearly died

due to steroids. Again, it is rare but like Tish said it doesn't hurt to

provide folks with this information and although rare, it does happen. I

can say that I have had several close calls where my body burned the little

20mg you get so quickly that I went into a hypoglycemic episode followed by

3 days of pure exhaustion and severe symptoms. To the degree my doctor

doubled my steroid dose for 3-4 days so I could recover without going to the

hospitol. Certainly I don't want to scare anyone, but I think it's

important to share our expieriences though and my expierience is...don't

self dose the adrenals...it's dangerous. Hope this helps ....

Be well!

LaCretia

>

>

>

>I started out on just on 25 mcg of Levoxyl and if I had not had such

>devastating effects from just that tiny amount without adrenal

>support, I would not be so paranoid and cautious as I am. Because it

>did such terrible things to me, I do not want to make light of the

>dangers. If the person was older and had been hypo many years and

>had developed cardiovascular disease, this sort of self medicating

>could cause serious problems and even death in my opinion. So, Ok it

>is probably rare, but I sure do not want that guilt on my concience

>from someone not taking the risks seriously and me making too light

>of them.

>

>Tish

>

>

>

>

>

>

>

>

[Guest guest]

I know some out here think Tish is over exagerating the adrenal issue but,

join the 's group and you will see why. They will tell you it can

kill you and will warn you to be extremely careful with any kind of steroid

treatment. Not to mention nearly everyone on the board has osteo due to the

steroids robbing their body of calcium. You have pretty severe muscle

waisting that occurs also when taking steroids. If it were not for me

spending time listening to other patients on the board, I would not

have realized just how dangerous it can get. A couple have seriously nearly

died from not getting enough Cortisone. Like Tish said, it is rare but does

happen. If you look at 's disease as a whole it is labeled a rare

disease and there are not that many diagnosed with it vs. thyroid patients.

I also have been on treatment for adrenal fatigue for a year and I can say

there were a few times that I thought I would have to go to the hospital

from it. If you go interview some of the folks on the board they

will inform you that they will not give you adrenal dosage information...the

first thing they will emphasize is to get a doctor who KNOWS how to treat

the adrenals first due to how dangerous it can be. I think Meg on the yahoo

addisons board can tell you first hand how many times she has nearly died

due to steroids. Again, it is rare but like Tish said it doesn't hurt to

provide folks with this information and although rare, it does happen. I

can say that I have had several close calls where my body burned the little

20mg you get so quickly that I went into a hypoglycemic episode followed by

3 days of pure exhaustion and severe symptoms. To the degree my doctor

doubled my steroid dose for 3-4 days so I could recover without going to the

hospitol. Certainly I don't want to scare anyone, but I think it's

important to share our expieriences though and my expierience is...don't

self dose the adrenals...it's dangerous. Hope this helps ....

Be well!

LaCretia

>

>

>

>I started out on just on 25 mcg of Levoxyl and if I had not had such

>devastating effects from just that tiny amount without adrenal

>support, I would not be so paranoid and cautious as I am. Because it

>did such terrible things to me, I do not want to make light of the

>dangers. If the person was older and had been hypo many years and

>had developed cardiovascular disease, this sort of self medicating

>could cause serious problems and even death in my opinion. So, Ok it

>is probably rare, but I sure do not want that guilt on my concience

>from someone not taking the risks seriously and me making too light

>of them.

>

>Tish

>

>

>

>

>

>

>

>

[Guest guest]

LOL... I feel your pain Kathy! Especially today! As many know...I'm

weaning off the Cortef and about 2 PM (right about now) I feel the yawn's

beginning...from there I get more and more tired until I just feel like

collasping! All my adrenal fatigue symptoms are coming back due to weaning

off. The only positive thing that I can pull from this at this moment is

the nausea is coming back... that will help me lose that 15lbs I put on

while on Cortef for sure. Hey... you have to find the positive somewhere

right...lol!

LaCretia

>

>

>

>Not to make light of all this, but.... " Just shoot me " .

>

>Kathy

>

>

>

>

>

> > I know some out here think Tish is over exagerating the adrenal

>issue but,

> > join the 's group and you will see why. They will tell you

>it can

> > kill you and will warn you to be extremely careful with any kind of

>steroid

> > treatment. Not to mention nearly everyone on the board has osteo

>due to the

> > steroids robbing their body of calcium. You have pretty severe

>muscle

> > waisting that occurs also when taking steroids. If it were not for

>me

> > spending time listening to other patients on the board, I

>would not

> > have realized just how dangerous it can get. A couple have

>seriously nearly

> > died from not getting enough Cortisone. Like Tish said, it is rare

>but does

> > happen. If you look at 's disease as a whole it is labeled

>a rare

> > disease and there are not that many diagnosed with it vs. thyroid

>patients.

> > I also have been on treatment for adrenal fatigue for a year and I

>can say

> > there were a few times that I thought I would have to go to the

>hospital

> > from it. If you go interview some of the folks on the

>board they

> > will inform you that they will not give you adrenal dosage

>information...the

> > first thing they will emphasize is to get a doctor who KNOWS how to

>treat

> > the adrenals first due to how dangerous it can be. I think Meg on

>the yahoo

> > addisons board can tell you first hand how many times she has

>nearly died

> > due to steroids. Again, it is rare but like Tish said it doesn't

>hurt to

> > provide folks with this information and although rare, it does

>happen. I

> > can say that I have had several close calls where my body burned

>the little

> > 20mg you get so quickly that I went into a hypoglycemic episode

>followed by

> > 3 days of pure exhaustion and severe symptoms. To the degree my

>doctor

> > doubled my steroid dose for 3-4 days so I could recover without

>going to the

> > hospitol. Certainly I don't want to scare anyone, but I think it's

> > important to share our expieriences though and my expierience

>is...don't

> > self dose the adrenals...it's dangerous. Hope this helps ....

> >

> > Be well!

> > LaCretia

> >

> > >

> > >

> > >

> > >I started out on just on 25 mcg of Levoxyl and if I had not had

>such

> > >devastating effects from just that tiny amount without adrenal

> > >support, I would not be so paranoid and cautious as I am. Because

>it

> > >did such terrible things to me, I do not want to make light of the

> > >dangers. If the person was older and had been hypo many years and

> > >had developed cardiovascular disease, this sort of self medicating

> > >could cause serious problems and even death in my opinion. So, Ok

>it

> > >is probably rare, but I sure do not want that guilt on my concience

> > >from someone not taking the risks seriously and me making too light

> > >of them.

> > >

> > >Tish

> > >

> > >

> > >

> > >

> > >

> > >

> > >

> > >

[Guest guest]

LOL... I feel your pain Kathy! Especially today! As many know...I'm

weaning off the Cortef and about 2 PM (right about now) I feel the yawn's

beginning...from there I get more and more tired until I just feel like

collasping! All my adrenal fatigue symptoms are coming back due to weaning

off. The only positive thing that I can pull from this at this moment is

the nausea is coming back... that will help me lose that 15lbs I put on

while on Cortef for sure. Hey... you have to find the positive somewhere

right...lol!

LaCretia

>

>

>

>Not to make light of all this, but.... " Just shoot me " .

>

>Kathy

>

>

>

>

>

> > I know some out here think Tish is over exagerating the adrenal

>issue but,

> > join the 's group and you will see why. They will tell you

>it can

> > kill you and will warn you to be extremely careful with any kind of

>steroid

> > treatment. Not to mention nearly everyone on the board has osteo

>due to the

> > steroids robbing their body of calcium. You have pretty severe

>muscle

> > waisting that occurs also when taking steroids. If it were not for

>me

> > spending time listening to other patients on the board, I

>would not

> > have realized just how dangerous it can get. A couple have

>seriously nearly

> > died from not getting enough Cortisone. Like Tish said, it is rare

>but does

> > happen. If you look at 's disease as a whole it is labeled

>a rare

> > disease and there are not that many diagnosed with it vs. thyroid

>patients.

> > I also have been on treatment for adrenal fatigue for a year and I

>can say

> > there were a few times that I thought I would have to go to the

>hospital

> > from it. If you go interview some of the folks on the

>board they

> > will inform you that they will not give you adrenal dosage

>information...the

> > first thing they will emphasize is to get a doctor who KNOWS how to

>treat

> > the adrenals first due to how dangerous it can be. I think Meg on

>the yahoo

> > addisons board can tell you first hand how many times she has

>nearly died

> > due to steroids. Again, it is rare but like Tish said it doesn't

>hurt to

> > provide folks with this information and although rare, it does

>happen. I

> > can say that I have had several close calls where my body burned

>the little

> > 20mg you get so quickly that I went into a hypoglycemic episode

>followed by

> > 3 days of pure exhaustion and severe symptoms. To the degree my

>doctor

> > doubled my steroid dose for 3-4 days so I could recover without

>going to the

> > hospitol. Certainly I don't want to scare anyone, but I think it's

> > important to share our expieriences though and my expierience

>is...don't

> > self dose the adrenals...it's dangerous. Hope this helps ....

> >

> > Be well!

> > LaCretia

> >

> > >

> > >

> > >

> > >I started out on just on 25 mcg of Levoxyl and if I had not had

>such

> > >devastating effects from just that tiny amount without adrenal

> > >support, I would not be so paranoid and cautious as I am. Because

>it

> > >did such terrible things to me, I do not want to make light of the

> > >dangers. If the person was older and had been hypo many years and

> > >had developed cardiovascular disease, this sort of self medicating

> > >could cause serious problems and even death in my opinion. So, Ok

>it

> > >is probably rare, but I sure do not want that guilt on my concience

> > >from someone not taking the risks seriously and me making too light

> > >of them.

> > >

> > >Tish

> > >

> > >

> > >

> > >

> > >

> > >

> > >

> > >

[Guest guest]

LOL... I feel your pain Kathy! Especially today! As many know...I'm

weaning off the Cortef and about 2 PM (right about now) I feel the yawn's

beginning...from there I get more and more tired until I just feel like

collasping! All my adrenal fatigue symptoms are coming back due to weaning

off. The only positive thing that I can pull from this at this moment is

the nausea is coming back... that will help me lose that 15lbs I put on

while on Cortef for sure. Hey... you have to find the positive somewhere

right...lol!

LaCretia

>

>

>

>Not to make light of all this, but.... " Just shoot me " .

>

>Kathy

>

>

>

>

>

> > I know some out here think Tish is over exagerating the adrenal

>issue but,

> > join the 's group and you will see why. They will tell you

>it can

> > kill you and will warn you to be extremely careful with any kind of

>steroid

> > treatment. Not to mention nearly everyone on the board has osteo

>due to the

> > steroids robbing their body of calcium. You have pretty severe

>muscle

> > waisting that occurs also when taking steroids. If it were not for

>me

> > spending time listening to other patients on the board, I

>would not

> > have realized just how dangerous it can get. A couple have

>seriously nearly

> > died from not getting enough Cortisone. Like Tish said, it is rare

>but does

> > happen. If you look at 's disease as a whole it is labeled

>a rare

> > disease and there are not that many diagnosed with it vs. thyroid

>patients.

> > I also have been on treatment for adrenal fatigue for a year and I

>can say

> > there were a few times that I thought I would have to go to the

>hospital

> > from it. If you go interview some of the folks on the

>board they

> > will inform you that they will not give you adrenal dosage

>information...the

> > first thing they will emphasize is to get a doctor who KNOWS how to

>treat

> > the adrenals first due to how dangerous it can be. I think Meg on

>the yahoo

> > addisons board can tell you first hand how many times she has

>nearly died

> > due to steroids. Again, it is rare but like Tish said it doesn't

>hurt to

> > provide folks with this information and although rare, it does

>happen. I

> > can say that I have had several close calls where my body burned

>the little

> > 20mg you get so quickly that I went into a hypoglycemic episode

>followed by

> > 3 days of pure exhaustion and severe symptoms. To the degree my

>doctor

> > doubled my steroid dose for 3-4 days so I could recover without

>going to the

> > hospitol. Certainly I don't want to scare anyone, but I think it's

> > important to share our expieriences though and my expierience

>is...don't

> > self dose the adrenals...it's dangerous. Hope this helps ....

> >

> > Be well!

> > LaCretia

> >

> > >

> > >

> > >

> > >I started out on just on 25 mcg of Levoxyl and if I had not had

>such

> > >devastating effects from just that tiny amount without adrenal

> > >support, I would not be so paranoid and cautious as I am. Because

>it

> > >did such terrible things to me, I do not want to make light of the

> > >dangers. If the person was older and had been hypo many years and

> > >had developed cardiovascular disease, this sort of self medicating

> > >could cause serious problems and even death in my opinion. So, Ok

>it

> > >is probably rare, but I sure do not want that guilt on my concience

> > >from someone not taking the risks seriously and me making too light

> > >of them.

> > >

> > >Tish

> > >

> > >

> > >

> > >

> > >

> > >

> > >

> > >

[Guest guest]

That's the way I feel alot even now. I did alittle physical exertion yesterday

and woke this morning at 5:30am with a massive headache. Don't know if it is

adrenal related or thyroid related but if I keep having them one of you nice

ladies can just come round and cut my head off!!! it couldn't feel any worse.

Deb

Re: Deb's experience with needing adrenal

support-- comments

Not to make light of all this, but.... " Just shoot me " .

Kathy

> I know some out here think Tish is over exagerating the adrenal

issue but,

> join the 's group and you will see why. They will tell you

it can

> kill you and will warn you to be extremely careful with any kind of

steroid

> treatment. Not to mention nearly everyone on the board has osteo

due to the

> steroids robbing their body of calcium. You have pretty severe

muscle

> waisting that occurs also when taking steroids. If it were not for

me

> spending time listening to other patients on the board, I

would not

> have realized just how dangerous it can get. A couple have

seriously nearly

> died from not getting enough Cortisone. Like Tish said, it is rare

but does

> happen. If you look at 's disease as a whole it is labeled

a rare

> disease and there are not that many diagnosed with it vs. thyroid

patients.

> I also have been on treatment for adrenal fatigue for a year and I

can say

> there were a few times that I thought I would have to go to the

hospital

> from it. If you go interview some of the folks on the

board they

> will inform you that they will not give you adrenal dosage

information...the

> first thing they will emphasize is to get a doctor who KNOWS how to

treat

> the adrenals first due to how dangerous it can be. I think Meg on

the yahoo

> addisons board can tell you first hand how many times she has

nearly died

> due to steroids. Again, it is rare but like Tish said it doesn't

hurt to

> provide folks with this information and although rare, it does

happen. I

> can say that I have had several close calls where my body burned

the little

> 20mg you get so quickly that I went into a hypoglycemic episode

followed by

> 3 days of pure exhaustion and severe symptoms. To the degree my

doctor

> doubled my steroid dose for 3-4 days so I could recover without

going to the

> hospitol. Certainly I don't want to scare anyone, but I think it's

> important to share our expieriences though and my expierience

is...don't

> self dose the adrenals...it's dangerous. Hope this helps ....

>

> Be well!

> LaCretia

>

> >

> >

> >

> >I started out on just on 25 mcg of Levoxyl and if I had not had

such

> >devastating effects from just that tiny amount without adrenal

> >support, I would not be so paranoid and cautious as I am. Because

it

> >did such terrible things to me, I do not want to make light of the

> >dangers. If the person was older and had been hypo many years and

> >had developed cardiovascular disease, this sort of self medicating

> >could cause serious problems and even death in my opinion. So, Ok

it

> >is probably rare, but I sure do not want that guilt on my concience

> >from someone not taking the risks seriously and me making too light

> >of them.

> >

> >Tish

> >

> >

> >

> >

> >

> >

> >

> >

[Guest guest]

That's the way I feel alot even now. I did alittle physical exertion yesterday

and woke this morning at 5:30am with a massive headache. Don't know if it is

adrenal related or thyroid related but if I keep having them one of you nice

ladies can just come round and cut my head off!!! it couldn't feel any worse.

Deb

Re: Deb's experience with needing adrenal

support-- comments

Not to make light of all this, but.... " Just shoot me " .

Kathy

> I know some out here think Tish is over exagerating the adrenal

issue but,

> join the 's group and you will see why. They will tell you

it can

> kill you and will warn you to be extremely careful with any kind of

steroid

> treatment. Not to mention nearly everyone on the board has osteo

due to the

> steroids robbing their body of calcium. You have pretty severe

muscle

> waisting that occurs also when taking steroids. If it were not for

me

> spending time listening to other patients on the board, I

would not

> have realized just how dangerous it can get. A couple have

seriously nearly

> died from not getting enough Cortisone. Like Tish said, it is rare

but does

> happen. If you look at 's disease as a whole it is labeled

a rare

> disease and there are not that many diagnosed with it vs. thyroid

patients.

> I also have been on treatment for adrenal fatigue for a year and I

can say

> there were a few times that I thought I would have to go to the

hospital

> from it. If you go interview some of the folks on the

board they

> will inform you that they will not give you adrenal dosage

information...the

> first thing they will emphasize is to get a doctor who KNOWS how to

treat

> the adrenals first due to how dangerous it can be. I think Meg on

the yahoo

> addisons board can tell you first hand how many times she has

nearly died

> due to steroids. Again, it is rare but like Tish said it doesn't

hurt to

> provide folks with this information and although rare, it does

happen. I

> can say that I have had several close calls where my body burned

the little

> 20mg you get so quickly that I went into a hypoglycemic episode

followed by

> 3 days of pure exhaustion and severe symptoms. To the degree my

doctor

> doubled my steroid dose for 3-4 days so I could recover without

going to the

> hospitol. Certainly I don't want to scare anyone, but I think it's

> important to share our expieriences though and my expierience

is...don't

> self dose the adrenals...it's dangerous. Hope this helps ....

>

> Be well!

> LaCretia

>

> >

> >

> >

> >I started out on just on 25 mcg of Levoxyl and if I had not had

such

> >devastating effects from just that tiny amount without adrenal

> >support, I would not be so paranoid and cautious as I am. Because

it

> >did such terrible things to me, I do not want to make light of the

> >dangers. If the person was older and had been hypo many years and

> >had developed cardiovascular disease, this sort of self medicating

> >could cause serious problems and even death in my opinion. So, Ok

it

> >is probably rare, but I sure do not want that guilt on my concience

> >from someone not taking the risks seriously and me making too light

> >of them.

> >

> >Tish

> >

> >

> >

> >

> >

> >

> >

> >

[Guest guest]

That's the way I feel alot even now. I did alittle physical exertion yesterday

and woke this morning at 5:30am with a massive headache. Don't know if it is

adrenal related or thyroid related but if I keep having them one of you nice

ladies can just come round and cut my head off!!! it couldn't feel any worse.

Deb

Re: Deb's experience with needing adrenal

support-- comments

Not to make light of all this, but.... " Just shoot me " .

Kathy

> I know some out here think Tish is over exagerating the adrenal

issue but,

> join the 's group and you will see why. They will tell you

it can

> kill you and will warn you to be extremely careful with any kind of

steroid

> treatment. Not to mention nearly everyone on the board has osteo

due to the

> steroids robbing their body of calcium. You have pretty severe

muscle

> waisting that occurs also when taking steroids. If it were not for

me

> spending time listening to other patients on the board, I

would not

> have realized just how dangerous it can get. A couple have

seriously nearly

> died from not getting enough Cortisone. Like Tish said, it is rare

but does

> happen. If you look at 's disease as a whole it is labeled

a rare

> disease and there are not that many diagnosed with it vs. thyroid

patients.

> I also have been on treatment for adrenal fatigue for a year and I

can say

> there were a few times that I thought I would have to go to the

hospital

> from it. If you go interview some of the folks on the

board they

> will inform you that they will not give you adrenal dosage

information...the

> first thing they will emphasize is to get a doctor who KNOWS how to

treat

> the adrenals first due to how dangerous it can be. I think Meg on

the yahoo

> addisons board can tell you first hand how many times she has

nearly died

> due to steroids. Again, it is rare but like Tish said it doesn't

hurt to

> provide folks with this information and although rare, it does

happen. I

> can say that I have had several close calls where my body burned

the little

> 20mg you get so quickly that I went into a hypoglycemic episode

followed by

> 3 days of pure exhaustion and severe symptoms. To the degree my

doctor

> doubled my steroid dose for 3-4 days so I could recover without

going to the

> hospitol. Certainly I don't want to scare anyone, but I think it's

> important to share our expieriences though and my expierience

is...don't

> self dose the adrenals...it's dangerous. Hope this helps ....

>

> Be well!

> LaCretia

>

> >

> >

> >

> >I started out on just on 25 mcg of Levoxyl and if I had not had

such

> >devastating effects from just that tiny amount without adrenal

> >support, I would not be so paranoid and cautious as I am. Because

it

> >did such terrible things to me, I do not want to make light of the

> >dangers. If the person was older and had been hypo many years and

> >had developed cardiovascular disease, this sort of self medicating

> >could cause serious problems and even death in my opinion. So, Ok

it

> >is probably rare, but I sure do not want that guilt on my concience

> >from someone not taking the risks seriously and me making too light

> >of them.

> >

> >Tish

> >

> >

> >

> >

> >

> >

> >

> >

[Guest guest]

*SUGGESTIONS FOR AN*

*APPROACH TO THE*

*MANAGEMENT OF THYROID*

*DEFICIENCY*

by Dr Barry J Durrant-Peatfield

M.B., B.S., LR.C.P., M.RCS.

Approved Civil Aviation Medical Examiner

The clinical syndrome of thyroid deficiency is very much more common

than is generally realized; , 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 myxoedema 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 favor 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 prescribe

anti-depressants. 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 thoughtfully

planned trial of treatment with an informed and cooperative 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 over-activity

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 T4-T3 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, UK)

(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 TSH

Vit B Riboflavin, Niacin, Pyridoxine play a role in thyroid

hormone manufacture.

VitC & VitE - 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, hyperkinesia, 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 recognized, 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 recognized 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 TSH,

so that a vicious spiral may slip into being. The danger of a low or

normal TSH in this situation being misinterpreted 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 over-activity, discussed below. Thyroid cysts,

adenomas or carcinomas are necessarily removed by surgery; and it is

sometimes necessary to remove goiters 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 over-activity, by surgery or I131

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 patients, 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, or

depression is frequently admitted to. Menstrual dysfunction may remain a

feature. Skin problems, fluid retention, digestive problems, or

arthralgia may remain in some degree. Many patients will continue to

complain 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 (Free T4), 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 Free T4 test 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 Free T4 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

under-dose. 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.l 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 tear 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 patient's assessment as the physician*'s 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 her response to treatment. This is satisfactorily done by three

simple exercises.

a. Basal Temperature, this is the temperature (10 mins axillary, or 3

mins 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.

b. Basal Pulse. This may be taken at the same time as temperature;

overdose will result in a rise of the resting pulse. 80 bpm will usually

signify overdose.

c. " Feel good factor " . It is possible to ask the patient 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 she is better.

Considerations will be given to actual dosage shortly.

2. Vehicle. There are three options to choose from.

a. Thyroxin (T4)

b. Tertroxin (T3)

c. Dried, natural thyroid U.S.P

a. In this country (Great Britain), Thyroxin (marketed usually as

Eitroxin--Synthroid in the US), is almost invariably used. Of the

naturally occurring thyroid hormones it is the most plentiful. The

thyroid hormone in the natural state is made up of around 80% Thyroxine

(T4), 15% Triiodothyronine (Tertroxin T3--Cytomel in the US), and 5%

Diiodothyronine (T2),Mono idothyronine (T1), and Thyronine (T0).

Thyroxine has a half-life of 8 days and works fairly 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.

b. Triiodothyronine - (T3) Tertroxin or Cytomel. This is quite

considerably more potent than T4, four or five times so, but unlike T4,

the half life of T3 is about 8 hours.

c. Dried Natural Thyroid. Used from about 1900, desiccated thyroid

fell into disfavour in Great Britain and availability ceased in 1985.

The synthetic Thyroxine (T4) was considered to be a better, purer

preparation. Though, of course, it /is /purer in that it does not

contain the other thyronines. However, *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 some of the load. Natural thyroid is

widely used in USA, as Natural Thyroid U.S.P., but in the UK has to be

specifically imported. *It almost invariably works better than the

synthetic T4*, and is generally preferred by the patient. About half of

the patients in the writer's practice are maintained on this

preparation. (obtained from Gold Line Laboratories, Fort Lauderdale; or

Armour thyroid, from The Foundation, Trumbull, Connecticut).

3. Conversion. Thyroxine (T4) 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 Triiodothyronine (T3) -

available as Tertroxin (Cytomel in the US). This is achieved by the

(largely liver produced), 5'deiodinase 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 that prolonged and/or severe hypothyroidism

may be associated with partial failure of the 5'deiodinase enzyme.

Although suspected, this situation may be diagnosed in default when

failure of response in thyroid replacement occurs*. The effect of

Thyroxine (T4) 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

hypothyroid 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

Free T4 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.

4. 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 levels de-sensitizes the receptors. This will

improve with time, and treatment of any Adrenal insufficiency present.

*5. Adrenal Insufficiency*

This might be more properly described as low adrenal reserve. Since

hypothyroidism adversely affects every cell, every tissue, and 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:*

*a. Longstanding and severe hypothyroidism.*

*b. **Episodes of extreme exhaustion, or collapse.*

*c. **Bad response to minor illness.*

*d. **Multiple allergies.*

*e. **Digestive problems - alternate diarrhea and constipation*

*f. **Flatulence*

*g. **Weight loss*

*h. **Increasing arthralgia (fibromyalgia) and morning stiffness.*

*i. **Pallor, yellow pigmentation (due to poorly metabolized

carotene)*

*j. **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 's Disease.

A single 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--even the thyroid replacement therapy itself

initially. 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; Cortisonehydrocortisone, 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 5mg qds; after a

week, 10 mg 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

inversely proportional to age. It is metabolized 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 Levothyroxine 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 100mg or more

levothyroxine is used, Tertroxin (T3) is added. 10mg for each 100mg of

T4 is to be preferred. 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 (30

mg). (Commensurate with its 100 years of use by the medical profession,

natural thyroid is still measured in grains). Dosage is increased by 1/2

gr. every two weeks; usually by six weeks 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 60mg 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 5mg hydrocortisone qds, and after a week, double the

dose. Alternatively Prednisolone 2.5 mg (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 levothyroxine (T4), but far from well, have to

be considered separately. If the condition is really quite severe, and

increasing thyroxine makes matters worse, it should be stopped for a

short while and cortisone prescribed*. 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; 10 mg for a few days, then 20 mg and so on*. After the

improvement *is seen to be full, and sustained*, natural thyroid can be

reintroduced*. 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 25mg daily,

and men 50mg 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 his 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 patients with prolonged ill health, and the

diagnosis rely on history and examination. *The reliance of the

profession on the pathological tests in favor 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 patients' lives.

*REFERENCES*

1. The Unsuspected Illness. . Harper and Row. 1976

2. . 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: Dec 1996

4. ORD W.M, On Myxoedema, a term proposed to be applied to an

essential 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. & 1976. ROBINSON PRESS. ISSN 0-913730-27-0

7. 7. Interindividual Differences in The Pituitary-Thyroid

Axis Influence The Interpretation Of Thyroid Function Tests. Clinial

endo crinology . 39:101-107:1993

8. 8. Staub et aI. Spectrum Of SubClinical And Overt

Hypothyroidism. American Journal Of Medicine 92: June 1992 pp 631

9. 9. . Temperature v Basal Metabolism. Journal Of

American Medical Association. 119:1072,1942

10. 10. Klause Wenzel. Osteoporosis. Lancet 340 15. 8. 92 pp 435-6

11. 11. Franhyn et al. Long-term Thyroxine treatment and bone

mineral density. Lancet 340 4.7.92

12. 12. Jeffries. W.M. Safe Uses Of Cortisone. C.

. 1981

13. 13. Klinefelter et al. Single Dose Prednisone Therapy.

J.A.M.A. 241 No 25 22.6.79

14. . Etiology And Treatment Of Lowered Resistance To U.R.I.s

Federation Proceedings 12 No I March 1953

FOXLEY LANE CLINIC

86 Foxley Lane,

Purley

Surrey CR8 3EE

U.K.

Copyright © All rights reserved

>

[Guest guest]

*SUGGESTIONS FOR AN*

*APPROACH TO THE*

*MANAGEMENT OF THYROID*

*DEFICIENCY*

by Dr Barry J Durrant-Peatfield

M.B., B.S., LR.C.P., M.RCS.

Approved Civil Aviation Medical Examiner

The clinical syndrome of thyroid deficiency is very much more common

than is generally realized; , 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 myxoedema 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 favor 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 prescribe

anti-depressants. 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 thoughtfully

planned trial of treatment with an informed and cooperative 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 over-activity

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 T4-T3 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, UK)

(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 TSH

Vit B Riboflavin, Niacin, Pyridoxine play a role in thyroid

hormone manufacture.

VitC & VitE - 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, hyperkinesia, 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 recognized, 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 recognized 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 TSH,

so that a vicious spiral may slip into being. The danger of a low or

normal TSH in this situation being misinterpreted 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 over-activity, discussed below. Thyroid cysts,

adenomas or carcinomas are necessarily removed by surgery; and it is

sometimes necessary to remove goiters 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 over-activity, by surgery or I131

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 patients, 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, or

depression is frequently admitted to. Menstrual dysfunction may remain a

feature. Skin problems, fluid retention, digestive problems, or

arthralgia may remain in some degree. Many patients will continue to

complain 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 (Free T4), 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 Free T4 test 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 Free T4 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

under-dose. 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.l 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 tear 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 patient's assessment as the physician*'s 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 her response to treatment. This is satisfactorily done by three

simple exercises.

a. Basal Temperature, this is the temperature (10 mins axillary, or 3

mins 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.

b. Basal Pulse. This may be taken at the same time as temperature;

overdose will result in a rise of the resting pulse. 80 bpm will usually

signify overdose.

c. " Feel good factor " . It is possible to ask the patient 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 she is better.

Considerations will be given to actual dosage shortly.

2. Vehicle. There are three options to choose from.

a. Thyroxin (T4)

b. Tertroxin (T3)

c. Dried, natural thyroid U.S.P

a. In this country (Great Britain), Thyroxin (marketed usually as

Eitroxin--Synthroid in the US), is almost invariably used. Of the

naturally occurring thyroid hormones it is the most plentiful. The

thyroid hormone in the natural state is made up of around 80% Thyroxine

(T4), 15% Triiodothyronine (Tertroxin T3--Cytomel in the US), and 5%

Diiodothyronine (T2),Mono idothyronine (T1), and Thyronine (T0).

Thyroxine has a half-life of 8 days and works fairly 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.

b. Triiodothyronine - (T3) Tertroxin or Cytomel. This is quite

considerably more potent than T4, four or five times so, but unlike T4,

the half life of T3 is about 8 hours.

c. Dried Natural Thyroid. Used from about 1900, desiccated thyroid

fell into disfavour in Great Britain and availability ceased in 1985.

The synthetic Thyroxine (T4) was considered to be a better, purer

preparation. Though, of course, it /is /purer in that it does not

contain the other thyronines. However, *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 some of the load. Natural thyroid is

widely used in USA, as Natural Thyroid U.S.P., but in the UK has to be

specifically imported. *It almost invariably works better than the

synthetic T4*, and is generally preferred by the patient. About half of

the patients in the writer's practice are maintained on this

preparation. (obtained from Gold Line Laboratories, Fort Lauderdale; or

Armour thyroid, from The Foundation, Trumbull, Connecticut).

3. Conversion. Thyroxine (T4) 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 Triiodothyronine (T3) -

available as Tertroxin (Cytomel in the US). This is achieved by the

(largely liver produced), 5'deiodinase 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 that prolonged and/or severe hypothyroidism

may be associated with partial failure of the 5'deiodinase enzyme.

Although suspected, this situation may be diagnosed in default when

failure of response in thyroid replacement occurs*. The effect of

Thyroxine (T4) 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

hypothyroid 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

Free T4 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.

4. 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 levels de-sensitizes the receptors. This will

improve with time, and treatment of any Adrenal insufficiency present.

*5. Adrenal Insufficiency*

This might be more properly described as low adrenal reserve. Since

hypothyroidism adversely affects every cell, every tissue, and 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:*

*a. Longstanding and severe hypothyroidism.*

*b. **Episodes of extreme exhaustion, or collapse.*

*c. **Bad response to minor illness.*

*d. **Multiple allergies.*

*e. **Digestive problems - alternate diarrhea and constipation*

*f. **Flatulence*

*g. **Weight loss*

*h. **Increasing arthralgia (fibromyalgia) and morning stiffness.*

*i. **Pallor, yellow pigmentation (due to poorly metabolized

carotene)*

*j. **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 's Disease.

A single 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--even the thyroid replacement therapy itself

initially. 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; Cortisonehydrocortisone, 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 5mg qds; after a

week, 10 mg 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

inversely proportional to age. It is metabolized 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 Levothyroxine 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 100mg or more

levothyroxine is used, Tertroxin (T3) is added. 10mg for each 100mg of

T4 is to be preferred. 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 (30

mg). (Commensurate with its 100 years of use by the medical profession,

natural thyroid is still measured in grains). Dosage is increased by 1/2

gr. every two weeks; usually by six weeks 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 60mg 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 5mg hydrocortisone qds, and after a week, double the

dose. Alternatively Prednisolone 2.5 mg (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 levothyroxine (T4), but far from well, have to

be considered separately. If the condition is really quite severe, and

increasing thyroxine makes matters worse, it should be stopped for a

short while and cortisone prescribed*. 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; 10 mg for a few days, then 20 mg and so on*. After the

improvement *is seen to be full, and sustained*, natural thyroid can be

reintroduced*. 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 25mg daily,

and men 50mg 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 his 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 patients with prolonged ill health, and the

diagnosis rely on history and examination. *The reliance of the

profession on the pathological tests in favor 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 patients' lives.

*REFERENCES*

1. The Unsuspected Illness. . Harper and Row. 1976

2. . 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: Dec 1996

4. ORD W.M, On Myxoedema, a term proposed to be applied to an

essential 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. & 1976. ROBINSON PRESS. ISSN 0-913730-27-0

7. 7. Interindividual Differences in The Pituitary-Thyroid

Axis Influence The Interpretation Of Thyroid Function Tests. Clinial

endo crinology . 39:101-107:1993

8. 8. Staub et aI. Spectrum Of SubClinical And Overt

Hypothyroidism. American Journal Of Medicine 92: June 1992 pp 631

9. 9. . Temperature v Basal Metabolism. Journal Of

American Medical Association. 119:1072,1942

10. 10. Klause Wenzel. Osteoporosis. Lancet 340 15. 8. 92 pp 435-6

11. 11. Franhyn et al. Long-term Thyroxine treatment and bone

mineral density. Lancet 340 4.7.92

12. 12. Jeffries. W.M. Safe Uses Of Cortisone. C.

. 1981

13. 13. Klinefelter et al. Single Dose Prednisone Therapy.

J.A.M.A. 241 No 25 22.6.79

14. . Etiology And Treatment Of Lowered Resistance To U.R.I.s

Federation Proceedings 12 No I March 1953

FOXLEY LANE CLINIC

86 Foxley Lane,

Purley

Surrey CR8 3EE

U.K.

Copyright © All rights reserved

>

[Guest guest]

*SUGGESTIONS FOR AN*

*APPROACH TO THE*

*MANAGEMENT OF THYROID*

*DEFICIENCY*

by Dr Barry J Durrant-Peatfield

M.B., B.S., LR.C.P., M.RCS.

Approved Civil Aviation Medical Examiner

The clinical syndrome of thyroid deficiency is very much more common

than is generally realized; , 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 myxoedema 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 favor 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 prescribe

anti-depressants. 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 thoughtfully

planned trial of treatment with an informed and cooperative 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 over-activity

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 T4-T3 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, UK)

(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 TSH

Vit B Riboflavin, Niacin, Pyridoxine play a role in thyroid

hormone manufacture.

VitC & VitE - 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, hyperkinesia, 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 recognized, 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 recognized 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 TSH,

so that a vicious spiral may slip into being. The danger of a low or

normal TSH in this situation being misinterpreted 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 over-activity, discussed below. Thyroid cysts,

adenomas or carcinomas are necessarily removed by surgery; and it is

sometimes necessary to remove goiters 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 over-activity, by surgery or I131

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 patients, 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, or

depression is frequently admitted to. Menstrual dysfunction may remain a

feature. Skin problems, fluid retention, digestive problems, or

arthralgia may remain in some degree. Many patients will continue to

complain 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 (Free T4), 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 Free T4 test 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 Free T4 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

under-dose. 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.l 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 tear 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 patient's assessment as the physician*'s 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 her response to treatment. This is satisfactorily done by three

simple exercises.

a. Basal Temperature, this is the temperature (10 mins axillary, or 3

mins 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.

b. Basal Pulse. This may be taken at the same time as temperature;

overdose will result in a rise of the resting pulse. 80 bpm will usually

signify overdose.

c. " Feel good factor " . It is possible to ask the patient 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 she is better.

Considerations will be given to actual dosage shortly.

2. Vehicle. There are three options to choose from.

a. Thyroxin (T4)

b. Tertroxin (T3)

c. Dried, natural thyroid U.S.P

a. In this country (Great Britain), Thyroxin (marketed usually as

Eitroxin--Synthroid in the US), is almost invariably used. Of the

naturally occurring thyroid hormones it is the most plentiful. The

thyroid hormone in the natural state is made up of around 80% Thyroxine

(T4), 15% Triiodothyronine (Tertroxin T3--Cytomel in the US), and 5%

Diiodothyronine (T2),Mono idothyronine (T1), and Thyronine (T0).

Thyroxine has a half-life of 8 days and works fairly 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.

b. Triiodothyronine - (T3) Tertroxin or Cytomel. This is quite

considerably more potent than T4, four or five times so, but unlike T4,

the half life of T3 is about 8 hours.

c. Dried Natural Thyroid. Used from about 1900, desiccated thyroid

fell into disfavour in Great Britain and availability ceased in 1985.

The synthetic Thyroxine (T4) was considered to be a better, purer

preparation. Though, of course, it /is /purer in that it does not

contain the other thyronines. However, *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 some of the load. Natural thyroid is

widely used in USA, as Natural Thyroid U.S.P., but in the UK has to be

specifically imported. *It almost invariably works better than the

synthetic T4*, and is generally preferred by the patient. About half of

the patients in the writer's practice are maintained on this

preparation. (obtained from Gold Line Laboratories, Fort Lauderdale; or

Armour thyroid, from The Foundation, Trumbull, Connecticut).

3. Conversion. Thyroxine (T4) 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 Triiodothyronine (T3) -

available as Tertroxin (Cytomel in the US). This is achieved by the

(largely liver produced), 5'deiodinase 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 that prolonged and/or severe hypothyroidism

may be associated with partial failure of the 5'deiodinase enzyme.

Although suspected, this situation may be diagnosed in default when

failure of response in thyroid replacement occurs*. The effect of

Thyroxine (T4) 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

hypothyroid 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

Free T4 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.

4. 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 levels de-sensitizes the receptors. This will

improve with time, and treatment of any Adrenal insufficiency present.

*5. Adrenal Insufficiency*

This might be more properly described as low adrenal reserve. Since

hypothyroidism adversely affects every cell, every tissue, and 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:*

*a. Longstanding and severe hypothyroidism.*

*b. **Episodes of extreme exhaustion, or collapse.*

*c. **Bad response to minor illness.*

*d. **Multiple allergies.*

*e. **Digestive problems - alternate diarrhea and constipation*

*f. **Flatulence*

*g. **Weight loss*

*h. **Increasing arthralgia (fibromyalgia) and morning stiffness.*

*i. **Pallor, yellow pigmentation (due to poorly metabolized

carotene)*

*j. **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 's Disease.

A single 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--even the thyroid replacement therapy itself

initially. 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; Cortisonehydrocortisone, 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 5mg qds; after a

week, 10 mg 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

inversely proportional to age. It is metabolized 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 Levothyroxine 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 100mg or more

levothyroxine is used, Tertroxin (T3) is added. 10mg for each 100mg of

T4 is to be preferred. 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 (30

mg). (Commensurate with its 100 years of use by the medical profession,

natural thyroid is still measured in grains). Dosage is increased by 1/2

gr. every two weeks; usually by six weeks 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 60mg 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 5mg hydrocortisone qds, and after a week, double the

dose. Alternatively Prednisolone 2.5 mg (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 levothyroxine (T4), but far from well, have to

be considered separately. If the condition is really quite severe, and

increasing thyroxine makes matters worse, it should be stopped for a

short while and cortisone prescribed*. 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; 10 mg for a few days, then 20 mg and so on*. After the

improvement *is seen to be full, and sustained*, natural thyroid can be

reintroduced*. 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 25mg daily,

and men 50mg 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 his 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 patients with prolonged ill health, and the

diagnosis rely on history and examination. *The reliance of the

profession on the pathological tests in favor 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 patients' lives.

*REFERENCES*

1. The Unsuspected Illness. . Harper and Row. 1976

2. . 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: Dec 1996

4. ORD W.M, On Myxoedema, a term proposed to be applied to an

essential 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. & 1976. ROBINSON PRESS. ISSN 0-913730-27-0

7. 7. Interindividual Differences in The Pituitary-Thyroid

Axis Influence The Interpretation Of Thyroid Function Tests. Clinial

endo crinology . 39:101-107:1993

8. 8. Staub et aI. Spectrum Of SubClinical And Overt

Hypothyroidism. American Journal Of Medicine 92: June 1992 pp 631

9. 9. . Temperature v Basal Metabolism. Journal Of

American Medical Association. 119:1072,1942

10. 10. Klause Wenzel. Osteoporosis. Lancet 340 15. 8. 92 pp 435-6

11. 11. Franhyn et al. Long-term Thyroxine treatment and bone

mineral density. Lancet 340 4.7.92

12. 12. Jeffries. W.M. Safe Uses Of Cortisone. C.

. 1981

13. 13. Klinefelter et al. Single Dose Prednisone Therapy.

J.A.M.A. 241 No 25 22.6.79

14. . Etiology And Treatment Of Lowered Resistance To U.R.I.s

Federation Proceedings 12 No I March 1953

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