Re: New to list and feel like hell....

March 8, 2005

Colleen,

The results that have been given to you are printed in a very

confusing fashion.

What the report is trying to say is that you have an ANA or 1:80 with

a speckled pattern. That is sort of a borderline titre that can

sometimes mean the start of an autoimmune disease - sometimes it does

not mean anything at all. It depends on your age, if you had a viral

infections, etc. at the time.

The speckled pattern that is reported is quite common. In high

titres, it can be an antibody to RNP (indicative of mixed connective

disease) or Sm (indicative of SLE) or SS-A/Ro or SS-B/La (indicative

of Sjogren's syndrome. The doctor would have to order tests to

further identify the antibody. Not all labs do additional

identification, he may have to find a lab specializing in testing for

autoimmune disorders. I managed such a lab for 17 years - not in that

area of research any more however.

The ANA by itself is not diagostic of anything. If your symptoms and

the ANA both point in the same direction, then the ANA can support a

diagnosis.

I hope that helps -

Winona

wrote:

> If anyone here can understand this, the following also came back in

my bloodwork:

>

> ANA SCR.....Borderline

> Result Comment:

> ANA TITER....1:80

> ANA PATTERN...Speckled

> Interpretations:

> REFERENCE RANGE

> Negative: <=1:40 TITER

> Borderline =1:80 TITER

> Positive: >=1:160 TITER

>

> INTERPRETATION:

>

> Pattern: Homogenous (Smooth); Antigen Detected: DNA (DSS, SS,N),

> Histone; Suggested Disease Association: High Titers - SLE

>

> Speckled: Antigen Detected: SM, RNP, SCL-70, SS-A/SS-B; Suggested

> Disease Association: SLE, MCTD, Scleroderma, Sjogrens

>

> Nucleolar: Antigen Detected: SCL-70, PM-1/SCL; Suggested Disease

> Association: High Titers

> Scleroderma

>

> Cemtromere: Antigen Detected: Centromere; Suggested Disease

> Association: PSS w/Crest Syndrome Variable

>

> DNA AB (EIA)... 19

>

> ~~~~~~~~~~~~~~~~~~~~~~~~~~~

>

> My question to all that, it appears to me that I am in the beginning

> stages of Scleroderma. Does it to you, as well? If so, I'm headed

> back to the doctor to find out why none of this was explained to me

at my last appointment.

March 8, 2005

Colleen,

The results that have been given to you are printed in a very

confusing fashion.

What the report is trying to say is that you have an ANA or 1:80 with

a speckled pattern. That is sort of a borderline titre that can

sometimes mean the start of an autoimmune disease - sometimes it does

not mean anything at all. It depends on your age, if you had a viral

infections, etc. at the time.

The speckled pattern that is reported is quite common. In high

titres, it can be an antibody to RNP (indicative of mixed connective

disease) or Sm (indicative of SLE) or SS-A/Ro or SS-B/La (indicative

of Sjogren's syndrome. The doctor would have to order tests to

further identify the antibody. Not all labs do additional

identification, he may have to find a lab specializing in testing for

autoimmune disorders. I managed such a lab for 17 years - not in that

area of research any more however.

The ANA by itself is not diagostic of anything. If your symptoms and

the ANA both point in the same direction, then the ANA can support a

diagnosis.

I hope that helps -

Winona

wrote:

> If anyone here can understand this, the following also came back in

my bloodwork:

>

> ANA SCR.....Borderline

> Result Comment:

> ANA TITER....1:80

> ANA PATTERN...Speckled

> Interpretations:

> REFERENCE RANGE

> Negative: <=1:40 TITER

> Borderline =1:80 TITER

> Positive: >=1:160 TITER

>

> INTERPRETATION:

>

> Pattern: Homogenous (Smooth); Antigen Detected: DNA (DSS, SS,N),

> Histone; Suggested Disease Association: High Titers - SLE

>

> Speckled: Antigen Detected: SM, RNP, SCL-70, SS-A/SS-B; Suggested

> Disease Association: SLE, MCTD, Scleroderma, Sjogrens

>

> Nucleolar: Antigen Detected: SCL-70, PM-1/SCL; Suggested Disease

> Association: High Titers

> Scleroderma

>

> Cemtromere: Antigen Detected: Centromere; Suggested Disease

> Association: PSS w/Crest Syndrome Variable

>

> DNA AB (EIA)... 19

>

> ~~~~~~~~~~~~~~~~~~~~~~~~~~~

>

> My question to all that, it appears to me that I am in the beginning

> stages of Scleroderma. Does it to you, as well? If so, I'm headed

> back to the doctor to find out why none of this was explained to me

at my last appointment.

March 9, 2005

I'm currently on 100 mcg Synthroid and back it up with 200 mcg

> Selinium in an effort to help the T4 convert to T3.

________________________________

I think your dose is far to low for you. You probably need 200 mcg

minimum. (See studies below.) Selinium is a good thing, but I don't

think it increases conversion unless you are deficient in the first

place. You might try night time melatonin. this is known to increase

conversion. The trouble with increasing conversion when your dose is

far too low is that you will deplete the T4 and still have hypo

symptoms because it is still not enough for you. However, if you

deplete T4, maybe this will raise TSH and get your doctor to

increase your dose.

_________________________________

> I have TED, rotting teeth, huge weight gain and of course, the

brittle

> nails and brain fog. These are the worst of the symptoms, though

> there are many more.

_______________________

Typical low thyroid symptoms and looks like mineral disturbances

from low thyroid and low adrenal.

________________________

>

> My last blood screen showed:

>

> FT4 1.67 [0.80-1.90]

> TSH sensitive 0.798 [0.400-4.000]

_________________________

These are pretty unhelpful. Since T4 is inactive, it doesn't help

you know if it's being converted well or where T3 the level of is.

T3 is the major one that does all the work. Typically, Synthroid

users have T4 that is higher with respect to T3. So, I'd be willing

to bet your free T3 levels are below the midline. I don't know

anybody who feels good with T3 down there. TSH is meaningless in my

book. Once people start on thyroid, TSH is overly suppressed by T4

meds most of the time. It has no correlation to your true status.

The TSH test is an the verge of being discredited. Many studies are

finding that it has no relationship to the health of thepatient.

________________________

> At the time of this last test (4 Jan) I was taking 112 mcg

Synthroid,

> but as of that day (2 March) am now on 100 mcg.

________________________

Let me guess, your idiot doctor is treating your TSH and not your

hypothryoidism.

______________________

>

> My eyes... oh, my eyes are currently my most major complaint.

> Extremely sensitivity to light, at this point I'd rather go to the

> dentist for a root canal than go to the neuro-opthalmologist to

have

> my eyes checked. I'm on 300mg 3x daily.

_________________________

I'm not sure what you are on at 300 mg 3x a day - a cortiosne? But,

sensitivity to light is a classic sign of adrenal hypfunction and

low cortisone levels. Adrenal hypofunction or adrenal fatigue is a

result of inadequate thyroid levels for a long time. The adrenals

need sufficient thyroid to work properly and be be the proper size

and to have enough hormones for stress and illness. Do a google

search ont he term " adrenal fatigue " or " adrenal hypofunction " When

the adrenals are not functioning right due to insufficient thyroid,

the pupils in the eyes cannot restrict properly in bright light and

basically, they have no defense against blocking excess light. You

can chek this yourself by shining a light in your eyes and watching

your pupils for about a minute. If they constrict for a bit and then

open back up or flutter in an attempt to constrict, this is a sign

of low cortosol or cortisone levels. Another test for adrenal

fatigue and low coetisone levels is to lie down and take your blood

pressure. Then stand up and take it again. If your blood pressure

drops when you stand, this means there is insufficient cortisol from

the adrenals. In this situation you will have very little capacity

for stress, poor immune function, pooling of blood in the abdomen

and lower extremities, hypoglycemia, maybe palipitations, mineral

disturbances such as high blood levels of calcium but leaching out

of the bones and teeth, excercise intolerance and on and on. The

adrenals play so many roles in the body that the symptoms of

insufficiency are many.

_________________________

>

> ANA SCR.....Borderline

> Result Comment:

> ANA TITER....1:80

> ANA PATTERN...Speckled

> Interpretations:

> REFERENCE RANGE

> Negative: <=1:40 TITER

> Borderline =1:80 TITER

> Positive: >=1:160 TITE

>

> INTERPRETATION:

>

> Pattern: Homogenous (Smooth); Antigen Detected: DNA (DSS, SS,N),

> Histone; Suggested Disease Association: High Titers - SLE

>

> Speckled: Antigen Detected: SM, RNP, SCL-70, SS-A/SS-B; Suggested

> Disease Association: SLE, MCTD, Scleroderma, Sjogrens

>

> Nucleolar: Antigen Detected: SCL-70, PM-1/SCL; Suggested Disease

> Association: High Titers

> Scleroderma

>

> Cemtromere: Antigen Detected: Centromere; Suggested Disease

> Association: PSS w/Crest Syndrome Variable

>

> DNA AB (EIA)... 19

__________________________

I think they are searching for other causes of you not feeling well.

Scleroderma and Rhumatoid arthritis are improved by proper thyroid

treatment and I have a feeling that the symptoms they want to

associate with these conditions are really mostly low thyroid.

Rhumatoid arthritis and Scleroderma have been associated with

hypothyroidism.

________________________

> My question to all that, it appears to me that I am in the

beginning

> stages of Scleroderma.

_________________________

I'd be willing to guess that this will greatly deminish or go away

if you were on enough thyroid so that your immune system could work

properly, since this is an auto-immune condition. There have been

cases of auto-immune diseases that stop in their tracks from proper

thyroid treatment.

_________________________

This is my opinion: You need to be on at least 3 grains of Armour

and I think your whole life would turn around. After all, most of

these problems started after the thyroid treatment with RAI.

You need to be able to adjust your thyroid dose to where you feel

best. It could be anywhere from 3 to 5 grains or more. To find out

for yourself if you are undertreated and I bet you sure are:

http://www.drrind.com/tempgraph.asp

http://www.thyrophoenix.com/self_monitor.htm

http://www.alternate-health.com/thyroid.html

I think you need to find a new doctor. Not and endocrinologist, but

a holistic, anti-aging or other natural hormone doctor, who will

adjust thryoid by symptoms not your TSH. This was how thyroid was

adjusted for over 75 years before the TSH test came along. I think

this will allow your immune system to work properly and help you

with whatever is beginning to happen.

Tish

Here are some extracts of books and papers:

_________________________

Personal correspondence from DR. Derry to Edna Kyrie of

http://www.thyroidhistory.net

Dear Edna

The statement by C.P. Lalonde in 1948 review: " When thyroxine is

administered to a thyroidectomized or myxedematous patient, it takes

250 -350 micrograms (mcg) of thyroxine (3.4 grains to 4.7 grains) to

maintain a normal metabolism.

( et al, 1935, Means, 1937) "

C. P. Leblond. Iodine metabolism. Advanc Biol Med Phys 1:353-386,

1948.

It does not say but I believe they gave it intravenously because it

is so badly absorbed orally. But IV thyroxine works well.

_______________________

Author: Dr PBS Fowler

Date Published: 23-May-2001

Publication: Lancet 2001; 357: 619-24. Volume 357,

Number 9273 23 June 2001

Title: Letter in response to Colin Dayan's article '

Interpretation of thyroid function tests'.

Before the days of hormone assays, hypothyroid patients

received about double the average dose of thyroxine

given today, but did not develop osteoporosis or atrial

fibrillation. Doses should be judged clinically rather

than be governed by misinterpreted hormone results.

P B S Fowler

1 Dayan CM. Interpretation of thyroid function tests.

Lancet 2001; 357: 619-24.

________________________

From " Thyroid Guardian of Health " by G. Young

It is an important guidline in that if individuals are placed on and

excessive dose of thyroid hormone, the temperature should become

elevated within two weeks time. However, if the thyroid feedback

mechanisms are working properly it is impossible to make and

individual hyperthyroid untill they are given more thyroid that the

gland produces--about 4-1/2 grains (333mcg synthroid) for a small

individual and about

5 grains (370 mcg synthroid) for the usual adult. Their basal

temperature should rise up

over 98.2 deg F if they are truely hyperthyroid, and thus have too

much thyroid hormone. The pulse is important as well; a slow pulse

is typical of pure low thyroid condition. With low adrenal function,

the pulse speeds up and the rapid pulse may indicate inadequate

adrenal support. The blood pressure is also an important guid line.

A blood pressure with a systolic below one hundred indicates

inadequate adrenal support......

Some authorities believe that if autoantibodies are present, it

renders other thyroid testing invalid.

Clinical symptoms remain the best indicator of adequate dosage.

________________________

Prognosis and treatment of COMMON THYROID DISEASES

Proceedings of a Symposium held in San Francisco,

California, U.S.A. - G March 1970

Editors : HERBERT A. SELENKOW AND FREDRIC HOFFMAN

Thus, in the average patient requiring 280 mcg T4 daily (3.7 grains),

190 mcg (3 grains) are absorbed. Of this, 90-100 mcg replaces the T4

normally secreted daily

and the remainder provides the physiological equivalent of normal T3

secretion.

______________

(This article shows that people got no response to thyroid hormone

at doses less than 3-5 grains natural thyroid or 220 to 370 mcg

synthroid)

Author: MONTE A. GREER, M.D.

Date Published: 15-Mar-1951

Publication: The New England Journal of Medicine Volume 244 MARCH

15, 1951 Number 11

Title: THE EFFECT ON ENDOGENOUS THYROID ACTIVITY OF FEEDING

DESICCATED THYROID TO NORMAL HUMAN SUBJECTS

Category: research

Keywords: research, GREER, EFFECT, ENDOGENOUS, THYROID, ACTIVITY,

FEED, DESICCATED, NORMAL, HUMAN, SUBJECT, circulating, thyroxin,

thyrotrophin, radio, iodine, index, therapeutic, accurate, euthyroid

Text: 388

IT HAS been known for many years that a reciprocal relation appears

to exist between the levels of circulating thyroxin and thyrotrophin

in the vertebrate species so far investigated, Until recently,

however, direct tests of thyroid actiyity in man have not been

feasible. Within the last few years, radioactive iodine has provided

a new method .for the study of thyroid function, permitting

observations that would otherwise be impossible.

Using shielded G-M counters, it is possible to follow directly the

accumulation of radioiodine in the thyroid gland. Studies in several

clinics have indicated that this method is an accurate index of

thyroid function.

In view of the widespread therapeutic use of thyroid medication, it

was of interest to determine whether the administration of

physiologic amounts of the hormone to man would produce the same

compensatory depression of the thyroid gland as that observed in

laboratory animals. Previous investigators, using other measures of

thyroid function, have observed that the thyroid gland is depressed

by thyroid feeding. Farquharson and Squiresl found that the

administration of moderate doses of desiccated thyroid to apparently

euthyroid " hypometabolic " subjects produced no appreciable elevation

of the initially low basal metabolic rate. On the contrary, when

thyroid medication was stopped, the basal metabolic rate fell

rapidly below the pretreatment level and remained depressed for

several weeks before gradually rising up the initial level. Riggs

and his co-workers2 administered gradually increasing amounts of

thyroid up to 20 to 25 gr. dally to euthyroid subjects. It was found

that both the basal metabolic rate and the serum-precipitable iodine

remained relatively constant until daily doses in excess of 3 to 5

gr. (22o to 370mcg synthroid) were given, when both. indices of

thyroid activity began to rise

co-comltantly. When the admmlstratlon of thyroId was abruptly

stopped, the basal metabolic rate and serum-precipitable iodine fell

abruptly, but transiently, to abnorncally low levels, indicating an

inhibition of endogenous hormone production and a delayed return to

normal thyroid function.

The present investigation was designed primarily to determine how

rapidly depression of the normal human thyroid gland occurs after

the institution of daily physiologic doses of thyroid hormone, how

much hormone is required daily to produce complete depression of the

thyroid and how rapidly recovery of thyroid activity occurs after

the cessation of therapy.

MATERIALS AND METHODS

Fortv-seven normal human volunteers, consisting chiefly of

laboratory technicians, physicians and nurses, were employed. They

were between 17 and 67 years of age, and all but three were women.

All were clinically euthyroid so far as could be determined,

although basal metabolic rates were obtained in only a few

instances. About one fourth of the subjects had taken thyroid

previously at one time or another; three had stopped the hormone

only a few weeks before beginning the. experiment. Four had been

taking 3 or more grams (220 mcg synthroid) daily for several years,

the initial study of

all but one of these being made while they were still taking the

hormone.

Studies with radioactive iodine were made wIth a modification of the

technic devIsed by Astwood and Stanley.3 The isotope with an eight

day half-life, I131, was used. Following the admistratlon of a 50-

microcurie tracer dose of I13l, serIal counts were made over the

thyroid gland by means of an externally placed shieided gamma

counter. Since the 24-hour uptake had been found to be as relIable

as any index of thyroid function determined by eans of I131 only

this measurement was used. The Il31 was obtained from Oak RIdge; the

standardization made at that laboratory before shipment was

accepted. An amount of radic:active iodine approximating 50

microcuries. was pipetted into a 50-cc. Erlenmeyer flask and diluted

wIth 15 to 20 ml. of tap water. The flask was then placed in front

of the shielded gamma counter, and the absolute quantity of

radioactivity determined. The distance of the flask from the end of

the gamma tube was measured by a ruled steel slide, at the edge of

the shielding, which was connected to a thin

389

thyroid function, although without clinical evidence of

hypothyroidism, was associated with normal levels of circulating

thyroxin.

It is interesting that subjects who had been taking desiccated

thyroid for several years showed as rapid a return of thyroid

function as did those subjects who had been taking the drug only a

few days. This strongly indicates that chronic depression of the

thyroid gland produces no permanent injury. One other interesting

feature is that a " rebound " phenomenon seems concomitant with the

return of the depressed thyroid glands to normal. This was

especially evident in the continuously treated subjects,; two had

uptakes higher than 50 per cent in the first swing of recovery,

which subsequently dropped below this level. Uptakes of from 50 to

75 per cent have been observed in 5 other patients after withdrawal

of thyroid hormone, which they had been taking for several years,

but these were not included in the present study because only a

single determination of their thyroid function was made. This

rebound is presumably due to a lag in the adjustment of pituitary

thyrotrophin production.

The depressed pituitary may be stimulated to increased secretion of

thyrotrophin as the level of circulating thyroxin falls upon

cessation of therapy. However, there is perhaps a certain lag before

the pituitary again becomes inhibited by increased endogenous

thyroid secretion, the thyroid gland thus becoming overstimulated.

This same type of delayed readjustment is probably responsible for

the fall in basal metabolic rate and serum-precipitable iodine seen

after the withdrawal of exogenous thyroid. It is possible that the

occasional case of thyrotoxicosis seen to develop upon the

withdrawal of thyroid medication from euthyroid patients may be

partially explained on this basis.

.....

The data presented indicate that the administration of exogenous

thyroid hormone results in a corresponding depression of endogenous

thyroid function, whatever the mechanism by which this is produced.

Since it has been found that the serum-precipitable iodine and the

basal metabolic rate do not rise in normal subjects unless thyroid

in excess of 3 to 5 grains (220 to 370mcg syntroid) daily is given,

it seems reasonable to

assume that astable euthyroid level of circulating thyroxin is

maintained by a depression of endogenous hormone formation

equivalent to the amount administered. This stable level is probably

maintained through pituitary regulation.

The administration of small doses of thyroid to normal patients for

the control of obesity, menstrual disturbances, " fatigue " and so

forth would thus seem to be without reason or promise of therapeutic

effect, since excessive amounts would be required before any

elevation of the levels of circulating thyroxin and basal metabolic

rate could be produced. The doses commonly administered for these

disorders are certainly below what would be considered toxic levels,

and the only effect to be expected would be a compensatory

depression of endogenous thyroid activity. The disappointing

experiences of clinicians in their attempts to treat apparently

euthyroid patients for such disorders are thus readily explained.

The occasional patient who complains of symptoms of hyperthyroidism

while taking only 3 to 4 grains of thyroid daily may represent those

persons whose thyroid glands become markedly depressed by the

exhibition of 1 gr. or less of hormone daily. Three grains would

thus be

390

three times their daily requirements; this might possibly give rise

to symptoms of overdosage.

It is of interest to consider the " increased sensitivity " of

myxedematous patients to exogenous thyroid hormone. This supposition

seems to have existed since the days of the first successful

treatment with thyroid extract of patients with Gull's Disease. So

far as the author is aware, no evidence has been published that

establishes any difference in the tissue susceptibility to thyroid

hormone of euthyroid subjects from that of myxedematous subjects.

It is frequently stated that myxedematous patients show signs and

symptoms of " toxicity " at lower dosage levels than do those with

normal thyroid glands, but adequate data supporting this statement

have never been presented. There is no question that small doses of

hormone have a much greater effect in raising the basal metabolic

rate and relieving the evidences of hypothyroidism in myxedematous

than in euthyroid-patients. This is readily explained by the

necessity for first equaling endogenous hormone production before

any elevation of the basal metabolic rate can be produced in normal

subjects. Riggs and his co-workers2 seem to be correct in assuming

that the failure of the serum-precipitable iodine to rise until 3 to

5 grains of thyroid were administered daily to normal subjects was

due to the necessity of first depressing endogenous thyroid

activity. However, they stated that this did not adequately explain

the differences between the two groups, since hypothyroid patients

became " toxic " on such low doses that they could not obtain data

equivalent to that on euthyroid patients who took large doses. They

suggested that the thyroid gland in intact patients is capable

of " breaking down " thyroid hormone, an explanation that seems

unlikely in view of the evidence of Leblond and Sue7 that the

thyroid gland is incapable of concentrating organically bound,

iodine and that it is only when the element is available as

inorganic iodide that accumulation is possible.

Certainly the evidence presented by Riggs2. 8 indicated little

difference in the responses of subjects with and without thyroid

glands, since the basal metabolic rate increased as much for an

equivalent rise in serum-precipitable iodine in normal persons as in

those with myxedema.

As gradually increasing doses of thyroid are given to patients with

myxedema, there is a progressively diminishing augmentation of the

basal metabolic rate as it approaches normal. Thus, 1 grain of

thyroid taken daily will produce a much greater increment in the

basal metabolic rate of an untreated myxedematous patient with a

basal metabolic rate of -30 per cent than it will in a myxedematous

patient already being treated with 1 grain daily who has a basal

metabolic rate of -10 per cent. If the basal metabolic rate is

plotted against the dose of thyroid given in myxedematous patients,

a curve is seen that approaches a plateau as the metabolism returns

to normal.9 It seens quite possible that if this curve were extended

and thyroid given in doses equivalent to the 5 to 25 gr.

administered by Riggs to normal subjects, no difference would be

found between subjects with and those without thyroid glands. It

would be expeeted that much larger doses of thyroid would be

required to produce an equivalent rise of the metabolic rate if the

subject were near the euthyroid level before treatment was begun.

Such has in fact been found to be the case in investigations of

intact subjects.

SUMMARY

The effect of exogenous thyroid hormone on the endogenous thyroid

function of 47 normal human subjects has been investigated with the

use of radio-active iodine. Marked depression of the subject's

thyroid gland could be produced within one week by the

administration of adequate daily physiologic doses of hormone. The

daily amount of hormone required to produce marked thyroid

depression was between land 3 grains in 93 per cent of those

studied, although one girl required 9 grains. After the withdrawal

of therapy, thyroid function returned to normal in most subjects

within two weeks, although a few subjects showed depression for six

to eleven weeks. Thyroid function returned as rapidly in those

subjects whose glands had been depressed by several years of thyroid

medication as it did in those whose glands had been depressed for

only a few days. Thus no permanent injury to the thyroid gland seems

to be produced by long-continued hormone administration. It is felt

that the reduction in endogenous thyroid function was brought about

through a depression of pituitary thyrotrophin secretion. It is

suggested that no important difference in sensitivity to thyroid

hormone exists between athyreotic and intact subjects.

REFERENCES

I. Farquharson, R. F., and Squires. A. H. Inhibition of secretion of

thyroid gland by continued ingestion of thyroid substance. Tr. Am.

Physicians 56:87-97, 1941.

2. Riggs, D. S.. Man, E. B., and Winkier, A. W. Serum iodine of

euthyraid subjects treated with desiccated thyroid. j. Clin.

lnvestigalion 24:722-731, 1945.

3. Astwood. E. B., and Stanley, M. M. Use of radioactive iodine a

study of thyroid function in man. West. j. Surg. 55:625-639. 1947.

4. Cortell. R., and Rawson, R. W. Effect of thyroxin On response of

thyroid gland to thy,otropic hormone. Endocrina/ogy 35:488-498. 1944.

5. Stanley, M. M.. and Astwood, E. B. Response of thyroid gland in

normal human subjects to administration of thyrotropin, as shown by

Studies with II " . Endocrinology 44:49-60. 1949.

6. Stanley, M. M. Direct estimation of rate of thyroid ho,mone

formation in man: effect of iodide ion on thyroid iodine

utilization. j. C/in Endocrino/. 9:941-954, 1949.

7. Le blond, C. P., and Siie, P. Iodine fluctation in thyroid as

influenced by hypophysis and ulher factors. Am. j. Physiol. 134:549-

561, 1941.

8. Winkier, A. W., Riggs, D. S., and Man. E. B. Serum iodine in

hypothyroidism before and during thyroid therapy. J. Clin.

lnvestigalion 24:732-741.1945.

9. Means, ]. H., and Lerman, ]. Symptomatology of my:tedema: its

relation to metabolic levels. time intervals and rations of thyroid.

Arch. lnt. Med. 55:1-6, 1935.

___________________

Author: KENNETH STERLING

Date Published: 01-Jan-1975

Publication: CRC PRESS INC CLEVELAND OHIO 1975

Title: DIAGNOSIS AND TREATMENT OF THYROID DISEASES

Category: treating

Keywords: Sterling, diagnosis, treat, thyroid, euthyroid, T4, T3,

dose, sythetic, measure, serum, thyroid, hormone, desiccated, adult,

child, PBI, TSH, heart, normal

Text: 83

REPLACEMENT THERAPY OF HYPOTHYROIDISM

Thus, the ultimate maintenance dose in adult myxedema is usually

between 2 and 5 grains (although sometimes stated to be I to 3

grains in older texts),

(This is 148 mcg to 370 mcg of synthroid equivelent.)

_______________

http://thyroid.about.com/library/derry/bl3a.htm

Dr. Derry

The doses a patient gets when monitored by the TSH is currently two

thirds or less of the well established clinically effective doses

established from 83 years of clinical experience before the TSH

arrived. (5-6)

For example, in a sixteen part study of the effects of desiccated

thyroid on healthy prisoners Danowski et al found they tolerated

dosages of 9 grains of desiccated thyroid (540 mgs which equals

about 540 micrograms thyroxine) without ill effects. (9-11). On

studies on obesity and thyroid hormone where the dosages for three

months were between three grains and 25 grains (1500 mg of

desiccated thyroid equals about 1500 micrograms of Eltroxine) (12).

they said: " As in previous studies, these dosages of desiccated

thyroid were well tolerated by the subjects. Occasional nervousness,

increased sweating, and decreased endurance were reported.

Tachycardia and slight increase in the systolic blood pressure and

decreases in the diastolic blood pressure appeared in all.

Electrocardiogram changes were minimal. Body weight decreased by an

average of 26 pounds during the 22 weeks of treatment. " (7).

_________________

[study of hormone replacement therapy following total thyroidectomy

in thyroid cancer--with special reference to the analysis of thyroid

hormone peripheral effects, using indirect calorimetry]

[Article in Japanese]

Nozaki H, Funahashi H, Sato Y, Imai T, Oike E, Kato M, Takagi H.

Second Department of Surgery, Nagoya University School of Medicine,

Japan.

Five weeks after the beginning of hormone replacement, T4 and free

T4 were slightly within range, and no enhancement of energy

metabolism was noted. From these findings, the post-operative TSH

suppression therapy carried out at our department is considered to

be justifiable also from the viewpoint of energy metabolism.

(This paper points out that they were unable to raise the metabolic

rate

on thyroidectomized patients unless they suppressed TSH. By not

doing so, they were uable to raise the metabolic rate. I believe

they used ony 120mcg of synthroid for this and this did not raise the

metabolic rate.)

____________________

http://www.drlowe.com/QandA/askdrlowe/armourthyroid.htm

That optimal dosage range is highly individual, but historically,

the typical patient's therapeutic window has been somewhere between

120 to 240 mg (2 to 4 grains Armour or 148 to 296mcg synthroid).

There's no way to accurately predict

what your therapeutic window is.

(Some people can get by on 2 grains, but not very many.)

_____________________

Dr. Derry, " Breast Cancer and Iodine " :

Before the 1973-1974 change in laboratory diagnosis, the objective

of treatment in all cases was raise the thyroid dose up untill the

patient was in a state of well-being.

Before the 1973-74 change, the normal dose of thyroid was three

times the level seen now (2 -3 grains now or 148 to 222 mcg) and

there were no cases

of fractures or osteoporosis ever reported in the previous 80 years.

________________________

Broda , " Hypothyroidism, the Unsuspected Illness "

Dr. Pericles Menof of South Africa began treatment in his practice

with 5 grains of Armour and then reduced if needed. (pg 150) (This

caused problems for people with heart problems because starting dose

was too high.)

In 1925, the smallest starting dosage was 4 grains and dosages up to

30 grains had been used. (page 188)

The proper dosage is the minimum to relieve symptoms.

___________________

Dr. Barry Peatfield from his book " The Great

Thyroid Scandal " Page 87-88:

The disgraceful fact is that all these measurements (except the

last) may not be worth the paper they are written on; or may be so

flawed that treatment based on them is bound to be wrong. So what

goes wrong? And why are doctors not aware that they may be so badly

off the beam? And why do so many have minds so closed?

The reasons blood tests may be so flawed we need now to examine.

First and foremost these are measures only of the levels of thyroid

hormone in the blood. What we need to know is the level of thyroid

in the tissues, and, of course, this the blood test cannot tell us.

The nearest we can go is the Basal Temperature Test, or the Basal

Metabolic Rate. The first we have discussed; the second is now of

historical value. The patient is connected up to an oxygen uptake,

carbon dioxide excretion, measuring device, and the rate of usage

determines the metabolic rate. This is also subject to various

errors. The amount of thyroid hormones being carried by the

bloodstream varies in a highly dynamic way, and may be up at one

point and down the next. The blood test is simply a two-dimensional

snapshot of the situation at that moment. The slowed circulation may

cause haemo-concentration from fluid loss, so that the thyroid

levels are higher than they should be. (A simple way to explain this

is to think of a spoonful of sugar in your cup of tea. If it is only

half a cup of tea but you still put in your teaspoon of sugar, then

although the amount of sugar is the same, the tea will be twice as

sweet.)

But the blood levels depend mostly on what's happening to the

thyroid hormones. If the cellular receptors are sluggish, or

resistant, or there is extra tissue fluid, together with

mucopolysaccharides, the thyroid won't enter the cells as it should;

so that part of the hormone is unused and left behind, giving a

falsely higher reading to the blood test. It is simply building up

unused hormone. This may apply to both T3 and T4. Further

complications exist if the T4 + T3 conversion is not working

properly, with a 5'-diodinase enzyme deficiency. There will be too

much T4, and too little T3. If there is a conversion block, and a T3

receptor uptake deficiency, both T3 and T4 may be normal or even

raised. The patient will be diagnosed as normal or even over-active;

in spite of all other evidence to the contrary. It grieves me to

report that I have intervened several times to prevent patients,

diagnosed as hyperthyroid, having an under-active thyroid removed

when the only evidence was the high T4 level (due to receptor

resistance) and the patient was clinically obviously hypothyroid.

The patients thanked me, but not the consultants.

Adrenal insufficiency adds another dimension for error to the T4 and

T3 tests. Adrenal insufficiency, of which more anon, will adversely

affect thyroid production, conversion, tissue uptake and thyroid

response. It may make a complete nonsense of the blood tests.

The most commonly used test of all is the TSH. I have sadly come

across very few doctors who can accept the fact that a normal, or

low TSH may still occur with a low thyroid. The doctrine is high TSH

= low thyroid. Normal TSH = normal thyroid. But the pituitary may

not be working properly (secondary or tertiary hypothyroidism). It

may not be responding to the Thyrotrophin Release Hormone(TRH)

produced by the hypothalamus, which itself may not be producing

enough TRH for reasons we saw earlier. The pituitary may be damaged

by the low thyroid state anyway, and be sluggish in its TSH output.

______________________________

http://www.drlowe.com/frf/t4replacement/intro.htm

The most effective of these therapies involves adjusting patients'

dosages of combined T4/T3 or T3 alone according to several indices

other than TSH and thyroid hormone levels. Those indices are signs,

symptoms, and various objective measures of tissue response to

particular dosages. When patients' dosages are titrated according to

these indices, dosages that prove safe and effective are typically

TSH-suppressive.[44] Evidence is available that this therapeutic

approach relieves patients' signs, symptoms, and measurable tissue

abnormalities such as low resting metabolic rates (RMR) according to

indirect calorimetry.

This observation suggests that dosages higher than those dictated by

the replacement concept more effectively relieve patients'

hypothyroid symptoms. Other research has shown that patients report

feeling better with TSH-suppressive dosages of thyroid hormone.[23]

[24][25] Moreover, psychiatrists report that dosages of T3 higher

than replacement dosages augment the depression-relieving effects of

antidepressants.[9][28][29][30][31][34] In addition, in a study of

patients made hypothyroid by therapeutic destruction of the thyroid

gland, some used TSH-suppressive dosages of thyroid hormone and

others used T4-replacement. Those on TSH-suppressive dosages didn't

gain excess weight; those on T4-replacement did. The researchers

concluded that T4-replacement was the cause of the excess weight

gain.[55] These published reports are consistent with thousands of

cases in which hypothyroid patients recovered from their symptoms

and other health problems with TSH-suppressive dosages of thyroid

hormone after T4-replacement failed to help them.

Kaplan's observation also suggests another point: that T4-

replacement keeps many hypothyroid patients' dosages too low to

relieve their symptoms is an indictment of the concept of

replacement. As the cause of

(1) the continued suffering and debility of patients,

(2) an increased incidence of potentially life-threatening diseases,

and

(3) the need for the chronic use of medications,

___________________________

Dr. Derry article:

http://thyroid.about.com/library/derry/bl11.htm

The effective dose physicians used by clinical judgment and

experience before 1975 was around 2-3 times higher than the dose

used by TSH blood test monitoring. So everyone's dose of thyroid

after 1975 was decreased by about two thirds of well established

clinically effective doses.

__________________________

Another Derry article:

http://thyroid.about.com/library/derry/bl4a.htm

In the 1960s it was textbook material after 70 years of experience

using thyroid that a dose below 180 mg of desiccated thyroid (3

grains) could not be measured clinically or in the laboratory. In

other words it was without effect.(2) The approximate equivalent

dose of synthroid or thyroxine (T4) would be about 180 micrograms

(mcg).

(3)

So unless your dose is above 180 there is little chance of regaining

your hair back and the problem likely continue and get worse. You

can tell when you are approaching the right dose personally when the

itching starts to go away permanently. Depending on how old you are

and other medical history it is likely though you would get complete

relief with a dosage up around 200 micrograms of Synthroid or

higher. We know that there are no side effects at those dosages.

Dosages of thyroxine (Synthroid, T4) of up to 300 micrograms are

without morbidity or mortality. (no sickness or deaths) (4)

_____________________________

Dr. Lowe's wife:

http://www.drlowe.com/emailnewsletter/2003archive.htm

Instead, they adjust dosages according to how patients respond to a

particular dose. As studies have shown, this approach produces far

superior treatment results than does adjusting dosages according to

thyroid test results.[1][2]

___________________________

Dr. Lowe uses this guide:

http://www.drlowe.com/clincare/clinicalforms/areyouoverstimulated.pdf

to determine if the patient is on too high a dose. In other words,

they raise thyroid dose up untill the patient feels best and use

this form as a way to make sure they haven't gone too high. Dose is

determined purely by how the patient feels and no tests are used

_____________________

Author: JAMES C. WREN, M.D.

Date Published: 01-Jan-1971

Publication: JOURNAL OF THE AMERICAN GERIATRICS SOCIETY Vol. 19, No

1, p 7, 1971

Title: SYMPTOMATIC ATHEROSCLEROSIS: PREVENTION OR MODIFICATION BY

TREATMENT WITH DESICCATED THYROID

All patients were given desiccated thyroid in an initial dosage of

15 to 30 mg daily (single dose). This was increased slowly to 60 to

240 mg (4 grains) daily (single dose) within six months, the aim

being full replacement or physiological dosage. The final dosage was

a matter of clinical judgement rather than laboratory study. In most

cases the dosage at six months was maintained throughout the rest of

the study. In the majority of cases the daily dosage was 120 mg (104

patients) or 180 mg (190 patients).

RESULTS

Subjective findings

General. In the symptomatic group, 100 of 132 patients reported

benefit from thyroid therapy, in the form of an increased sense of

well-being, increased exercise tolerance, greater motivation and

greater alertness. Twenty-two remained unchanged and 10 died.

It is generally conceded that human atherosclerosis is irreversible,

but these results indicate that the administration of thyroid may be

of benefit in many cases.

Probably of most importance and significance was the statistical

observation that for these thyroid-treated patients the mortality

rate was lower than that for the population at large.

(Note the doses. They are quite high on average.)

_________________________

Report by by Dr. Hertoghe on his studies of thyroid function

Daily production of T4 is about 80 to 100 micrograms and T3 is

20 micrograms.

(This is equivelent to 3 grains armour or 222 mcg synthroid and does

not take into account the

amount of thyroid that would be lost to the digestive system by

taking pills. It is only measuring actual levels in the blood.)

_______________________

email correspondence, January 20, 8:33 am 2005

Dear Leitita,

according to the ROCHE medical encyclopedia, the daily turnover of

T3

and T4 is 30 and 80 microgramm respectively. I don't have further

information, but I think you can find plenty of data in the web.

Best regards

G. Proehl

Dr. Gerhard Proehl

GSF-Institute of Radiation Protection

Postfach 1129

D-85758 Neuherberg

Phone: +49-89-3187-2889

Fax: +49-89-3187-3363

Email: proehl@g...

(This is equivelent to 200 mcg or just under 3 grains. This does not

take into account losses to the digestive system by taking pills.)

______________________

Dr. Guberman

http://drguberman.com/news.cfm?date_range=8/01/04

7051 West Commercial Blvd., Suite 3-C

Tamarac, FL 33319

e-mail: drguberman@d...

That optimal dosage range is highly individual, but historically,

the typical patient's therapeutic window has been somewhere between

120 to 240 mg (2 to 4 grains Armour or 148 to 296 mcg synthroid).

There's no way to accurately predict

what your therapeutic window is. Until you find it, you may not

improve much from the Armour. But once you do, you're likely to feel

that the wait was well worth it.

_________________________

Author: P. B. S. Fowler

Date Published: 11-Aug-1973

Publication: BMJ 11 August 1973 Vol. III p 352 - 353

Title: LETTER: Treatment of Hypothyroidism

this infrequent phenomenon lies in the

fact that exogenous thyroid hormone in moderate

doses administered to normal subjects rarely has

appreciable effects, owing to compensatory suppression

of the subject's own thyroid gland through diminished

secretion by the pituitary of thyroid-stimulating

hormone (TSH). TIns feedback inhibition tends to

maintain a constant level of circulating thyroid hormone.

There are, in fact, instances of normal subjects

who have taken quite appreciably excessive doses of

thyroid with minimal or no manifestations of toxicity,

probably due to enhanced ability for degradation of

excessive

84

amounts of hormone in some individual

__________________________

http://www.thyroid-info.com/articles/dommisse.htm

An Interview with Dommisse, MD

Unique Theories About Hypothyroidism Treatment

I ran into too many patients who had classic hypothyroid symptoms,

which cleared completely on appropriate thyroid treatment, and whose

TSH was below 2.0 (but above 1.5) and with FT4 and FT3 levels in the

low ends of their 'normal ranges'….Finally, I found some patients

with several symptoms and signs of hypothyroidism whose TSH was

between 1.0-1.5; so I lowered my range, for the last time, to 0.1-

1.0; I now treat primary hypothyroidism with a TSH of >1.0 (if the

FT4 and FT3 are low-normal, not above the middle of their 'normal

ranges').

_______________________

.. " Optimum Diagnosis and Treatment of Hypothyroidism With Free T3

and Free T4 Levels " by Dr. ph Mercola (US), DO

http://www.mercola.com/article/hypothyroid/diagnosis_comp.htm

Most patients continue to have classic hypothyroid symptoms because

excessive reliance is placed on the TSH. This test is a highly

accurate measure of TSH but not of the height of thyroid hormone

levels.

The basic problem that traditional medicine has with diagnosing

hypothyroidism is the so called " normal range " of TSH is far too

high: Many patients with TSH's of greater than 1.5 (not 4.5) have

classic symptoms and signs of hypothyroidism.

______________________

Dr. Derry http://thyroid.about.com/library/derry/bl11.htm

Topic: Low Adrenal Function and Thyroid Problems

Physicians before 1975 found the minimum clinically

effective dose for hypothyroid patients was about 180

mg of desiccated thyroid or 180 micrograms of

eltroxine (T4).

____________________

Dr. Derry article:

http://thyroid.about.com/library/derry/bl4a.htm

In the 1960s it was textbook material after 70 years of

experience using thyroid that a dose below 180 mg of

desiccated thyroid (3 grains) could not be measured

clinically or in the laboratory. In other words it was

without effect.(2) The approximate equivalent dose of

synthroid or thyroxine (T4) would be about 180

micrograms.(3)

So unless your dose is above 180 there is little chance

of regaining your hair back and the problem likely

continue and get worse.

We know that

there are no side effects at those dosages. Dosages of

thyroxine (Synthroid, T4) of up to 300 micrograms are

without morbidity or mortality. (no sickness or deaths)

(4)

_____________________

Dr. Derry http://www.bites-medical.org/hypo/hist.html (Site

now gone)

There were

no problems with desiccated thyroid even at high

doses, and it was known as one of the safest drugs

available. Synthetic T4, on the other hand, has had a

long history of manufacturing and reliability problems.

_____________________

(This paper points out that some patients need suppressive doses of

thyroid to feel good.)

MINI REVIEW

Intrinsic imperfections of endocrine replacement therapy

J A Romijn, J WA Smit and S W J Lamberts

Department of Endocrinology, Leiden University Medical Center,

Leiden and Department of Internal Medicine, Erasmus Medical Center,

Rotterdam University, Rotterdam, The Netherlands

(Correspondence should be addressed to J A Romijn; Email:

j.a.romijn@l...)

However, many patients

treated for endocrine insufficiencies still suffer from more or less

vague complaints and a decreased

quality of life. It is likely that these complaints are, at least in

part, caused by intrinsic imperfections

of hormone replacement strategies in mimicking normal hormone

secretion.

......effects of

hormones in general, and thus of hormone replacement strategies in

particular, are difficult to

quantify at the tissue level. Therefore, in clinical practice we

rely mostly on plasma variables –

`plasma endocrinology' – which are a poor reflection of hormone

action at the tissue level.

Complaints of thyroid patients....They range from

musculoskeletal complaints, to vague feelings of being

unwell, and to depression. Two approaches have been

used to decrease the complaints experienced by these

patients: an increase in the dose of L-thyroxine, and

combination treatment of thyroxine with tri-iodothyronine.

In some of the patients, a decrease in complaints

can be achieved by increasing the dose of thyroxine

above that required to restore TSH concentrations to

normal (1). For this reason, such patients are often

allowed to take a dose of thyroxine that would be

judged as overtreatment with respect to TSH concentrations.

The second approach was evaluated by

Bunevicius et al. (2), who performed a randomised controlled

trial to compare the effects of thyroxine alone

with those of thyroxine plus tri-iodothyronine. Patients

with hypothyroidism benefitted when 12.5 mg triiodothyronine

was substituted for 50 mg thyroxine in

their treatment regimens. This resulted in improved

neuropsychological functioning. Pulse rates and

serum sex hormone-binding globulin concentrations

were greater after treatment with thyroxine plus

tri-iodothyronine, indicating a slightly greater effect

on the heart and liver. Serum thyroxine concentrations

were lower and tri-iodothyronine concentrations

were greater after treatment with thyroxine plus

tri-iodothyronine, but serum TSH concentrations, a

sensitive measure of thyroid hormone action, were

similar after the two treatments. It should be noted

that not all patients benefitted from this approach

because, even in the group with combination therapy,

patients continued to report complaints of depression.

Thyroxine:

The thyroid secretes tri-iodothyronine (T3) (,20%) in addition to

thyroxine (T4) (,80%). In the absence of

thyroid function, exogenous thyroxine is not able to normalise the

concentrations of T4 and T3 in all tissues in rodents, even in the

presence of normal TSH concentrations. Despite this knowledge,

currently available preparations of T3 have unfavourable

pharmacological profiles and adequate markers of biological effect

are lacking. Additional evidence is required before combination

therapy can be advised.

First, it is remarkable that the normal values

of TSH show a more than tenfold variation, between

0.4 and 4.5mU/l. Because, in clinical practice, the optimal

TSH concentration for individual patients within

this range is unknown, titration of the substitution

dose of thyroxine within this tenfold variation is

relatively crude. Secondly, the intrinsic assumption of

many doctors in this approach is that normal TSH

concentrations reflect adequate thyroid hormone

concentrations, not only at the tissue level of the

hypothalamus and the pituitary, but also in the other

tissues. However, it is likely that this assumption is

erroneous, because TSH is produced only by the

pituitary gland and therefore may not reflect thyroid

hormone status in tissues outside the hypothalamo–

pituitary axis. This notion is supported by data obtained

from animal experiments.

Thyroxine is considered to be an

inactive hormone, because a thyroxine-specific receptor

has not been identified. Rather, thyroxine serves as a

prohormone, because it is the precursor of tri-iodothyronine.

Some tissues, such as muscle, have a relatively low

deiodinase activity and are dependent, to a great

extent, on tri-iodothyronine derived from the thyroid

and the liver.

In rodents, it has been clearly demonstrated that

there is no single dose of thyroxine or tri-iodothyronine

that normalises thyroid hormone concentrations in all

tissues simultaneously in hypothyroid animals (3).

Therefore, it is highly likely that, in patients treated

with L-thyroxine, subtle derangements at the tissue

level are present with respect to thyroid hormone availability,

and probably also thyroid hormone action.

_______________________

Changes in serum triiodothyronine, thyroxine, and

thyrotropin during treatment with thyroxine in severe

primary hypothyroidism

M Maeda, N Kuzuya, Y Masuyama, Y Imai and H

Ikeda

J. Clin. Endocrinol. Metab., Jul 1976; 43: 10 - 17.

It is difficult to assess what is the

optimal dose for any one subject, for at present we

have no objective, easily quantifiable parameter to

assess response of body tissues to thyroid hormone

replacement. Measurements of serum TSH, kinetics of

reflex time, and oxygen consumption are helpful, but

not entirely reliable for this purpose.

Individuals on physiological replacement

replacement

doses of pure sodium levothyroxine have elevated

levels (high normal to hyperthyroid range) of serum

thyroxine (-Pattee). The resin uptake tests in

these persons are also elevated above normal, so that in

patients on 300 or 400 pg of sodium levothyroxine

(4.0 to 5.5 grains) a

day, the PBI or serum thyroxine level will

be in the high range and so will the free thyroxine

index.

(Note the very high doses of Synthroid needed to make the patient

feel well. This was before over reliance on the TSH test.)

_______________________

(This paper points out that healthy people have little responxe to

being given thyroid.)

Author: WILLIAM H. BEIERWALTES, M.D.

Date Published: 01-Jan-1955

Publication: Michigan Journal Clinical Endocrinology Vol. 15, 1955

p148 - 150 (Editorial)

Title: RESPONSE TO THYROID

Category: diagnosing

Keywords: thyroid, BEIERWALTES, desiccated, oral, research,

myxedqamatous, myxoedema, euthyroid , diagnose, basal, pulse rate,

iodine

Text: 1955 Editorial WILLIAM H. BEIERWALTES, M.D. University

Hospital, Ann Arbor, Michigan Journal Clinical Endocrinology Vol.

15, 1955 p148 - 150

p148

RESPONSE TO THYROID

WHEN desiccated thyroid is administered orally to myxedematous

humans, the resultant metabolic changes are quite different from

those observed in the euthyroid subject. The clinician can diagnose

or treat hypothyroid patients much more intelligently if he is aware

of these difference in response to thyroid. In addition, an unworked

field for clinical research becomes evident when one reviews the

known major differences between the myxedematous patient and the

euthyroid subject in response to desiccated thyroid administration.

The most striking difference observed may be summarized by the

statement that the patient who is truly deficient in circulating

thyroid hormone responds dramatically and with predictable

regularity to the administration of small doses of desiccated

thyroid. The euthyroid subject, on the other hand, shows no obvious

clinical response to small doses of thyroid. A simple and readily

available diagnostic test for borderline hypothyroidism, therefore,

is the administration of 1 grain of desiccated thyroid per day for a

period of six weeks after a careful history and physical examination

have been made and basal metabolic rate and serum cholesterol

determinations have been performed. The patient who is truly

deficient in thyroid hormone will generally respond to the

administration of 1 grain of desiccated thyroid per day for six

weeks with an increase in basal pulse rate and metabolic rate and a

fall in the serum cholesterol level. The patient not truly deficient

in thyroid hormone will show no significant change in these indices

of thyroid hormone effect.

p149

.....The myxedematous patient and the euthyroid subject also show a

different response to sudden cessation of desiccated thyroid

medication. The myxedematous patient at first shows a rapid drop in

his serum precipitable-iodine level and basal metabolic rate, then a

slower fall to pre-treatment levels over a period of six to eight

weeks (3). On the other hand, when the thyroid medication of a

euthyroid person is suddenly stopped, the serum precipitable-iodine

value falls to myxedematous levels in three to four weeks, but the

basal metabolic rate may take as long as nine to fifteen weeks to

reach its lowest level (3). These values then rise to pre-treatment

levels. The radioiodine uptake is also falsely depressed by thyroid

administration and has taken as long as eleven weeks to recover (4).

Furthermore, when the thyroid does recover its ability to

concentrate I131, the I131 pickup rate may rebound temporarily to

hyperthyroid levels. Obviously, if a physician were to stop the

desiccated thyroid medication of a euthyroid patient in an attempt

to evaluate the patient's underlying thyroid status, these ensuing

changes in indices of thyroid function, when sampled, might prove

very misleading and confusing.

The daily output of thyroid hormone by the normal thyroid gland is

thought to be equivalent to not more than 3 grains of desiccated

thyroid per day. Consequently, when the daily dosage of desiccated

thyroid is raised to 4 grains or more per day, any differences

observed between athyreotic and euthyroid subjects can not be

explained on the basis of further suppression of normal thyroid

function. Most practicing physicians have probably observed a

euthyroid patient who was comfortable while voluntarily taking 5 to

20 grains of desiccated thyroid a day, in an attempt to reduce

p149

his weight and rid himself of fatigue. Rarely, if ever, does one see

an athyreotic patient voluntarily take more than 3 grains of

desiccated thyroid per day. This situation suggests that the

athyreotic patient is more sensitive to thyroid substance than is

the euthyroid person, even after his myxedema has been controlled

with medication.

.....WILLIAM H. BEIERWALTES, M.D.

University Hospital, Ann Arbor, Michigan

REFERENCES

1. MEANS, J. H,: The Thyroid and Its Disease, ed. 2. Philadelphia,

J. B. Lippincott Co., 1948, p 249

2. WINKLER, A. W.; RIGGS, D. S., and MAN, E. B.: Serum iodine in

hypothyroidism before and during thyroid therapy, J. Clin. Invest.

24: 732, 1945

3. RIGGS, D. S.; MAN, E. B., and WINKLER, A. W.: Serum iodine of

euthyroid subjects treated with desiccated thyroid, J. Clin. Invest.

24: 722, 1945

4. GREER, M. A.: The effect on endogenous thyroid activity of

feeding desiccated thyroid to normal human subjects, New England J.

Med. 244: 385, 1951

5. JOHNSTON, M. W.; SQUIRES, A. H., and FARQHARSON, R. F.: The

effect of prolonged administration of thyroid, Ann. Int. Med. 35:

1008, 1951

6. THOMPSON, W. O.; THOMPSON, P. K.; TAYLOR, S. G., and DICKIE, L.

F. N.: Calorigenic action of single large doses of desiccated hog

thyroid: comparison with the action of thyroxine given orally and

intravenously, Arch. Int. Med. 54: 888, 1934

March 9, 2005