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Thyroid Antibodies
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January 17, 2005
Question: Recently, my doctor diagnosed me with autoimmune thyroid disease. My TSH and all other thyroid labs were in range, but she ordered thyroid antibodies and they were high.
She started me on small amount of Synthroid. I am thin, 5 ft. 2 in., and 108
lbs. I haven’t had a weight change, and my only symptom is tiredness. Is
Synthroid recommended even though all my labs are well within normal except
for the high antibodies?
Dr. Lowe: I regret to say that you're
embarking on what’s likely to prove a frustrating experience—one in
which your quality of life may progressive worsen over time. I say this
based on long clinical experience and the available scientific evidence.
Many clinicians believe that when a patient has high thyroid antibodies,
he or she should begin thyroid hormone therapy. I am among them. The patient
should begin therapy to prevent troubling hypothyroid symptoms from
developing.
If your antibodies remain high, they’ll most likely damage your thyroid
gland. Eventually, the damage may be so severe that the gland can no longer
produce enough thyroid hormone to keep your metabolism normal. When you
become deficient of thyroid hormone, your fatigue is likely to worsen, and
you’ll develop other hypothyroid symptoms. For example, on T4-replacement
therapy, which your doctor has prescribed,
you’ll most likely gain weight you can’t lose.
The problem I see for you is the T4-replacement. Late last year, we
published two critiques of T4-replacement on drlowe.com. If you’ll read
them, you'll see that there’s ample justification for my first paragraph
in this email. Links to the critiques are below:
http://www.drlowe.com/frf/t4replacement/intro.htm
http://www.drlowe.com/frf/guttler/critique1.htm
For your long-range welfare, I encourage you to print and read the
critiques. I also recommend that you share them with your doctor. Hopefully
she'll be responsive to logic and science, the bases of the critiques, and
not subject you to the possible adverse effects of T4-replacement—a
therapeutic approach based more on financial venture than science.
My hope is that your doctor will switch you to a T4/T3 product and adjust
your dosage by your symptoms rather than your TSH level. If she does, you
stand a good chance of overcoming your fatigue and preventing other
troubling hypothyroid symptoms from ever developing.
October 12, 2004
Question: I am a 32-year-old woman who was diagnosed with
fibromyalgia in 1999. During these five years, doctors have prescribed one
antidepressant after another. None of them have helped me at all. I’ve
felt hypothyroid the entire time, but my doctors have all said my TSH, T4,
and T3 are normal and I can’t be hypothyroid. In the past month, my
symptoms have changed. I now have rapid heart rate, weight loss (I’ve gone
from 120 to 110 in two weeks), tremors, extreme fatigue and weakness,
extreme nervousness, sweats, insomnia, and I just feel awful. These new
symptoms are terrible to deal with and I’m confused about them. From
reading your website, you seem to think fibromyalgia symptoms are caused by
hypothyroidism. But these new symptoms are like hyperthyroidism. Doesn’t
that contradict your theory about fibromyalgia? Last week, my doctor told me
the new symptoms are caused by anxiety, and he prescribed Xanax. The Xanax
hasn’t stopped them, so I’m confused. If the symptoms aren’t caused by
anxiety, then what is causing them? They sure don’t seem like
hypothyroidism.
Dr. Lowe: Your current symptoms don’t
contradict our theory that hypothyroidism underlies most patients’
fibromyalgia symptoms. If you meet the criteria for fibromyalgia, then
you've most likely been hypothyroid all along. The usual lab tests (TSH, T4,
and T3) doctors order to rule out or diagnose hypothyroidism often fail to
show that a patient is hypothyroid. This is especially true of the patient
who has a marginal thyroid hormone deficiency due to autoimmune thyroiditis.
You didn’t mention whether any of your doctors have ordered thyroid
antibodies. If not, it’s possible that all along, you’ve had undiagnosed
autoimmune thyroiditis with high thyroid antibodies. If so, it’s likely
that you’ve been marginally hypothyroid despite your "normal"
TSH, T3, and T4 levels.
If this is the case, then your "fibromyalgia" symptoms are most
likely misdiagnosed symptoms of hypothyroidism due to autoimmune
thyroiditis. This mechanism is actually compatible with your current
symptoms, which are characteristic of thyroid hormone overstimulation or
"thyrotoxicosis." Many patients with autoimmune thyroiditis go
through one or more phases of thyrotoxicosis. This happens when the
autoimmune process damages the follicles of the thyroid gland enough for
them to rupture. The follicles contain thyroid hormone, and when they
rupture, the hormone leaks into the blood. The leakage can be so great that
the patient’s tissues are exposed to too much thyroid hormone, and this
causes thyrotoxicosis. Fortunately, the leakage is time-limited, and because
of that, the thyrotoxicosis is transient.
If your symptoms are those of transient thyrotoxicosis, Xanax is not the
proper treatment. Instead, your doctor should prescribe a beta-blocker, such
as propranolol. Propranolol will control the symptoms until you pass through
the thyrotoxic phase. Afterward, your former hypothyroid
("fibromyalgia") symptoms will resume. It is possible, however,
that the symptoms will be worse than before. They’ll be worse if you’ve
lost so many thyroid follicles that your gland cannot produce as much
thyroid hormone as before.
If your thyroid gland follicles are releasing large amounts of thyroid
hormone into your blood, your free T3 and free T4 should now be high and
your TSH low. Your doctor should order these testes. It is more important,
however, that he order thyroid peroxidase and thyroglobulin antibody levels
to learn whether you have autoimmune thyroiditis. He should include in the
order a thyroid-stimulating antibody level, just in case you’ve developed
Graves’ disease. If your test results point to autoimmune thyroiditis and
not Graves’, then after your thyrotoxicosis has subsided, your doctor
should start you on thyroid hormone therapy. You should insist on a
product that contains both T4 and T3.
If your doctor refuses to order thyroid antibody levels, we’ll be happy
to order them for you long distance.
Read
our webpage on long-distance lab orders and then phone us at
303-413-6003. My assistant will answer any questions you have and arrange a
phone consultation so that we’re sure to order the right tests. If your
doctor does cooperate, however, and orders the tests, I hope you’ll let me
know the outcome. Meanwhile, I wish you the very best.
November 13, 2003
Question: I’m a 40-year old woman, and I need your advice. Two years ago, I went to my doctor
complaining of fatigue. He found that my TSH level was high and prescribed
Synthroid. I presently take a dosage of 0.88 mg.
Three months ago, I started having more hypothyroid symptoms. I’m
always tired, extremely cold, constipated, fatigue, my ankles feel swollen,
and I have aches and pains throughout my body. Because of these symptoms, my
doctor referred me to an endocrinologist.
The endocrinologist ordered a TSH level and antithyroid antibody levels.
My TSH level was 3.29, which he said was normal. My thyroglobulin antibodies
were high 32, and my thyroid peroxidase antibodies were high at 70.
When I questioned the endocrinologist about the elevated antibodies, he
told me to do nothing but stay on the same dose of Synthroid. I asked why
the two antibodies were high. His explanation was that it’s normal for the
levels to be high in people taking Synthroid, or it could be that high
antibodies are simply normal for me.
That doesn't make any sense to me! I still have the same hypothyroid
symptoms I mentioned above, and my spirits are down. Do you mind giving me
your opinion?
Dr. Lowe:
I’m sorry your spirits are
down, but I certainly understand why. Many patients feel let down when the
opinion of a specialist doesn’t seem to make sense. Patients should find
it uplifting, however, that through the Internet, they can usually find
answers that do make sense.
Some patients with hypothyroid symptoms due to autoimmune thyroiditis do
well on 0.88 mg of Synthroid. However, those are extremely rare
patients. For most such patients, that dosage constitutes grossly
inadequate treatment.
It’s plausible that your symptoms have recently worsened because your
Synthroid dose of 0.88 mg is too low to suppress the antithyroid antibody
attack on your thyroid gland. In other words, your low dose of thyroid
hormone may be allowing your autoimmune thyroiditis to progress and worsen
your hypothyroidism.
If your endocrinologist said your TSH of 3.29 is normal, his judgement
conflicts with the current lab standard. According to the American
Association of Clinical Endocrinologists, the new target TSH level is 3.0 to
3.04. Obviously, your TSH was above this target level.
Some patients’ antithyroid antibodies remain high despite thyroid
hormone therapy. Typically, though, the levels decline.[1][2]
In my experience, effective thyroid hormone therapy decreases the levels to into the reference range or close to it. And despite your endocrinologist’s opinion, it’s highly improbable that a high
antithyroid antibody level is normal for anyone who has your classic
hypothyroid symptoms. A high antibody level means the person has autoimmune
thyroiditis, and that’s clearly abnormal.
To understand the relation of antithyroid antibodies to hypothyroid
symptoms and proper thyroid hormone therapy, I strongly recommend my
extensive chapter on hypothyroidism in The
Metabolic Treatment of Fibromyalgia .
References
1. Jannson, R., Karlsson, A., and
Dahlberg, P.A.: Thyroxine, methimazole, and thyroid microsomal autoantibody
titres in hypothyroid Hashimoto’s thyroiditis. Br. Med. J., 290:
11, 1985.
2. Trbojevic, B., Lalic, N., and
Slijepcevic, D.: The effect of replacement therapy on thyroid antibody and
serum thyrotropin concentrations in Hashimoto’s thyroiditis. In The
Thyroid and Autoimmunity. Edited by H.A. Drexhage and W.M. Wiersinga,
Amsterdam, Excerpta Medica, 1986, p.113.
May 25, 2003
Question: I believe my thyroid gland is failing and that I’m hypothyroid. For years, I’ve
had most of the symptoms listed on
drlowe.com. Also, when I swallow, I feel like something is
swollen in the front of my neck. My doctor ordered a TSH and a free T4.
He said the results were normal and that my symptoms can’t be
hypothyroidism. He refused to order thyroid antibodies. He said that if
my antibodies were high, it would be reflected in a high TSH and low
thyroid hormone levels, which I don’t have. Is he right? Is there
something else I can do to find out if I’m hypothyroid.
Dr. Lowe:
Your doctor is wrong. Antibodies are often high despite "normal"
TSH and thyroid hormone levels. Thyroid function tests (TSH and measures of
thyroid hormone levels) often miss thyroid disease and hypothyroidism.
Two Scandinavian researchers, Aarflot and Bruusgaard, found this in their
study of 737 men and 771 women.[1]
They found that those with chronic widespread musculoskeletal pain (often
diagnosed as fibromyalgia) had a higher incidence of thyroid antibodies than
those without pain. But thyroid function test results did not differ
between the two groups. This means that the antibody test showed thyroid
disease while the TSH and thyroid hormone levels failed to show it. The
study raises a possibility that all patients with hypothyroid-like symptoms
and their doctors should note: Patients may be suffering from hypothyroid
symptoms due to autoimmune thyroid disease, and while thyroid function test
results may be "normal," high antibody levels will reveal the
disease. In fact, thyroid function test results may be "normal"
for years despite patients having autoimmune thyroiditis the whole
time.[2]
I recently evaluated a patient whose case illustrates the importance of not
depending solely on thyroid function tests. She had long suffered from
hypothyroid symptoms when her family doctor found a nodule on the left side
of her thyroid gland. A needle biopsy suggested that the nodule was benign.
The patient suspected, however, that the nodule meant she was hypothyroid.
To find out, she asked her doctor to refer her to an endocrinologist.
She ended up seeing two different endocrinologists. The first ordered
thyroid function tests and told her the results were normal. Based on this
result, he pronounced that her symptoms could not possibly be caused by
hypothyroidism.
The patient wanted another opinion and asked her doctor to refer her to
an endocrinologist at a Mayo Clinic. She hoped that the endocrinologist
being on staff at a Mayo clinic meant he was more competent than the first.
Like the first endocrinologist, he ordered thyroid function tests and said
the results were normal. And again like the first endocrinologist, he
confidently assured her that her symptoms couldn’t possibly be caused by
hypothyroidism.
While seeing the second endocrinologist, the patient consulted with a
surgeon about her thyroid nodule. The surgeon told her that his wife had
recently had the same type of benign nodule. She had chosen to have it
surgically removed because she didn’t want to chance it becoming
malignant. The patient saw the sense in the surgeon’s wife’s decision,
and she decided to have him remove the part of her thyroid gland that
contained the nodule.
The surgeon removed the left lobe of her thyroid gland and sent the
tissue to a lab for study. The lab report came back saying the patient’s
thyroid tissue had destruction characteristic of Hashimoto’s thyroiditis.
After reading this report, the patient’s family doctor ordered thyroid
antibodies. They turned out to be extremely high. He then diagnosed the
Hashimoto’s thyroiditis that the two endocrinologists had missed. This
finding made it likely that the patient’s hypothyroid-like symptoms were
indeed most likely hypothyroid symptoms.
When the patient’s family doctor ordered the thyroid antibody test, her
anti-microsomal (peroxidase) antibodies were 673. Anything above 2 was
considered abnormal. The doctor prescribed T4, but she—like many
hypothyroid patients—found T4-replacement ineffective. But when she began
taking 2 grains of Armour and 50 μg of Cytomel, her antibody level
plunged to 70. When her Cytomel dose was 75 mcg., her symptoms began to
distinctly improve—pretty strong evidence that the two endocrinologists
had misdiagnosed her symptoms as unrelated to hypothyroidism. She’s
presently undergoing metabolic rehab. Based on her similarity to other
hypothyroid Hashimoto’s patients who’ve undergone our program, I’m
confident that she’ll soon fully recover from her hypothyroid symptoms.
This patient’s story should make one thing clear: You should not let
your doctor—even if he or she is an endocrinologist—deny you thyroid
testing you believe you should have. For your own health and well-fare, you,
like other patients, must face a tragic fact: Most conventional doctors are
incompetent at identifying patients who need thyroid hormone therapy—even
when the evidence for the need is obvious or even overwhelming. And as this
patient’s case shows, endocrinologists are well represented among inept
conventional doctors.
You asked whether there’s anything else you can do to find out if you’re
hypothyroid. There is: Demand full and proper testing, and don’t
take no for an answer! If your current doctor won’t order the proper
tests, fire him or her and find one who will. You may have to "go
outside your insurance" to find one, but isn’t that worth getting
well when conventional doctors forsake you? If it is worth it to you, you can
get an accurate diagnosis and proper treatment; so-called "alternative
thyroid doctors" have made them readily available for patients whom
conventional doctors have failed. I wish you the best in your pursuit of a
competent doctor, proper testing, and effective treatment should it turn out
that you need it.
References
1. Aarflot, T. and Bruusgaard D.:
Association between chronic widespread musculoskeletal complaints and
thyroid autoimmunity. Results from a community survey. Scand. J. Prim.
Health Care, 14(2):1111-1115, 1996.
2. Volpé, R.: Autoimmune thyroiditis. In Werner and Ingbar’s The Thyroid: A Fundamental and
Clinical Text, 6th edition. Edited by L.E. Braverman and R.D. Utiger,
New York, J.B. Lippincott Co., 1991, pp.921-933.
Continued at top of right column
. . .
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November
20, 2002
Question: I am a Brazilian
hypothyroid patient and have been taking T4. My dosage is 50 mcg each day. I’m
now experiencing some changes in my vision capabilities. My vision is a
little fuzzy and blurred, and this started after a few months of taking T4.
My question is: Can T4 reduce my capacity to see things clearly? Should I
wear glasses? I’m very curious to know because it seems I’ll have to
take the T4 for the rest of my life.
Dr. Lowe:
Keep in mind that T4 alone is the least effective thyroid hormone
preparation, and 50 mcg is an extremely small amount. I seriously doubt that
50 mcg is benefiting you in any way. It may, however, be harming you.
T4 is highly effective at one thing: suppressing TSH secretion by the
pituitary gland. T4 can suppress pituitary TSH secretion while leaving the
metabolism of other tissues so slow that the patient continues to suffer
from hypothyroid symptoms. Consequently, the doctor concludes (from the
lowered TSH) that the patient is well; in the mean time, the patient suffers
from continuing hypothyroid symptoms. Even worse, if the T4 dose is too low,
the patient’s symptoms may actually worsen.
It's possible that the paltry amount of T4 you’re taking, by lowering
your TSH level, has reduced your thyroid gland’s release of T4 and T3. The
T4 you're taking may be far too little to compensate for your thyroid gland’s
reduced thyroid hormone output. As a result, the
small dose of T4 you’re taking may actually be worsening some harmful
effects of your hypothyroidism. The Physician’s Desk Reference
contains an important statement largely ignored by conventional doctors:
"Inadequate doses of Synthroid [and by extension, any other
brand of T4] may produce or fail to resolved symptoms of
hypothyroidism."[1,p.1500]
(Italics mine.) Doctors currently
restricting their hypothyroid patients to small doses of T4 would do well by
their patients to read and seriously consider the implications of this
quote.
Two possible mechanisms come to mind that could—at least theoretically—account
for the visual problems that began after you began using T4. A possible
harmful effect of a small T4 dose is myxedematous swelling behind the eyes
that distorts the patient’s vision. ("Myxedema" is the swelling that occurs
when too little thyroid hormone regulation of connective tissue cells causes
an increase in water-binding molecules in connective tissues.) The swelling
might cause you to feel pressure behind your eyes. And you may have other
body areas that have become swollen or puffy since you began to use T4. If
you have either of these symptoms, you should discuss this possibility with
your doctor.
Another possibility is that you have autoimmune thyroid disease, and as
part of the disease, you have anti-thyroglobulin antibodies. The suppression
of your thyroid gland by too small a dose of thyroid hormone may have
augmented the autoimmune process by increasing your anti-thyroglobulin
antibodies. In some patients, serum containing anti-thyroglobulin antibodies
was found to bind to human eye muscles.[2]
Apparently, an antigen within the
thyroglobulin molecule is the same or similar to one in an enzyme (acetylcholinesterase)
at the nerve-muscle junction in the eye muscles.[3]
The anti-thyroglobulin
antibodies apparently cross-reacts with this muscle enzyme. Destruction of
the enzyme could cause the eye muscles to stay contracted too long. This
would distort the eye ball’s shape and produce the fuzzy, blurred vision
you described.
The proper approach would be for your doctor to switch you to a more
effective thyroid hormone preparation—one containing both T4 and T3, such
as desiccated thyroid. Of course, if your doctor keeps your dosage as low as
he has your T4 dose, you might not fair much better. So, if your present
doctor won’t cooperate with your using a high enough dose of a more
effective thyroid hormone preparation, prudence will lead you to another
doctor who will.
References
1. Physician’s Desk Reference,
53red edition. Montvale, Medical Economics Company, Inc., 1999.
2. Mullins, B.R., et al.: Delayed hypersensitivity in Graves’disease
and exophthalmos: identification of thyroglobulin in normal human eye
muscle. Endocrinology, 100:351, 1977.
3. McKenzie, J.M. and Zakarija, M.: Antibodies in autoimmune
thyroid disease. In Werner and Ingbar’s The Thyroid: A Fundamental and
Clinical Text, 6th edition. Edited by L.E. Braverman and R.D. Utiger,
New York, J.B. Lippincott Co., 1991, pp.506-524.
September 25, 2002
Question: I have searched the Internet and found your articles which have been very interesting. My TSH
level is 4.15, and my thyroid peroxidase antibody result was high at 27.9.
My internist told me that high levels of these antibodies don’t affect the
function of my thyroid gland. But for the past four to six months, I’ve
had hair breaking off, and my hair is not growing. I gained 9 lbs. in two
months, and I’ve been depression. I have for the past two years thought I
had arthritis and take Motrin for that. After reading about fibromyalgia on
your website, I think maybe I have it. I just assumed I’d just have to
live with these symptoms. Anyway, do you think I need thyroid treatment?
Dr. Lowe:
Thank you for your very interesting email. Your internist is patently wrong
about the thyroid peroxidase (anti-microsomal) antibodies—they do
indeed impair thyroid gland function. The antibodies are considered
"cytotoxic,"meaning they’re damaging to thyroid gland cells.[1,p.926]
The antibodies interfere with the activity of the enzyme "thyroid
peroxidase," and the interference impairs function of the thyroid
gland.[2]
Your elevated antibodies indicate that you have "autoimmune thyroiditis," and that is clearly a process destructive to the thyroid
gland.
Your TSH level also suggests that the
function of your thyroid gland is impaired. A few years ago, clinicians
would’ve considered your TSH level of 4.15 "normal." Based on
recent evidence, however, a TSH level that high suggests impaired thyroid
gland function—especially in someone with elevated thyroid peroxidase
antibodies. So your TSH, like your antibody titer, indicates hypothyroidism.
Treatment with thyroid hormone usually
suppresses anti-thyroid antibodies and slows or stops the process of
autoimmune thyroiditis.[3][4]
Based on your symptoms and your lab test results, I have no doubt that you are
hypothyroid and need treatment.
References
1. Volpé, R.: Autoimmune
thyroiditis. In Thyroid Function and Disease. Edited by G.W. Burrow,
J.H. Oppenheimer, and R. Volpé, Philadelphia, W.B. Saunders, 1989,
pp.921-933.
2. Kohno, Y., Hiyama, Y., Shface="Verdana" imojo, N., Nakajima, H., and Hosaya,
T.: Autoantibodies to thyroid peroxidase in patients with chronic
thyroiditis. Clin. Exp. Immunol., 65: 534, 1986.
3. Jannson, R., Karlsson, A., and Dahlberg, P.A.: Thyroxine,
methimazole, and thyroid microsomal autoantibody titres in hypothyroid
Hashimoto’s thyroiditis. Br. Med. J., 290: 11, 1985.
4. Trbojevic, B., Lalic, N., and Slijepcevic, D.: The effect of
replacement therapy on thyroid antibody and serum thyrotropin concentrations
in Hashimoto’s thyroiditis. In The Thyroid and Autoimmunity. Edited
by H.A. Drexhage and W.M. Wiersinga, Amsterdam, Excerpta Medica,
1986, p.113.
November 18, 2001
Question: My fibromyalgia (hypothyroid) symptoms started six months after I had
silicone breast implants put in. Several months later my doctor found that I
had high thyroid antibodies. Tests over the next three years showed that my
antibodies stayed high. Several months after I had the implants removed, two
different tests showed that my antibodies were normal again. My doctor told
me there’s no relation between fibromyalgia, hypothyroidism, and breast
implants. Instinctively, I don’t believe him, but I’d like to know what
you think.
Dr. Lowe:
Many patients with silicone breast implants have fibromyalgia symptoms.
These symptoms are the same as those of many patients with hypothyroidism
caused by autoimmune thyroid disease. Some implant patients have positive
immune function test results. The most common positive immune test result is
a high level of anti-nuclear antibodies. This test result, however, isn’t
specific to any of the body's organ systems. Some implant patients have high
levels of "anti-thyroglobulin" and "thyroid peroxidase"
antibodies. These antibodies, of course, are highly specific to the thyroid
gland.
As I wrote at length in The
Metabolic Treatment of Fibromyalgia, studies clearly show that silicone
implants commonly rupture and leak, and bacteria often colonize the
implants. These findings make it plausible that decomposing implants
activate the immune system, and that this activation leads to autoimmune
disease in susceptible women. It’s equally tenable that the autoimmune
disease in some breast implant patients involves the thyroid gland. If the
autoimmune disease suppresses thyroid gland function, the women may develop
so-called "fibromyalgia" symptoms. If the women had fibromyalgia
before getting the implants, their symptoms may worsen.
In 1997, researchers published a report of
two patients who developed Hashimoto’s
thyroiditis
after receiving
silicone breast implants for cosmetic purposes.[1]
A 45-year-old woman
received her implants 1976. In 1991, she developed Hashimoto’s thyroiditis
that led to a deficiency of thyroid hormone. For treatment, she took T4
alone. As often happens, the T4 alone was ineffective, and her symptoms
continued. She was chronically fatigued and had joint pain and morning
stiffness; her eyes were so dry that she had to use artificial tears. In
1995, she had a high level of both antinuclear antibodies and thyroid
peroxidase antibodies. Her gamma globulin level was elevated by 22.6%, and
her thyroid gland was diffusely enlarged. Because her implants were painful,
she had them removed in 1996. A pathologist performed a microscopic exam of
the implant materials from the woman. He reported that each implant had a
fibrous capsule with extremely dense connective tissue and fibrosis. This,
of course, is evidence of immune reaction to the implant materials. The
second patient was 55 years old. She received silicone breast implants in
1984. In 1995, she developed Hashimoto’s thyroiditis. Her thyroid gland
was painful and tender when palpated. She had mild hyperthyroidism and
positive anti-thyroglobulin antibodies. She underwent corticosteroid
treatment for five months. In 1996, her test for antinuclear antibodies was
positive. She had the implants removed because her breasts were painful.
The researchers who reported these two cases
wrote that Hashimoto’s thyroiditis is only rarely associated with silicone
breast implants. They also wrote that the patients’ implants may have had
nothing to do with the thyroiditis.[1]
If silicone implants have nothing to do with patients' autoimmune
thyroiditis, however, we could accurately predict that women with breast
implants would have no higher incidence of anti-thyroid antibodies than
women in the general population. But this prediction is refuted by a report
I just read from AAL Reference Laboratories. The report states, "We
have found [thyroglobulin and thyroid peroxidase antibodies] present in the
sera of 24% of patients with silicone gel breast implants."[2]
For comparison, let's consider the
percentages of 1,314 health individuals with high levels of the antithyroid antibodies. Of 870 males, 2.6% had high thyroglobulin
antibodies, 3.9% had high thyroid peroxidase antibodies, and 2.2% had high
levels of both. Of 484 females, 6.2% had high thyroglobulin antibodies, 9.5%
had high thyroid peroxidase antibodies, and 6.0% had high levels of both.[3]
Obviously, by comparison, the
24% incidence of antithyroid antibodies among implant patients is a far
higher than in the population at large. The higher percentage suggests that
silicone implants leads to autoimmune thyroid disease in a significant
percentage of women. We certainly need more studies of this issue by
unbiased researchers. For the time being, though, I personally believe women
with silicone implants have reasonable concerns—despite firm reassurances
of medical researchers with financial ties to the silicone implant industry.
References
1. Vayssairat, M., Mimoun, M., Houot, B., Abuaf, N., Rouquette, A.M., and
Chaouat, M.: Hashimoto’s thyroiditis and silicone breast implants: two
cases. J. Mal. Vasc., 22(3): 198-199, 1997.
2. AAL Reference Laboratories, Inc., in Santa Ana, California, May 8, 2001.
3.Tajiri,
J., Higashi, K., Morita, M,., et al.: Thyroid antibodies in healthy blood
donors. Endocrinol. Jpn., 31(6):837-843, 1984.
October 5, 2000
Question: My symptoms include
drowsiness, fatigue, and occasional muscle aches. I have a
"normal" TSH of 4.5 (range of 0.4 to 5.0), but my thyroid
antibodies were elevated. My internist overrode my endocrinologist's
suggestion of "doing nothing." But the internist prescribed
Synthroid, the medication you say doesn't work well. My symptoms have
continued despite my using Synthroid. Should I ask the internist to
prescribe something else? Your advice would be helpful.
Dr. Lowe: In an important recent
study, researchers followed patients for 20 years after their initial
thyroid function testing. At follow-up, patients who initially had TSH
levels above 2.0 had a much higher incidence of overt hypothyroidism. Many
researchers, including me, have reached a conclusion from this study—that
the upper half of the "normal" reference range for the TSH is
contaminated with TSH values of patients with incipient thyroid disease. In
practical terms, this means that when a patient's TSH is over 2.0,
suspecting that she has thyroid disease is reasonable, although the disease
may only be dawning. The most common thyroid disease that results in primary
hypothyroidism is chronic autoimmune thyroiditis. Elevated thyroid
antibodies show autoimmune thyroiditis. Your elevated antibodies suggest
that this disease is already under way in your thyroid gland.
Together, your lab test results and your symptoms (which are
characteristic of hypothyroidism) suggest some degree of hypothyroidism.
Even if your thyroiditis waxes and wanes for years, ultimately you’re
likely to progress to overt hypothyroidism. During those waxing and waning
years, you’ll have low thyroid hormone levels at intervals. When your
hormone levels are low, you’ll suffer from hypothyroid symptoms. Some
clinicians will diagnose these symptoms as "fibromyalgia,"
"chronic fatigue syndrome," or one of the other "new
diseases." But you can avoid the symptoms and these pointless diagnoses
simply by using the proper form and dosage of thyroid hormone.
In view of all this, your endocrinologist's do-nothing position doesn’t
make good sense to me. I heartily agree with your internist that you should
be taking thyroid hormone. However, I emphatically qualify that you
should use an effective dosage of a proper thyroid hormone preparation! As
to proper preparations, your prospects for improving with any brand of T4
alone (including Synthroid) are far less than with two other preparations.
Treatment results are far superior when the hypothyroid patient uses either
(1) plain T3, or (2) a T4/T3 combination that has four parts T4 to one part
T3. Two excellent brands of the latter preparation are Armour Thyroid and
Thyrolar.
Regarding effective dosages, our typical patient achieves optimal
treatment results only when we adjust her dosage by the responses of
her tissues to the hormone. Results are less than optimal when the patient’s
thyroid hormone dosage is adjusted according to blood levels of hormones
(such as the TSH and the free T3 and free T4). Every patient and every
doctor should always bear in mind critical advice of Dr. Broda Barnes: Blood
levels of any thyroid-related hormone are thoroughly irrelevant to finding a
patient’s optimal dosage. What's important is the patient’s tissue
response to a particular dosage of thyroid hormone. Unless you and your
doctor follow Dr. Barnes’ sage advice (which I have echoed in The
Metabolic Treatment of Fibromyalgia), you're simply not likely to get
optimal therapeutic results.
October 15, 1997
Question:
I'm wondering if you test your patients for presence of thyroid
antibodies, and if so, whether these values correlate with any other observations. What is
the significance of thyroid antibodies?
Dr. Lowe: We are concerned with thyroid antibodies
in our care of fibromyalgia patients. Our concern is based on our finding that primary
hypothyroidism (inadequate thyroid gland production of thyroid hormone) is the mechanism
of fibromyalgia in some 10% to 14% of patients. We have clearly shown that when these
patients are treated properly, virtually all of them markedly improve or recover. (By
"properly," I mean with the form of thyroid hormone that is effective for the
individual patient, and with a safe dosage that is high enough based on the patient's
response to treatment rather than TSH levels.) It is important to recognize that of
fibromyalgia patients with primary hypothyroidism, fibromyalgia symptoms and signs are a
product of the thyroid hormone deficiency.
We are interested in thyroid antibodies for two main reasons. First, the presence of
antithyroid antibodies strengthens the diagnosis of primary hypothyroidism (which is only
suggested by an elevated TSH level). Second, an elevated titer of antithyroid antibodies
indicates impaired thyroid gland function, even when thyroid function test results do not
show a thyroid hormone deficiency. Before hormone deficiency is detectable by thyroid
function tests, slight reductions in thyroid hormone levels may be causing fibromyalgia
symptoms in a patient whose cells are highly responsive to minor reductions in thyroid
hormone levels. In this subset of patients, antithyroid antibodies are a clue that reduced
thyroid hormone levels may account for fibromyalgia symptoms.
This view is supported by a recent study by Aaarflot and Bruusgaard. They conjectured that
evidence of thyroid autoimmunity is more important than thyroid function tests in patients
with widespread musculoskeletal pain. [Aaarflot, T. and
Bruusgaard, D.: Association of chronic widespread musculoskeletal complaints and thyroid
autoimmunity: results from a community survey. Scandinavian Journal of Primary Health
Care, 14(2):111-115, 1996.]
Also, antithyroid antibodies may indicate that other tissues are involved in the
autoimmune process—possibly accounting for features of fibromyalgia other than pain
and fatigue. In some primary hypothyroid fibromyalgia patients, for example, the
autoimmune process might account for dry mucous membranes (sicca syndrome) [Hansen, B.U., Ericsson, U.B., Henricsson, V., Larsson, A.,
Manthorpe, R., and Warfvinge, G.: Autoimmune thyroiditis and primary Sjogren's syndrome:
clinical and laboratory evidence of the coexistence of the two diseases. Clinical and
Experimental Rheumatology, 9(2):137-141, 1991.]
Corticosteroids lower thyroid antibody titers, but immunosuppressive therapy isn't
necessary because autoimmune thyroiditis can be treated easily with thyroid hormone. All
patients with any degree of hypothyroidism due to autoimmune thyroiditis should be treated
with thyroid hormone. This treatment should be for life, as the patient remains
hypothyroid when he or she stops the use of thyroid hormone. After the patient begins
taking thyroid hormone, thyroid antibody levels usually decrease.
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