Sludge Watch ==> Sewage Sludge - Tobacco - Cadmium - Graves Disease (bulging eyes)

[Maureen Reilly]

Sludgewatch Admin:

That previous post on composting tobacco sludge reminded me of an excellent 
discussion on Graves Disease (think Barabara Bush and her googly eyes).

Graves Disease is a thyroid condition related to cadmium, which is inhaled 
from cigarettes or eaten (especially spinach or swiss chard) and sludged 
soil get more cadmium since sewage sludge has lots of cadmium.

Cadmium has no beneficial role to play in the chemistry of plants or people.

This is such an interesting article!  And another great reason to stop the 
land application of sludge.

Here it is in text format ... but you may enjoy the pictures so look it up 
on the web.


>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

http://www.ithyroid.com/thyroid_eye_disease.htm

THYROID EYE DISEASE (TED)

Thyroid eye disease (TED) is one of the stranger aspects of thyroid disease 
and  particularly interesting from three reasons:  first, it is such a 
bizarre phenomenon making the investigation very interesting; two, it 
provides some very interesting clues about what causes it and what causes 
Graves' disease; and third, it can be extremely uncomfortable for the person 
suffering from it and this makes finding a cure very motivating.

TED is also known as ophthalmopathy, orbitopathy, or exophthalmia.  The eyes 
bulge out and if this becomes severe enough the eyelids no longer close, 
causing the eye to dry out.  Sufferers may have to tape their eyes shut at 
night to keep their eyes from becoming dry and damaged.

The cause of this bulging of the eye is the growth of fibroblasts at the 
back of the eye.  This tissue grows so much that the eye is pushed outward.  
Even more interesting is that there is often another growth in the same 
person--the tissue at the front of the shin, which is also full of 
fibroblasts, grows and this thickened skin is called pretibial myxedema.  
This myxedema is sometimes found on the corresponding underside of the lower 
arm and at other places in the body.

Interestingly, Graves' patients are not the only ones which get TED and 
pretibial myxedema.  People with Hashimoto's thyroiditis also get it and 
even some people who don't have obvious thyroid dysfunction may get it.

Scientists don't know for sure what causes this fibroblast growth, but 
studies show that the immune system seems to be involved.  Immune system 
agents called immunoglobins seem to stimulate the growth of the fibroblasts. 
  The same antibodies that seem to cause Graves' and Hashimoto's seem to be 
the ones involved.

One of the fascinating clues about the cause of Graves', TED, and possibly 
Hashimoto's is that smokers are more likely than nonsmokers to get all of 
these conditions.  There seems to be something ingested in the tobacco smoke 
that causes these conditions to develop and worsen.

While there are many substances in tobacco smoke which affect the thyroid, 
most of these seem to have short-lived effects.  I believe that the agent in 
tobacco which causes thyroid disease must stay in the body a long time.

My theory is that the agent in tobacco smoke which stimulates the onset of 
Graves' and TED is cadmium.  Cadmium is a very toxic heavy metal which is 
found in the Periodic Table of Elements right below zinc, which in turn is 
just to the right of copper.

Cadmium is a metal found naturally in soil which is taken up by green leafy 
plants such as tobacco.  Other green leafy plants like lettuce, spinach, 
beet greens, and Swiss chard also are high in cadmium.  Some root vegetables 
like carrots seem to accumulate cadmium.  The fact that cadmium is taken up 
by these plants and humans and other animals eat and enjoy these plants 
suggests that cadmium might be an essential nutrient.

There is a protein in the body called metallothionein, which is formed from 
the amino acid cysteine, that transports cadmium, zinc, copper and possibly 
other metals in the body.  It's possible that excessive cadmium competes for 
transport sites with copper and zinc and may even be preferentially 
transported by metallothionein and this is the reason why cadmium in 
excessive amounts is so toxic to the body.

Cadmium is a very useful metal because it provides corrosion resistance and 
has electrical properties.  It is used extensively in industry and cadmium 
waste goes into the sewage system.  Sewage sludge is an inexpensive 
fertilizers used in agriculture.  Because of growing awareness of the high 
cadmium content and the dangers of cadmium are becoming more well known, 
most progressive and organic farmers do not use sewage sludge.  However 
sewage sludge is still used in some agriculture.  Tobacco is one of the 
crops which are fertilized extensively with sewage sludge, and this is one 
reason why tobacco is so high in cadmium.  However, even tobacco not 
fertilized this way has high cadmium because the plant naturally accumulates 
cadmium from the soil. When tobacco is smoked, relatively large amounts of 
cadmium are ingested into the body.

Batteries are another source of cadmium.  Ni-Cad or nickel-cadmium batteries 
are used extensively and we all handle these.  It is highly likely that 
cadmium particles cling to the outside of these batteries and we may ingest 
this cadmium if we don't thoroughly wash our hands after handling these 
batteries.

There are some very big problems with cadmium entering the body. First of 
all, cadmium is known to be toxic to the thyroid gland cells.  Thyroid cells 
can be taken from an animal and put into a dish and kept alive.  Then 
various substances including heavy metals can be added to the cells to study 
the effects.  From these studies cadmium has been determined to be a metal 
which is  particularly damaging to thyroid cells.  It's not surprising that 
smoking might cause thyroid malfunction.

Another interesting thing about cadmium is that female animals tend to 
accumulate cadmium while male animals tend to not accumulate it as much. 
This is an extremely strange phenomenon but it lends support to the theory 
that cadmium is a culprit in autoimmune thyroid disease and TED.

Consider these experiments:  Scientists took male and female rats and 
castrated them, thereby eliminating the bulk of their naturally produced sex 
hormones, testosterone and estrogen.  Then they gave half the animals (both 
male and female) cadmium.  The groups were further divided so that half of 
each group was injected with testosterone and half with estradiol (the most 
potent of the estrogens).  The animals that were given estradiol, whether 
male or female, were found to accumulate cadmium, and the animals given 
testosterone were found to excrete the cadmium.  By this experiment it was 
shown that estrogen (estradiol) causes the accumulation of cadmium, while 
testosterone causes the excretion of cadmium.

What does this mean?  It means that women are much more likely to accumulate 
cadmium and to suffer from the toxic effects of cadmium.  (I will discuss 
this situation in more detail in the cadmium story.)  Since women make up 
close to 90% of thyroid disease cases, this offers very suggestive evidence 
that cadmium might be an important factor.  Women's bodies are not well 
suited for being exposed to toxic metals.

Another interesting aspect of TED is that studies show that TED increases 
following radioiodine therapy (RAI).  When you think about it, this is a 
very strange, but intriguing phenomenon also.

My feeling is that this might also be connected to cadmium.  When 
radioactive iodine is administered in RAI, we know that this radioiodine 
must break down into alpha particles and other elements.  Iodine is element 
number 53, so when it breaks down it presumably breaks down into elements 
with smaller atomic numbers.

Cadmium is element number 48, only five elements below iodine.  It's 
possible that as radioiodine breaks down into cadmium which is the stable 
breakdown product.  I hope to find out if this is possible, but this would 
fit in with the observations and theory that cadmium toxicity is a prime 
cause of TED and Graves'.

If the theory that cadmium toxicity is a major causative factor in TED and 
Graves', then there is another bizarre conclusion:  that consumption green 
leafy vegetables might be very damaging to sufferers of Graves' and TED.  I 
have to laugh every time I think about this because it is a very strange 
conclusion.  It's extremely difficult for me or most people to think of 
salads filled with green leafy vegetables as possibly being culprits in 
Graves'.

Remember that this is just a theory, but interestingly this agrees with my 
experience when I had hyperthyroidism.  It seemed that whenever I ate a 
green salad my hyper symptoms would increase and that night would be a more 
difficult night than usual.

Also, recently I met a woman who was the first person I've known with TED.  
I was amazed at how her eyes protruded and she told me that she had just 
concluded a series of ten radiation sessions in which the radiation was 
directed to the fibroblasts at the back of the eyes.  I felt very sorry for 
her--it's not a pretty sight.

I explained many of my theories to her including the one about how eating 
green leafy vegetables might be very damaging because of the cadmium 
content.  I was very amazed when she told me that she practically lived on 
salads loaded with green leafy vegetables.  This is just observation, but it 
didn't contradict the theory.  Pretty strange theory, if true.

March 5, 2002

Some group members have said that flax seed oil or eggs from chickens fed 
flax seed oil have benefited their thyroid eye disease. It's definitely 
worth a try.

STUDIES

The following study may be extremely significant for the understanding of 
Graves' disease and Graves' ophthalmopathy (TED). While I hesitate to jump 
to conclusions, this study seems to indicate that manganese superoxide 
(MnSOD), which is an antioxidant, may stimulate retroocular fibroblast 
growth which is the root of TED. The retroocular fibroblasts seem to grow in 
response to stimulation by the TSH receptor antisera (anti-p1). MnSOD has a 
similar structure to the TSH receptor peptide and apparently in Graves' 
there is an autoimmune response to MnSOD. Therefore it is possible that an 
excess amount of manganese in the diet causes excessive production of MnSOD 
which in turn causes and autoimmune response to MnSOD and this stimulates 
the retroocular fibroblasts. While this would be very interesting, I don't 
know if my interpretation of this is correct. However, this does fit in with 
the fact that manganese is a copper antagonist and high levels of manganese 
would suppress copper levels. Copper supplementation could, in turn, help 
reduce manganese levels and help suppress this autoimmune response.

Immunodetection of manganese superoxide dismutase in cultured human 
retroocular fibroblasts using sera directed against the thyrotropin 
receptor.
Burch HB, Barnes S, Nagy EV, Sellitti D, Burman KD, Bahn RS, Lahiri S
Endocrine-Metabolic Service, Kyle Metabolic Unit, Walter Reed Army Medical 
Center, Washington, DC 20307-5001, USA.

The identification of antigenic targets in the retroocular autoimmune 
response of Graves' ophthalmopathy is likely to increase our understanding 
of mechanisms underlying this disorder. While a number of putative 
autoantigens have been identified on the basis of molecular weight or cell 
of origin, a determination of the significance of these antigens is 
contingent upon an identification of the amino acid sequence. Our group has 
previously identified immunoreactive retroocular fibroblast (ROF) proteins 
recognized by thyrotropin receptor (hTSH-R) antisera (anti-p1), at molecular 
weights of 95, 71, 41, and 14-25 kDa. In the present study, proteins 
detected by anti-p1 and visualized by Ponceau staining were isolated and 
processed for microsequencing. Ponceau staining revealed dense bands at 
molecular weights of 14 and 23 kDa, and a weak band at 41 kDa. N-terminal 
sequencing was performed on the prominent band at approximately 23 kDa, 
showing it to be manganese superoxide dismutase (MnSOD), a mitochondrial 
enzyme responsible for protection against oxygen free radical-associated 
cellular damage. Sequence comparison of MnSOD to the hTSH-R peptide, p1, 
revealed a linear segment of amino acid homology. Preincubation of anti-p1 
with p1 blocked immunodetection of the 23 kDa band corresponding to MnSOD, 
and immunoprecipitation of ROF protein using anti-pi yielded protein 
recognized by anti-MnSOD. Autoimmunity against human recombinant MnSOD was 
further assessed by ELISA. Patients with Graves' disease (n = 53) had 
significantly higher ELISA indices than normal control subjects (n = 29), 
while patients with Hashimoto's thyroiditis had intermediate values. These 
results document MnSOD autoantibodies in patients with Graves' disease and 
suggest that this may result from an immune cross-reactivity between MnSOD 
and the TSH-receptor.

The following study suggests that selenium deficiency is involved in 
fibrosis. This proliferation of fibroblasts is also seen in Thyroid Eye 
Disease, therefore this condition may be a result of selenium deficiency.

Title

Selenium deficiency and thyroid fibrosis. A key role for macrophages and 
transforming growth factor beta (TGF-beta).

Author

Contempre B; Le Moine O; Dumont JE; Denef JF; Many MC

Address

Institute of Interdisciplinary Research (IRIBHN), Free University of 
Brussels, Medicine Faculty, Belgium. bcontemp at med.ulb.ac.be

Source

Mol Cell Endocrinol, 124(1-2):7-15 1996 Nov 29

Abstract

Free radical damage and fibrosis caused by selenium deficiency are thought 
to be involved in the pathogenesis of myxoedematous cretinism. So far, no 
pathway explains the link between selenium deficiency and tissue fibrosis. 
Pharmacological doses of iodine induce necrosis in iodine-deficient 
thyroids. Necrosis is much increased if the glands are also 
selenium-deficient, which then evolve to fibrosis. This rat model was 
reproduced to explore the role of selenium deficiency in defective tissue 
repair. At first, proliferation indexes of epithelial cells and fibroblasts 
were comparable between selenium-deficient and control groups. Then, in 
selenium-deficient thyroids the inflammatory reaction was more marked being 
mainly composed of macrophages. The proliferation index of the epithelial 
cells decreased, while that of the fibroblasts increased. These thyroids 
evolved to fibrosis. TGF-beta immunostaining was prominent in the 
macrophages of selenium-deficient rats. Anti TGF-beta antibodies restored 
the proliferation indexes, and blocked the evolution to fibrosis. In 
selenium deficiency, an active fibrotic process occurs in the thyroid, in 
which the inflammatory reaction and an excess of TGF-beta play a key role.
The following is a study which suggests that a bone marrow transplantation 
cured Graves', TED, and anemia.  This could also be interpreted that the 
Graves' and TED were caused by the anemia and correction of the anemia by 
the bone marrow transplantation corrected these conditions.  The bone marrow 
is where the red blood cells are manufactured. Be aware that this is just 
one case and not scientific evidence.


Clin Endocrinol (Oxf) 1999 Feb;50(2):267-70


Apparent cure of Graves-Basedow disease after sibling allogeneic bone marrow 
transplantation.

Diez S, Banias H, Diez-Martin JL, Briz M, Estrado J, Barcelo B

Department of Endocrinology, Universidad Autonioma, Madrid, Spain.

Evidence that allogeneic bone marrow transplantation (BMT) can cure or alter 
the course of intractable autoimmune diseases comes from both extensive 
experimental work in animal models and anecdotal case reports in humans. We 
describe a female patient diagnosed as having severe aplastic anaemia (SAA), 
hyperthyroidism and ophthalmopathy of Graves-Basedow disease who received a 
BMT from her histocompatible sister. Fifty-three months after BMT, complete 
remission of hyperthyroidism and ocular signs persists. The SAA is cured and 
she is free of any chronic graft-versus-host disease (GVHD). In the early 
post-BMT period, PCR analysis of bone marrow and peripheral blood cells 
confirmed a complete chimerism of donor origin. Thus, it is plausible to 
attribute the resolution of the patient's thyroid hyperfunction and 
opththalmopathy to the replacement of the host immune system.

PMID: 10396372, UI: 99324694
The following study shows that radiation therapy for ophthalmopathy (TED) 
does not produce any beneficial effects that can be measured (by the methods 
used in this test).  There does not seem to be any benefit from 
radiotherapy, leaving only the negative effects of radiation.  I see 
absolutely no reason to undergo radiation therapy for TED.

A PROSPECTIVE, RANDOMIZED, DOUBLE-BLIND CONTROLLED STUDY OF ORBITAL 
RADIOTHERAPY FOR GRAVES' OPHTHALMOPATHY.

C. Gorman, J. Garrity, V. Fatourechi, R.S. Bahn, I. Petersen, S. Stafford, 
J. Earle, G. Forbes, R. Kline,E. Bergstralh, K. Offord, D. Rademacher, N. 
Stanley and G. Bartley Division of Endocrinology and Departments of 
Ophthalmology, Radiation Oncology, Diagnostic Radiology and the Section of 
Biostatistics, Mayo Clinic, Rochester, Minnesota USA and University of 
California Davis at Sacramento, Division of Radiation Oncology, Sacramento, 
California USA

Background: Although widely used for treatment of Graves' ophthalmopathy 
(GO), the efficacy of orbital radiotherapy (OT) has not been established in 
a prospective randomized double-blind controlled trial.

Specific aims: To determine: 1) If 20 Gy of external beam OT directed to one 
orbit of patients with GO resulted in improvement in comparison with the 
untreated orbit when evaluated three and six months after therapy; 2) If 20 
Gy of OT to the second orbit six months later produced effects similar to 
those observed when the first orbit was treated; 3) To relate the magnitude 
of the treatment effect to the time since onset of eye symptoms.

Patients and Methods: Forty-two euthyroid patients with mild to moderate GO 
and elevated TSI levels received 20 Gy of megavoltage radiation to a 
randomly selected orbit. Six months later the second orbit was treated. 
Every three months, measurements were made of thyroid function and antibody 
status, proptosis, volume of extraocular muscle (EOM) and fat, range of EOM 
motion, eyelid fissures and extent of diplopia. The study had 80% power to 
detect 0.5 mm change in proptosis and 0.75 mL in volume measures.

Results: Six month - baseline measurements were recorded for the untreated 
(UT) and the treated (T) orbit. They revealed (mean±SD): Fat volume(cc) UT 
-0.3(1.3), T 0.3(1.3), P 0.87. Muscle volume(cc) UT -0.4(1.3), T -0.6(1.4), 
P 0.14. Proptosis(mm) UT 0.0(1.0), T -0.1(1.3), P 0.46. Range of motion area 
(cm2) UT 8.7 (33), T 8.8(35), P 0.98. Lid fissures(mm) UT 0.0(2.0), T 
-0.1(1.7), P 0.42.

Results at three months were similar to those at six months. Diplopia field 
area at baseline, six and 12 months was 42, 41, and 39 cm2. P=0.09 for six 
months - baseline and 0.02 for 12 months - baseline. Subset analyses of 
early vs. late treated orbits, or smokers vs. non-smokers, and of patients 
treated <1.3 vs. >1.3 years since onset disclosed no significant differences 
for any group.

With one exception, patients were euthyroid on commencing and throughout the 
study.

Conclusion: If radiotherapy is beneficial for Graves' ophthalmopathy, its 
ameliorative effects did not reach the detection level of the techniques 
used in this study. No clinically significant benefit was observed.

>From Mercola.com:

Radiotherapy Does Not Help Graves' Disease Eye Problems
For years, radiation therapy to the eye has been used to treat eye problems 
associated with the thyroid condition Graves' disease. Now a new study 
questions whether this treatment is actually useful.

Graves' disease triggers an overproduction of hormones from the body's 
thyroid gland, a key regulator of metabolism and other vital functions. A 
small percentage of people with the disorder have a complication called 
Graves' ophthalmopathy, which is characterized by bulging eyes, double 
vision and other eye problems.

To investigate the effectiveness of radiotherapy for these eye 
complications, investigators studied 42 patients with Graves' 
ophthalmopathy. The patients exhibited a variety of symptoms including 
higher-than-normal volumes of eye muscle and fat, bulging of the eyes, less 
eye range of motion and double vision.

The patients received radiotherapy in one eye and a "sham" treatment in the 
other eye.

At follow-up, 3 and 6 months after treatment, no significant differences 
were observed between the treated and untreated eyes.

And this was true regardless of whether a patient was a smoker. Smokers, the 
researchers note, have been found to be more vulnerable to Graves' 
ophthalmopathy, and this could theoretically affect their response to 
treatment.

Graves' disease is a naturally remitting condition, and over a period of 
time many of the symptoms, including [those related to] the eyes, may 
improve. This tendency to natural remission, together with the imprecision 
of measurements used in most previous studies, has allowed the perception to 
persist that the treatment is effective.

Overall, in 44% of the patients, the eye treated with radiotherapy did not 
appear any different from the non-treated eye. In about 27% of patients the 
treated eye appeared better than the untreated eye, but in 30% it appeared 
worse.

Ophthalmology September 2001;108:1523-


If you look at the following study you'll see that a significant improvement 
was obtained in TED (Graves' ophthalmopathy) with vitamin B3 
(nicotinamide--a form of niacin). 300 mgs of nicotinamide a day was used. 
Allopurinol is an inhibitor of xanthine oxidase. Xanthine oxidase is a 
molybdenum-based enzyme. Since molybdenum and copper are antagonists, a 
copper deficiency could allow excess xanthine oxidase to proliferate. If 
xanthine oxidase is involved in the genesis of TED, then this is a possible 
explanation of why copper might help reduce TED.

The significance of this study is that it really offers evidence that TED is 
a nutritional deficiency disease.

A note on molybdenum: it's possible that excess molybdenum is involved in 
TED. If you have TED and are trying molybdenum, be especially aware to see 
if molybdenum might increase the symptoms of the TED.

<<http://forums.about.com/n/main.asp?webtag=ab-thyroid&msg=11222.1&Find=Find

Am J Ophthalmol 2000 May;129(5):618-22 Related Articles, Books, LinkOut

Antioxidant agents in the treatment of Graves' ophthalmopathy.

Bouzas EA, Karadimas P, Mastorakos G, Koutras DA Department of 
Ophthalmology, Red Cross Hospital, Athens, Greece.
mastorak at matrix.kapatel.gr

PURPOSE: To report the effect of antioxidant agents in the treatment of mild
and moderately severe Graves' ophthalmopathy. METHODS: Prospective,
nonrandomized, comparative study performed at a referral center. A series of
11 patients with mild or moderately severe, active, newly diagnosed Graves'
ophthalmopathy were included in the study. Allopurinol (300 mg daily) orally
and nicotinamide (300 mg daily) orally were used for 3 months. A complete
ophthalmologic examination was performed before and 1 and 3 months after
initiation of treatment. The response to treatment was estimated separately
for each component of the disease and overall by its effect on a total eye
score. Eleven patients with mild or moderately severe, active, newly
diagnosed Graves' ophthalmopathy who received placebo were also examined at
the same time points. Patients in each group were recruited consecutively.
Although nonsmoking was not an exclusion criterion, all patients were
cigarette smokers. RESULTS: Nine (82%) of 11 patients treated with oral
antioxidants showed improvement of mild to moderately severe Graves'
ophthalmopathy versus three (27%) of 11 patients in the control group (P
<.05). Soft tissue inflammation was the component of the disease that
responded more to treatment. No side effects of antioxidant treatment were
recorded. Patients' satisfaction was high. CONCLUSIONS: This pilot study
presents encouraging results in the treatment of mild and moderately severe
Graves' ophthalmopathy with antioxidant agents. To evaluate these 
preliminary
results, randomized prospec-tive studies are needed.

Mary Shomon told me about a website called www.TEDCURE.com.

When potassium is deficient the cell membrane allows more water to enter the 
cell than escape so cells swell up with water. This is manifested in people 
as edema and many hypers report gaining weight on very little calorie intake 
and generally having edema. Myxedema which is another form of edema and 
which is seen in Graves' as pretibial myxedema or orbital fibroblast 
proliferation may have the same origin: from potassium deficiency. I 
consider it quite likely that potassium deficiency is a major contributing 
cause to TED and worthy of further investigation. However, I doubt if 
potassium deficiency is the only cause. Most likely it is one of several 
deficiencies whose combination leads to the condition.

Following is a list of potassium deficiency symptoms from Dr. Gupta's 
website:

HEAD : heavy; lethargy, drowsy, yawning, mild headche; dull thinking
& concentration, emotional, Hairs slowly turning grey with
weak roots.
EYES  : heavy; tired, photophobia.
EARS : buzzing.
NOSE  : irritation & repeated sneezing.
FACE : abnormal feel of superficial skin.
MOUTH : dry; gum bleeding, recurrent cuts inside the mouth while eating; 
side of tongue having abnormal feel, hiccups & reflux oesophagitis; hoarse 
voice.
NECK : muscles tired as while driving; jerky movements at neck.
UPPER LIMBS : cold hands; arms tired while working; numbness & tingling of 
hands; corns on fingers; arms & hands as if falling down when outstretched; 
grip not strong & handwriting not clear with less pressure while writing; 
bilateral tender points near elbows; visible pulsating vessels.
BACK : itchy; often lumbar sprains.
HEART : pulsation & palpitations; high recordable B.P.
CHEST : rapid breathing; suffociation while lying down.
ABDOMEN : constipation; excessive gas formation & urination.
LOWER LIMBS : painful buttocks while prolonged sitting on hips; pain in 
thigh muscles while going upstairs & pain in lower leg muscles while sitting 
on foot; bilateral tender points on lower legs near ankles; stamping gait 
multiple corns; cold & numb feet.
JOINTS : pain on pressing joint crease.
WHOLE BODY  : as if squeezed out, with the desire to lie down; dull &
apprehensive;
And History of falling down on ground.

This problem of K-loss results in early maturity, early decay and early 
death.

The following study shows that smoking and RAI greatly increase the risk for 
developing Thyroid Eye Disease. Also note

Risk factors for thyroid optic neuropathy include smoking, radioactive 
iodine treatment
Patients should be followed closely. Visual-field and color-vision testing 
help in early detection.
by Bob Kronemyer


  May 15, 1999

---Disc edema in a patient with thyroid optic neuropathy and field defect.

WAIKOLOA, Hawaii — Smoking and radioactive iodine treatment alone are two 
risk factors for developing thyroid optic neuropathy among patients with 
Graves’ hyperthyroidism.

“We now know that smoking is a significant risk factor,” said Robert L. 
Lesser, MD, a neuro-ophthalmologist in private group practice in Waterbury, 
Conn. “This is another reason to warn these patients that they should not be 
smoking. In fact, patients who have thyroid disease in general are seven 
times more likely to develop a more severe form of ophthalmopathy if they 
smoke.”


Combined treatment may be better
---Clinical photograph of a patient with marked limitation of gaze with 
thyroid optic neuropathy and minimal proptosis.

Radioactive iodine treatment alone also increases the risk of contracting or 
worsening ophthalmopathy. One study published last year showed that 15% of 
patients who were treated only with radioiodine developed or had worsening 
ophthalmopathy. In contrast, none of the patients who were treated with both 
radioiodine and prednisone had progression, and two-thirds showed 
improvement. Further, only 3% of those treated with methimazole had any 
worsening of eye disease.

“Presumably what happens with thyroid ophthalmopathy is that the lymphocytes 
that are targeting against the thyroid also react to the eye muscles. You 
end up with lymphocytic infiltration and mucin deposition,” said Dr. Lesser, 
who spoke here at Hawaii ‘99, sponsored by Ocular Surgery News and the New 
England Eye Center.

The inferior rectus, medial rectus and superior rectus are the most commonly 
involved muscles, “so it is really an eyeball diagnosis,” said Dr. Lesser, 
who recommends “a computerized tomography [CT] scan or magnetic resonance 
imaging [MRI] of the orbit with fat suppression to document enlargement of 
the muscles.”

Dr. Lesser cited a female patient with white eyes. “That doesn’t necessarily 
make a difference, though. Sometimes the eyes are congested and sometimes 
they are not,” he said. However, the patient also had minimal proptosis. 
“That is one of the tip-offs that there is a greater risk for thyroid optic 
neuropathy, be cause of the simple mechanical crowding phenomenon.”

Although the risk of developing the disease is relatively low (1% to 5%), 
vision loss is possible; therefore, these patients should be tested and 
followed closely. Moreover, the absence of disk edema does not exclude the 
diagnosis.


Test useful for early detection
Visual-field and color-vision testing help in early detection. “Patients 
need to be alerted about the possibility of a change in vision and need to 
arrange to see you if this happens,” Dr. Lesser said. Low-dose radiation may 
be appropriate for even some of the congestive findings.

Once the diagnosis is made, Dr. Lesser starts patients on short-term 
steroids. “I do not favor using steroids on a long-term basis because I 
think the treatment becomes worse than the disease,” he said. He also 
mentioned that high-dose steroids may be appropriate in certain situations. 
“We are now becoming comfortable with 1 g of methylprednisolone intravenous 
for 3 to 5 days and seeing if that rapidly decompresses the muscle.”

Dr. Lesser’s patients are maintained on steroids throughout radiation 
treatment. “It is at that point that I taper the steroids and then measure 
the effect,” he said. “Results are quite good in most cases.” Surgical 
decompression of the orbit is reserved for those patients with a 
contraindication or intolerance. “You have several choices with 
decompression, including lateral wall, medial wall and inferior wall,” he 
said.

Overall, patients are “psychologically devastated” by thyroid orbitopathy, 
Dr. Lesser said. “A lot of these patients need counseling and support.”

For Your Information:  Robert L. Lesser, MD, can be reached at 1201 W. Main 
St., Waterbury, CT 06708; (203) 597-9100; fax: (203) 597-1696. Dr. Lesser 
has no direct financial interest in any of the products mentioned in this 
article, nor is he a paid consultant for any companies mentioned.
Reference:  Bartalena L, Marcocci C, Bogazzi F, et al. Relation between 
therapy for hyperthyroidism and the course of Graves’ ophthalmopathy. N Engl 
J Med. 1998;338(2):73-78.




WAIKOLOA, Hawaii — Smoking and radioactive iodine treatment alone are two 
risk factors for developing thyroid optic neuropathy among patients with 
Graves’ hyperthyroidism.

“We now know that smoking is a significant risk factor,” said Robert L. 
Lesser, MD, a neuro-ophthalmologist in private group practice in Waterbury, 
Conn. “This is another reason to warn these patients that they should not be 
smoking. In fact, patients who have thyroid disease in general are seven 
times more likely to develop a more severe form of ophthalmopathy if they 
smoke.”

Blindness following orbital irradiation for Graves' ophthalmopathy.

Arch Ophthalmol. 1984 Oct;102(10):1473-6.


Radiation retinopathy after orbital irradiation for Graves' ophthalmopathy.

Kinyoun JL, Kalina RE, Brower SA, Mills RP, Johnson RH.

Recent reports indicate that orbital irradiation for Graves' ophthalmopathy 
is sometimes beneficial, particularly for dysthyroid optic neuropathy, and 
is not associated with serious complications. We are aware, however, of four 
patients who were found to have radiation retinopathy after orbital 
irradiation for Grave's ophthalmopathy. All four patients have decreased 
central acuity, and three of the four are legally blind in one or both eyes. 
Computer reconstruction of the dosimetry, based on computed tomography and 
beam profiles, shows that errors in dosage calculations and radiotherapy 
technique probably account for the radiation retinopathy in three of the 
four patients. Radiotherapy for Graves' ophthalmopathy should be 
administered only by competent radiotherapists who are experienced in the 
treatment of this disease. Similar errors in dosage calculations and 
treatment techniques may account for other reports of radiation retinopathy 
after reportedly safe dosages.

Publication Types:  Case Reports

PMID: 6548374 [PubMed - indexed for MEDLINE]