THYROID DISEASE

Read and learn more about thyroid disease goiter. For more, visit the Thyroid Disease website ThyroidDiseaseWiki.com.

Q: If you have an enlarged goiter will you develop thyroid disease?
my mother had a hyper active thyroid and everyone on her fathers side had problems…ive had a goiter for about 12 years and my blood comes back ok….is there other tests besides blood and ultasound that they can take …like antibodies?? or am i just fine i am on my fourth child and they say pregnancy can make it misbehave.

A: No.

And why is this question in the “marraige and divorce” section?

Q: was diagnosed with thyroid disease (hyper) I had a goiter, and I have bad allergies, and I also suffer from b?
I have RA and the symptoms come and go

A: http://autoimmunedisease.suite101.com/discussion.cfm/4197/877-886

Q: is it possible to have a thyroid disease and not show up in the bloods?
I have many symptoms to many to mention but my thyroid is painful at times.I am developing a goiter and my thyroid gland is definitetly enlarged.Yet i had two thyroid tests one before christmas and one recently but my doctors says its comeback normal again.This is so annoying as i feel sick and still know results.

A: What kind of blood test did you have? Did the doctor just do a TSH? If so that is not enough. You need to have your Ft4 and Ft3 checked. Also if you have a goiter you may be Iodine defincent. Check out the following web site.
www.stopthethyroidmadness.com

Q: thyroid disease?
hows it like being pregnant and being hyperthyroid or hypothyroid. wat meds do you take while pregnant. and if anybody has a goiter or mass on their necks. thanks for the answers.

A: I had carried 2 children while on thyroid med
and now my 3rd
your doc will take care of your med dosage and he will make you have blood test monthly to make sure that the baby is healthy as well as you
Good luck

Q: Is having Hypothyoidism a Thyroid Disease?
Long story short.. I got a lump in my neck very big they removed it ( I thought they removed my right thyroid but now im not sure if they did that and the lump or just the goiter ) Then a year later found out my thyroid wasnt working again and now im on medication Eltroxin 0.05 mg ( levothyroxin) Now when i go to get over the counter stuff it says do not take if you have thyroid disease so im wondering if hyprothryoidism a thyroid disease.

A: I’ve been taking synthroid for low thyroids for over 10 years and I’ve taken many over the counter medications that say not to take with thyroid disease, without any problems. However, the best thing to do would be to ask your doctor. Better safe then sorry. Have a great day. : )

Q: Operation to remove part of swollen thyroid (goiter). Risks associated with operation?
My friend is having an operation to remove part of her thyroid as she has Hashimotos disease and the gland has become quite large. Does anyone have any experience with this and does anyone know of the risks associated with the operation? I have been told it is quite a delicate operation and she will have to be off work for 4 weeks. Many thanks.

A: Surgery is always risky. I think the other post did well describing what to expect.

But what about the autoimmune disorder? Cutting out the thyroid isn’t going to solve the problem.

Also, you kind of need your thyroid. You can supplement with exogenous sources, but there are side effects that can cause you to be placed into not so nice categories (like more susceptible to stroke, Alzheimer’s, etc).

Here is some food for thought.

Autoimmune means that your body’s immune system is attacking itself, in your case the thyroid gland.

It does this by recognizing certain protein strands and tagging it with antibodies. Then your body sends out it seek and destroy immune mediators to kill off the tagged protein structures.

Usually this is how your body defends itself from viruses, bacteria, fungi, ect. There is a problem with your tagging system that has caused your body to attack itself.

This is usually diagnosed by testing for antibodies in blood work, as well as clinical symptoms.

How does this happen?

There is no one pin pointed cause. The most popular reason is because of some break down in your filtering system. You normally keep bad things out through things like your skin, gut lining etc.

If there is a problem with your gut, things get through that shouldn’t, your body recognizes it as foreign, tags it and destroys it.

Sometimes the protein structures of the things that get through look like the protein structures that make up certain cells in your body. That is why you see some of the other post saying that this autoimmune disorder is related to other autoimmune disorders (diabetes, lupus, RA, etc).

It is really a problem with your filter, not your thyroid (or at least primarily the problem). Treating the thyroid might help somewhat, but it will not address the problem (in my example, the gut lining (filter) being disrupted).

I got more information on this and other thyroid problems on my blog.

Q: I have a Thyroid disease and my multiple doctors can’t diagnose it. Please HELP!!?
Ok I was first told I have a thyroid disease about 2 years ago. I was 19yrs old and had a 9 month old son. My first and only symptom was I was tired and draging myself through a day. At first I thought it was just having a new baby but when he started sleeping through the night I thought something has got to be wrong. Well my TSH has always been extremeley low and sometime undetectable. But my t3 and t4 have always been normal. First they thought it was secondary hypothyroidism and put me on synthroid. Then that wasn’t helping so they did more tests and ruled it out again. My symptoms now are anxiety attacks, shakiness, my mind feels like it’s racing and I just can’t get enough done. I walk fast and I am now anti social. Which I used to love to talk but now I’m scared of conversation. I have hot flashes, migraines, can’t tolerate noise, but the worst one is my extreme fatigue. I’ve had numerous tests that shows I have a multi nodular goiter, enlarged thyroid, and 4 swallen lymphnodes.

A: I have grave’s disease – extreme hyperthyroidism. You may have been suffering from Chronic Fatigue Syndrome at first and when they gave you synthroid – it could have pushed your thyroid into overdrive! You symptoms are classic hyperthyroid symptoms, but I would see another doctor/specialist to determine exactly what the diagnosis would be. You never have to settle on what one doctor tells you. Remember – they call it a practice for a reason!! Good Luck and I hope you feel better soon!
Feel free to e-mail me if you have any other questions.
=)

Q: i want informations about goiter disease?
it’s a disease which infect thyroid gland… i want to make presentation about it so i want detailed regulated infgormations about this disease

A: A goiter is an enlargement of the thyroid gland. Persons with enlarged thyroids may have normal function of the gland (euthyroidism), thyroid deficiency (hypothyroidism), or overproduction of the hormones (hyperthyroidism). Goiter may be congenital or acquired, endemic or sporadic.
The goiter often results from increased pituitary secretion of thyrotropic hormone in response to decreased circulating levels of thyroid hormones. Thyroid enlargement may also result from infiltrative processes that may be inflammatory or neoplastic. Goiter in patients with thyrotoxicosis is caused by thyrotropin receptor-stimulating antibodies.

Figure 561-1 Congenital goiter in infancy. A, Large congenital goiter in an infant born to a mother with thyrotoxicosis who had been treated with iodides and methimazole during pregnancy. B, A 6-wk-old infant with increasing respiratory distress and cervical mass since birth. The operation revealed a large goiter that almost completely encircled the trachea. Notice the anterior deviation and posterior compression of the trachea. Partial thyroidectomy completely relieved the symptoms. It is apparent why a tracheostomy is not adequate treatment for these infants. The cause for the goiter was not found.
561.1 Congenital Goiter
Congenital goiter is usually sporadic and may result from a fetal thyroxine (T4 ) synthetic defect or the administration of antithyroid drugs or iodides during pregnancy for the treatment of thyrotoxicosis. Goitrogenic drugs and iodides cross the placenta and at high doses may interfere with synthesis of thyroid hormone, resulting in goiter and hypothyroidism in the fetus. The concomitant administration of thyroid hormone with the goitrogen does not prevent this effect, because insufficient amounts of T4 cross the placenta. Iodides are included in many proprietary preparations used to treat asthma; these preparations must be avoided during pregnancy because they have often been a cause of unexpected congenital goiter. Amiodarone, an antiarrhythmic drug with a 37% iodine content, has also caused congenital goiter with hypothyroidism. Even when the infant is clinically euthyroid, there may be retardation of osseous maturation, low levels of T4 , and elevated levels of thyroid-stimulating hormone (TSH). In women with Graves disease on antithyroid drugs, these effects can occur when the mother takes only 100–200?mg of propylthiouracil/24?hr; all such infants should undergo thyroid studies at birth. Administration of thyroid hormone to affected infants may be indicated to treat clinical hypothyroidism, to hasten the disappearance of the goiter, and to prevent brain damage. Because the condition is rarely permanent, thyroid hormone may be safely discontinued after the antithyroid drug has been excreted by the neonate, usually after a week.
Enlargement of the thyroid at birth may occasionally be sufficient to cause respiratory distress that interferes with nursing and may even cause death. The head may be maintained in extreme hyperextension. When respiratory obstruction is severe, partial thyroidectomy rather than tracheostomy is indicated ( Fig. 561–1 ).
Goiter is almost always present in the congenitally hyperthyroid infant. These goiters usually are not large; the infant manifests

1882
clinical symptoms of hyperthyroidism, and the mother often has a history of Graves disease (see Chapter 562.1 ). TSH receptor-activating mutations are also a recognized cause of congenital goiter.
When no causative factor is identifiable, a defect in synthesis of thyroid hormone should be suspected. Neonatal screening programs find congenital hypothyroidism caused by such a defect in 1/30,000–50,000 live births. If the infant is hypothyroid, it is advisable to treat immediately with thyroid hormone and to postpone more detailed studies for later in life. Because these defects are transmitted by recessive genes, a precise diagnosis is helpful for genetic counseling. Monitoring subsequent pregnancies with ultrasonography can be useful in detecting fetal goiters (see Chapters 85.2 ).
Iodine deficiency as a cause of congenital goiters is rare in developed countries, but persists in isolated endemic areas (see below). More important is the recent recognition that severe iodine deficiency early in pregnancy may cause neurologic damage during fetal development, even in the absence of goiter. The iodine deficiency may result in maternal and fetal hypothyroidism, preventing the partially protective transfer of maternal thyroid hormones.
When the “goiter” is lobulated, asymmetric, firm, or large to an unusual degree, a teratoma within or in the vicinity of the thyroid must be considered in the differential diagnosis (see Chapter 563 ).
561.2 Endemic Goiter and Cretinism
Etiology
IODINE DEFICIENCY.
The association between dietary deficiency of iodine and the prevalence of goiter or cretinism has been recognized for more than half a century. A moderate deficiency of iodine can be overcome by increased efficiency in the synthesis of thyroid hormone. Iodine liberated in the tissues is returned rapidly to the gland, which resynthesizes triiodothyronine (T3 ) preferentially at a higher rate than normal. This increased activity is achieved by compensatory hypertrophy and hyperplasia, which satisfy the demands of the tissues for thyroid hormone. In geographic areas where deficiency of iodine is severe, decompensation and hypothyroidism may result. It is estimated that 2 billion individuals in developing countries live in areas of iodine deficiency.
Seawater is rich in iodine, and the iodine content of fish and shellfish is also high. Endemic goiter is rare therefore in populations living along the sea. Iodine is deficient in the water and native foods in the Pacific West and the Great Lakes areas of the United States. Deficiency of dietary iodine is even greater in certain Alpine valleys, the Himalayas, the Andes, the Congo, and the highlands of Papua New Guinea. In areas such as the United States, where iodine is provided in foods from other areas and in iodized salt, endemic goiter has disappeared. Iodized salt in the United States contains potassium iodide (100?µg/g) and provides excellent prophylaxis. Further iodine intake in the United States is contributed by iodates used in baking, iodine-containing coloring agents, and iodine-containing disinfectants used in the dairy industry. The recommended daily allowance of iodine for infants is greater than 30?µg/kg/24?hr; this amount is exceeded fourfold in breast-fed infants and 10-fold in infants fed cow’s milk in the United States.
Clinical Manifestations.
If the deficiency of iodine is mild, thyroid enlargement does not become noticeable except when there is increased demand for the hormone during periods of rapid growth, as in adolescence and during pregnancy. In regions of moderate iodine deficiency, goiter observed in schoolchildren may disappear with maturity and reappear during pregnancy or lactation. Iodine-deficient goiters are more common in girls than in boys. In areas where iodine deficiency is severe, as in the hyperendemic highlands of Papua New Guinea, nearly half the population has large goiters, and endemic cretinism is common.
Serum T4 levels are often low in individuals with endemic goiter, although clinical hypothyroidism is rare. This is true in New Guinea, the Congo, the Himalayas, and South America. Despite low serum levels of thyroid hormone, serum TSH concentrations are often only moderately increased. In such patients, circulating levels of T3 are elevated. Moreover, T3 levels are also elevated in patients with normal T4 levels, indicating a preferential secretion of T3 by the thyroid in this disease.
Endemic cretinism is the most serious consequence of iodine deficiency; it occurs only in geographic association with endemic goiter. The term endemic cretinism includes two different but overlapping syndromes—a neurologic type and a myxedematous type. The frequency of the two types varies among different populations. In Papua New Guinea, the neurologic type occurs almost exclusively, but in Zaire, the myxedematous type predominates. Both types are found in all endemic areas, and some individuals have intermediate or mixed features.
The neurologic syndrome is characterized by mental retardation, deaf-mutism, disturbances in standing and gait, and pyramidal signs such as clonus of the foot, the Babinski sign, and patellar hyperreflexia. Affected individuals are goitrous but euthyroid, have normal pubertal development and adult stature, and have little or no impaired thyroid function. Individuals with the myxedematous syndrome also are mentally retarded and deaf and have neurologic symptoms, delayed sexual development and growth, myxedema, and absence of goiter; serum T4 levels are low, and TSH levels are markedly elevated. Delayed skeletal maturation may extend into the 3rd decade or later. Ultrasonographic examination shows thyroid atrophy.
Pathogenesis.
The pathogenesis of the neurologic syndrome has been attributed to iodine deficiency and hypothyroxinemia during pregnancy, leading to fetal and postnatal hypothyroidism. Although some investigators have attributed brain damage to a direct effect of elemental iodine deficiency in the fetus, most believe the neurologic symptoms are caused by fetal and maternal hypothyroxinemia. There is evidence that the human fetal brain has receptors for thyroid hormone before development of the fetal thyroid, and there is also evidence of transplacental passage of maternal thyroid hormone into the fetus, which normally might ameliorate the effects of fetal hypothyroidism on the developing nervous system. The pathogenesis of the myxedematous syndrome leading to thyroid atrophy is more bewildering. Searches for additional environmental factors that may provoke continuing postnatal hypothyroidism have led to incrimination of selenium deficiency, goitrogenic foods, thiocyanates, and Yersinia. Studies from Western China suggest that thyroid autoimmunity may play a role. Myxedematous cretins with thyroid atrophy, but not euthyroid cretins, were found to have thyroid growth-blocking immunoglobulins of the kind found in infants with sporadic congenital hypothyroidism. Others are skeptical about any role of thyroid growth-blocking immunoglobulins to explain these findings.
Treatment.
In many developing countries, administration of a single intramuscular injection of iodinated poppy seed oil to women prevents iodine deficiency during future pregnancies for about 5 yr. This form of therapy given to children younger than 4 yr of age with myxedematous cretinism results in a euthyroid state in 5 mo. However, older children respond poorly and adults not at all to iodized oil injections, indicating an inability of the thyroid gland to synthesize hormone; these patients require treatment with T4 . In the Xinjiang province of China, where the usual methods of iodine supplementation had failed, iodination of irrigation water has increased iodine levels in soil, animals, and human beings.

1883
561.3 Sporadic Goiter
The term sporadic goiter encompasses goiters developing from a variety of causes; patients are usually euthyroid but may be hypothyroid. The most common cause of sporadic goiter is lymphocytic thyroiditis (see Chapter 560 ). Intrinsic biochemical defects in the synthesis of thyroid hormone are almost always associated with goiter. The occurrence of the disorder in siblings, onset in early life, and possible association with hypothyroidism (goitrous hypothyroidism) are important clues to the diagnosis.
Iodide Goiter.
A small percentage of patients treated with iodide preparations for prolonged periods acquire goiters. Iodides are commonly included for their expectorant effect in cough medicines and in proprietary mixtures for asthma. Goiters resulting from iodine administration are firm and diffusely enlarged, and in some instances hypothyroidism may develop. In normal individuals, acute administration of large doses of iodine inhibits the organification of iodine and the synthesis of thyroid hormone (Wolff-Chaikoff effect). This effect is short-lived and does not lead to hypothyroidism. When iodide administration continues, an autoregulatory mechanism in normal persons limits iodine trapping and permits the level of iodide in the thyroid to decrease and organification to proceed normally. In patients with iodide-induced goiter, this escape does not occur because of an underlying abnormality of biosynthesis of thyroid hormone. The persons most susceptible to the development of iodide goiter are those with lymphocytic thyroiditis or with a subclinical inborn error in thyroid hormone synthesis and those who have had a partial thyroidectomy.
Lithium carbonate also causes goiters; it is currently widely used as a psychotropic drug. Lithium competes with iodide; the mechanism producing the goiter or hypothyroidism is similar to that described earlier for iodide goiter. Lithium and iodide also act synergistically to produce goiter; their combined use should be avoided.
Amiodarone, a drug used to treat cardiac arrhythmias, can cause thyroid dysfunction with goiter because it is rich in iodine. It is also a potent inhibitor of 5′-deiodinase, preventing conversion of T4 to T3 . It can cause hypothyroidism, particularly in patients with underlying autoimmune disease; in other patients, it may cause hyperthyroidism.
Simple Goiter (Colloid Goiter).
A few children with euthyroid nontoxic goiters have simple goiters, a condition of unknown cause not associated with hypothyroidism or hyperthyroidism and not caused by inflammation or neoplasia. The condition predominates in girls and has a peak incidence before and during the pubertal years. Histologic examination of the thyroid either is normal or reveals variable follicular size, dense colloid, and flattened epithelium. The goiter may be small or large. It is firm in half the patients and is occasionally asymmetric or nodular. Levels of TSH are normal or low, scintiscans are normal, and thyroid antibodies are absent. Differentiation from lymphocytic thyroiditis may not be possible without a biopsy, but biopsy ordinarily is not indicated. Therapy with thyroid hormone may help avoid progression to a large multinodular goiter, although it is difficult to separate any treatment effects from the natural history, which is for the goiter to decrease in size. Untreated patients should be re-evaluated periodically. This condition must be differentiated from lymphocytic thyroiditis (see Chapter 560 ).
Multinodular Goiter.
Rarely, a firm goiter with a lobulated surface and single or multiple palpable nodules is encountered. Areas of cystic change, hemorrhage, and fibrosis may be present. The incidence of this condition has decreased markedly with the use of iodine-enriched salt. A mild goitrogenic stimulus, acting over a long time, is thought to be the cause. Ultrasonographic examination may reveal multiple echo-free and echogenic lesions that are nonfunctioning on scintiscans. Thyroid studies are usually normal, but TSH may be elevated and thyroid antibodies may be present. The condition occurs in children with McCune-Albright syndrome (usually resulting in hyperthyroidism) and has been described in three children (including two siblings) with digital anomalies and cystic renal disease. Dominant nodules within a multinodular goiter, particularly those not suppressed by replacement therapy with T4 , may be an indication for evaluation by fine-needle aspiration because malignancy cannot readily be ruled out.
Toxic Goiter (Hyperthyroidism).
See Chapter 562 .
561.4 Intratracheal Goiter
One of the many ectopic locations of thyroid tissue is within the trachea. The intraluminal thyroid lies beneath the tracheal mucosa and is frequently continuous with the normally situated extratracheal thyroid. The thyroid tissue is susceptible to goitrous enlargement, which involves the normally situated and the ectopic thyroid. When there is obstruction of the airway associated with a goiter, it must be ascertained whether the obstruction is extratracheal or endotracheal. If obstructive manifestations are mild, administration of sodium-l-thyroxine usually causes the goiter to decrease in size. When symptoms are severe, surgical removal of the endotracheal goiter is indicated (also see Chapter 561.1

Q: Thyroid goiter/nodule and size?
I have been diagnosed with Hashimoto’s disease and a multinodular goiter. I am having it removed next week due to the size, the ultrasound showed it at 6cm, two years ago it was about 4.5cm. The fnab showed it as benign back then. I have not taken any medication until last week. Here is my question: When I am stressed out the lump in the left side of my neck looks very large, when I’m not it is much smaller. (It’s not just be thinking this, my husband and co workers have noticed this as well) Has anyone experienced this?

A: Yes, it happens—Hasimotos’ can cause your thryroid to be very vascular & it will enlarge! Best of luck to you–My Mom has an appt w/her surgeon tomorrow–her nodule is 3cm, not sure if its malignant or not.

You should do just fine–I was back to work in 2 wks after my surgery! Feeling much more energetic since it was removed!!1

Good luck!♥♥♥

Q: Each year, i have to get an ultrasound for a goiter on the right side of my thyroid. Any suggestions ?
I am on synthroid for Hashimoto’s disease but I am not sure if this is what I should be treated for as the dr is not sure if it is actually hashimoto’s. Any input would be greatly appreciated

A: Hashi’s can be diagnosed by testing for thyroid antibodies. So that can be verified

Synthroid is a synthetic form of the thyroid hormone T4. It replaces what the thyroid gland is no longer able to produce.

In the case of Hashi’s, you should be given enough replacement hormone, of the proper type, to bring the TSH as close to zero as possible without the level of the thyroid hormones (Free T4 and Free T3) going so high as to cause you to become hyperthyroid (excess thyroid hormone).

By proper type I mean that for some folks synthetic T4 products (like synthroid) dont’ work for us, either our bodies can not break them down to the absorbable stage and/or our bodies are not able to convert it to the active hormone, Free T3, for our body to be able to use to function.

It’s another reason that it’s a good idea to check your labs to be sure that they are running the correct tests to determine if your body is properly converting hormone, if it’s not, you can take all the T4 you want and still be a miserable heap on the floor suffering from hypothyroidism (insufficient thyroid hormone)

If you are still dealing with goiter (enlarged thyroid) in the right lobe, that is suggesting that your dosage is not yet correct for your body’s needs and/or your gland is dealing with continuing damage from the thyroid antibodies

A good first step would be to request copies of your labs so that you can see if your levels are where they need to be and that your dosage is correct. In my own experience … a ‘lets look at it next year to see if it’s gotten any worse’ attitude is unacceptable. I don’t want it to be worse, I want it to be properly managed now.

IMHO That inexcusable work ethic, be it from laziness, greed, or lack of knowledge, is something we, as paying customers, should not have to tolerate.

Q: Thyroid disease – specialist needed?
My family doctor does not want to refer me to an endocrinologist, but I am wondering how far I should go in insisting on one. I’m Canadian, so it’s all covered under Medicare.
In January, I was diagnosed hypothyroid and began taking synthroid (my doc didn’t even physically examine my neck) . Four weeks ago, a different doctor ordered a neck ultrasound and it was discovered that I have thyroiditis and a multinodular goiter (each lobe about 5cm). Despite being on synthroid, my TSH went up more than fourfold in the last few weeks, so he has decided to double my synthroid dose. My doctor has finally agreed to order a biopsy of the nodules after much insistence on my part. My understanding is that you automatically biopsy any thyroid nodule to be on the safe side. Furthermore, there is a history of thyroid cancer in my family. I don’t feel all that confident leaving it to a general practitioner, especially one that doesn’t seem to be all that thorough without a lot of prompting.

A: First of all, it’s pretty odd that the doctor didn’t palpate your thyroid gland. We do rely on advanced scanning technology a lot, but I don’t know if that means we should forgoe standardized physical exam procedures. I’m not an expert, only a med student, but any time we suspect something about the thyroid, you stand behind the patient, lightly palpate, and feel it as the patient swallows for any bumps.
Anyway, I think that since you do have such concern, you should let your doctor know that you’d feel most comfortable with a specialist and see what he/she says. I don’t know why the doctor didn’t agree the first time you requested a specialist, maybe there is some reason? But, either way, it’s best for the relationship just to clear the air and say how you feel. The doctor shouldn’t try to prevent you from seeking care how you see best. An endocronologist might have some additional insight into this, also. Good luck.

Q: I have a multinodule goiter. Why do I have this and why does it continue to grow?
I have had biospy done, it is benien. My TSH was .5 and my T3 and T4 were in the high end of the normal range. I am a fifth generation woman to have a goiter in my family. I am a 30 years old female. I am trying to figure out why this runs so heavily in my family and by the way my family has a history of autoimmune disease such as R.A. and Reiter’s Syndrome (I am the first to have Reiter’s syndrome in my family) and so on. I am trying to make since of all of this since my goiter continues to grow. I am having another ultrasound next Tuesday. I live in the US so iodine is not the issue. There has to be a reason even a hidden one because this goiter issue just runs to hard on the family to be just simple gentics-except maybe a certain thyroid or pitutary disease.

A: From what you wrote, I guess you’ve already read extensively regarding multinodular goitre (MNG) and other autoimmune diseases.

All i can tell you is this: the more it runs in the family, the more likely that this is due to genetics. Autoimmune diseases have a tendency to occur together (ie. if you have grave’s disease, there’s a higher likelihood that you’ll have other autoimmune problems like reiter’s and RA.).

My advice is for you not to search too hard for some other cause of the hereditary MNG. It may be difficult for you to blame it all on genetics, but that’s the way it is.

Besides iodine, you should ask your doctor about other alternatives. Many centres in the world will offer a total thyroidectomy for MNGs that continue increasing in size, as there is a possibility that one of the nodules may turn malignant in the future. The downside of surgery is that you’ll have to be on thyroid replacement medication for life. On the other hand, radioactive iodine can sometimes make one more prone to cancer, and will also eventually lead to hypothyroidism and need for thyroid replacement.

Q: I am getting a total thyroidectomy for a goiter on the left side of my thyroid that may or not be cancerous.?
I’ve known about this disease since I was 15, and have been on Levoxyl/synthroid since. I’m really just wondering what to expect for someone of my age (19) after the surgery. All responses appreciated! Thanks.

A: Wow sweetie…thats awful…..I was diagnosed with hypothyroidism at age 15…the normal levels are supposed to be 0.4-5….mine was in the 170s…So they put me on synthroid (synthetic thyroid: meaning they made it in a lab)
I was on that for 5-6 years, then I heard about ARMOUR thyroid….its a natural thyroid extract from pigs…
I was on it for 3 months before I started getting signs that my thyroid was kicking back on…Under doctor supervision, I quit all medications…
Its been two years now and, due to an illness my thyroid level is at 5.2, which isn’t bad considering….

With all of the research I’ve done, I suggest you do some as well, I read that alot of times doctors will jump to conclusions with their diagnoses…
At 15, your thyroid is doing crazy sh#t anyway!!!YOUR GROWING!! the levels are going to be crazy!!!
If your doctor throws you on medication when the thyroid is acting irrational, the chemicals in the lab created pills will kill off any good thyroid thats left!!!

Do you eat the correct type of iodine? Thats the biggest cause of thyroid goiters and malfunctions….that and sodium….or salt…
Make sure to buy 100% sea salt (it has the sodium that is good for thyroid health)
Also seaweed, or kelp has the perfect amount of natural iodine which nurishes the thyroid….

And as always, diet change affects the thyroid as well as the whole body….
Remember “good goes in…good comes out…..bad goes in, and well, you get the idea”

Good luck and try these things before surgery, sometimes just a diet change can cause a goiter to go down, unless it is cancerous….
Don’t stress, that makes it worse…if you need any more help or just someone to listen to all of the worries you have let me know….I’ve dealt with the thyroid long enough!!!

Q: How long does it take to develop a goiter?
I was recently diagnosed with an autoimmune disease which resulted in a goiter (Hashimoto’s Disease). Does anyone know how long it would have taken for it to develop after being infected with an autoimmune disorder? My thyroid is 2-3 times larger than the normal size. How long has my goiter been developing? Months? Years?
Please, help. Thanks to everyone who answers.

I would reallllllllyyyyyyyyyyy like to know!

A: I had a goiter for about 5 years,from what i remembered my neck started swelling uop from nowhere when i was out with my friend and then it went down on its own again. However before the swelling i noticed major changes in my mood and craving for alot of food. I thought nothing of it…and a couple of weeks later the goiter finally formed and it was huge.long story short i controlled it with medicine and radioactiive but neither worked as my body threw out the radioactive. so ten days ago i finally decided to have surgery and removed my entire thyroid because i simply could not control it with mediciation anymore and taking herbs and natural remedies did not work for me either. i feel great after the surgery,my heart is not longer pounding,no more breaking out in hives etc. I found an excellent surgeon who did not destroy my voice and my calcium levels were a little low after the operation but its back to normal now. however if u get save ur thyroid n radioactive works for u,then great,surgery should be your last option for graves disease.

Q: graves disease, radioactive pill or surgery for thyroid?
I jus wanted to hear from those who had the radio active pill, and from those who had the thryoid surgery, which one is better. and if you could choose again, which one you would choose. im relying more to the surgery. but i wanted to hear from those who have gone thru this. i have a goiter and i am so tired of taking a bunch of medications. also, i wanted to know how the recovery was. thank you so much for the answers. appreciate it.

A: I had the radio active pill. Either way you’ll continue to be on meds because in most cases you’ll need a replacement hormone (like synthroid) once you had the RAI or the surgery. With the RAI (radio active idodine) you’ll need to live alone for about 3 days, use only disposal plates/forks (unless you have a dishwasher). It doesn’t hurt and I really wouldn’t say there is a “recovery time” you just can’t be close to people for 3 days because of the radiation in your body. And if you are planning on getting pregnant, you have to wait about 6 months. If you are pregnant, you can NOT have the radio active treatment. There is a mandatory pregnancy test before they will give you treatment.

With the surgery, you’ll have longer recovery time, plus the scar from the surgery (which fades pretty quickly… my sister just had it done). But she had to have the RAI after the surgery, so we was stuck with both.

Either way, good luck to you. Hope this helped.