Lupus

Monday, June 24, 2013

Lupus and Autoimmune Thyroid Issues

     I was diagnosed with graves disease before my lupus diagnosis.  Graves disease is an autoimmune thyroid disease which causes your thyroid to be hyper.  The symptoms are: weight loss, nervousness, irregular periods/light periods, shakiness, moodiness, hair loss, more bowel movements, breathing problems, rapid heart rate, dry skin, itchy skin, bulging eyes, feeling hot and sweaty.  Graves disease can be dangerous if it is severe and if not treated can lead to heart problems, bone problems and something called a thyroid storm.  I had my thyroid killed with radio active iodine, it wasn't painful and caused me no side effects.  The hardest part of the radiation was staying away from my family for a few days.  Then after my treatment I had a normal thyroid for a month but couldn't walk due to lupus, at this time the doctors were speculating what was wrong with me because the thyroid disease could not cause all of my symptoms and I had these symptoms before my thyroid disease.  My health took a turn for the worst, my thyroid was killed and the replacement hormone my Endocrinologist put me on a generic form of synthroid.  I had a reaction to the thyroid replacement, my Endocrinologist would take me off for a few days and then start me back on, due to not having a thyroid anymore this playing led me into the hospital.  Before going into the hospital I had my general practitioner put me on Armour thyroid replacement which is basically pig thyroid, but I had a reaction to that also.  My Endocrinologist would not put me on Armour thyroid because it is controversial in the medical community and she said she didn't know how to administer the proper dose.  My general practitioner did research for me through the internet and with the other patients that he had that were on Armour.  Due to the reaction to Armour and my Endocrinologist not acting properly I ended up EXTREMELY ill and in the hospital.  It took 8-10 months for me to recover from the thyroid issues on top of being very ill from lupus.  While in the hospital another Endocrinologist, put me on Synthroid no generic pill the name brand replacement.  He said that the generic and Armour have fillers that I had a reaction to and that the Synthroid was the most pure form of replacement, it had less fillers.  I have had no issues on Synthroid as of yet and I pray that I don't because that is all I have to give me thyroid function.  One bad doctor can cause severe, life threatening consequences, and there are so many out there practicing.  All my Endo had to do was switch me from generic to name brand synthroid and I would have been fine.  
     Now I have my thyroid levels checked every few months, and it does tend to flucuate and my synthroid needs adjusted about once a year.  It always has to be upped never lowered.  It is common to have lupus and autoimmune thyroid disease, however having autoimmune thyroid disease doesn't mean that you will have a higher chance of having lupus. 


Hypothyroidism

On this page:

What is hypothyroidism?

Hypothyroidism is a disorder that occurs when the thyroid gland does not make enough thyroid hormone to meet the body’s needs. Thyroid hormone regulates metabolism—the way the body uses energy—and affects nearly every organ in the body. Without enough thyroid hormone, many of the body’s functions slow down. About 4.6 percent of the U.S. population age 12 and older has hypothyroidism.1
1Golden SH, Robinson KA, Saldanha I, Anton B, Ladenson PW. Prevalence and incidence of endocrine and metabolic disorders in the United States: a comprehensive review. Journal of Clinical Endocrinology & Metabolism. 2009;94(6):1853–1878.
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What is the thyroid?

The thyroid is a 2-inch-long, butterfly-shaped gland weighing less than 1 ounce. Located in the front of the neck below the larynx, or voice box, it has two lobes, one on each side of the windpipe. The thyroid is one of the glands that make up the endocrine system. The glands of the endocrine system produce and store hormones and release them into the bloodstream. The hormones then travel through the body and direct the activity of the body’s cells.
The thyroid gland makes two thyroid hormones, triiodothyronine (T3) and thyroxine (T4). T3 is made from T4 and is the more active hormone, directly affecting the tissues. Thyroid hormones affect metabolism, brain development, breathing, heart and nervous system functions, body temperature, muscle strength, skin dryness, menstrual cycles, weight, and cholesterol levels.
Drawing of the head and neck showing the thyroid and pituitary glands..
The thyroid gland makes two thyroid hormones, T3 and T4. Thyroid hormone production is regulated by TSH, which is made by the pituitary gland in the brain.
Thyroid hormone production is regulated by thyroid-stimulating hormone (TSH), which is made by the pituitary gland in the brain. When thyroid hormone levels in the blood are low, the pituitary releases more TSH. When thyroid hormone levels are high, the pituitary responds by dropping TSH production.
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What causes hypothyroidism?

Hypothyroidism has several causes, including
  • Hashimoto’s disease
  • thyroiditis, or inflammation of the thyroid
  • congenital hypothyroidism, or hypothyroidism that is present at birth
  • surgical removal of part or all of the thyroid
  • radiation treatment of the thyroid
  • some medications
Less commonly, hypothyroidism is caused by too much or too little iodine in the diet or by abnormalities of the pituitary gland.

Hashimoto’s Disease

Hashimoto’s disease, also called chronic lymphocytic thyroiditis, is the most common cause of hypothyroidism in the United States.1 Hashimoto’s disease is a form of chronic inflammation of the thyroid gland. Hashimoto’s disease is also an autoimmune disorder.
Normally, the immune system protects the body against foreign invaders—such as viruses and bacteria—that can cause illness. But in autoimmune diseases, the immune system attacks the body’s own cells and organs. With Hashimoto’s disease, the immune system attacks the thyroid, causing inflammation and interfering with its ability to produce thyroid hormones.
More information about Hashimoto’s disease can be found in the National Endocrine and Metabolic Diseases Information Service (NEMDIS) fact sheetHashimoto’s Disease at www.endocrine.niddk.nih.gov.

Thyroiditis

Thyroiditis causes stored thyroid hormone to leak out of the thyroid gland. At first, the leakage raises hormone levels in the blood, leading to hyperthyroidism—when thyroid hormone levels are too high––that lasts for 1 or 2 months. Most people then develop hypothyroidism before the thyroid is completely healed.
Several types of thyroiditis can cause hyperthyroidism followed by hypothyroidism:
  • Subacute thyroiditis. This condition involves painful inflammation and enlargement of the thyroid. Experts are not sure what causes subacute thyroiditis, but it may be related to a viral or bacterial infection. The condition usually goes away on its own in a few months.
  • Postpartum thyroiditis. This type of thyroiditis develops after a woman gives birth. For more information, see the section titled “What happens with pregnancy and thyroid conditions?”
  • Silent thyroiditis. This type of thyroiditis is called “silent” because it is painless, as is postpartum thyroiditis, even though the thyroid may be enlarged. Like postpartum thyroiditis, silent thyroiditis is probably an autoimmune condition and sometimes develops into permanent hypothyroidism.

Congenital Hypothyroidism

Some babies are born with a thyroid that is not fully developed or does not function properly. If untreated, congenital hypothyroidism can lead to mental retardation and growth failure. Early treatment can prevent these complications, so most newborns in the United States are screened for hypothyroidism.

Surgical Removal of the Thyroid

When part of the thyroid is removed, the remaining part may produce normal amounts of thyroid hormone, but some people who have this surgery develop hypothyroidism. Removal of the entire thyroid always results in hypothyroidism.
Part or all of the thyroid may be surgically removed as a treatment for
  • hyperthyroidism
  • a large goiter, which is an enlarged thyroid that may cause the neck to appear swollen and can interfere with normal breathing and swallowing
  • thyroid nodules, which are noncancerous tumors, called adenomas, or lumps in the thyroid that can produce excess thyroid hormone
  • thyroid cancer

Radiation Treatment of the Thyroid

Radioactive iodine, a common treatment for hyperthyroidism, gradually destroys the cells of the thyroid. Most people who receive radioactive iodine treatment eventually develop hypothyroidism. People with Hodgkin’s disease, other lymphomas, and head or neck cancers are treated with radiation, which can also damage the thyroid.

Medications

Some drugs can interfere with thyroid hormone production and lead to hypothyroidism, including
  • amiodarone, a heart medication
  • interferon alpha, a cancer medication
  • lithium, a bipolar disorder medication
  • interleukin-2, a kidney cancer medication
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What are the symptoms of hypothyroidism?

Hypothyroidism has many symptoms that can vary from person to person. Some common symptoms of hypothyroidism are
  • fatigue
  • weight gain
  • a puffy face
  • cold intolerance
  • joint and muscle pain
  • constipation
  • dry skin
  • dry, thinning hair
  • decreased sweating
  • heavy or irregular menstrual periods and impaired fertility
  • depression
  • slowed heart rate
However, hypothyroidism develops slowly, so many people don’t notice symptoms of the disease.
Symptoms more specific to Hashimoto’s disease are a goiter and a feeling of fullness in the throat.
Hypothyroidism can contribute to high cholesterol, so people with high cholesterol should be tested for hypothyroidism. Rarely, severe, untreated hypothyroidism may lead to myxedema coma, an extreme form of hypothyroidism in which the body’s functions slow to the point that it becomes life threatening. Myxedema requires immediate medical treatment.
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Who is likely to develop hypothyroidism?

Women are much more likely than men to develop hypothyroidism. The disease is also more common among people older than age 60.1
Certain factors can increase the chances of developing thyroid disorders. People may need more regular testing if they
  • have had a thyroid problem before, such as a goiter
  • have had surgery to correct a thyroid problem
  • have received radiation to the thyroid, neck, or chest
  • have a family history of thyroid disease
  • have other autoimmune diseases, including
    • Sj√∂gren’s syndrome, characterized by dry eyes and mouth
    • pernicious anemia, a vitamin B12 deficiency
    • type 1 diabetes
    • rheumatoid arthritis
    • lupus, a chronic inflammatory condition
  • have Turner syndrome, a genetic disorder that affects females
  • are older than age 60
  • have been pregnant or delivered a baby within the past 6 months
People should get tested regularly to help uncover thyroid problems—especially subclinical problems. Subclinical means a person has no apparent symptoms.
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What happens with pregnancy and thyroid conditions?

Hypothyroidism. During pregnancy, hypothyroidism is usually caused by Hashimoto’s disease and occurs in three to five out of every 1,000 pregnancies.2
Uncontrolled hypothyroidism raises the chance of miscarriage, preterm delivery, and preeclampsia—a dangerous rise in blood pressure during late pregnancy.
Untreated hypothyroidism during pregnancy may also affect the baby’s growth and brain development. Thyroid medications can help prevent these problems and are safe to take during pregnancy. Women with hypothyroidism should discuss their condition with their health care provider before becoming pregnant.
Postpartum thyroiditis. This inflammation of the thyroid gland affects about 4 to 9 percent of women in the first year after giving birth.2 Postpartum thyroiditis is believed to be an autoimmune condition and causes hyperthyroidism that usually lasts for 1 to 2 months.
Women with postpartum thyroiditis often develop hypothyroidism before the thyroid gland is completely healed. The condition is likely to recur with future pregnancies.
Postpartum thyroiditis sometimes goes undiagnosed because the symptoms are mistaken for postpartum blues—the exhaustion and moodiness that sometimes follow delivery. If symptoms of fatigue and lethargy do not go away within a few months or if a woman develops postpartum depression, she should talk with her health care provider. If the hypothyroidism symptoms are bothersome, thyroid medication can be given.
More information can be found in the NEMDIS fact sheet Pregnancy and Thyroid Disease at www.endocrine.niddk.nih.gov.
2Ogunyemi DA. Autoimmune thyroid disease and pregnancy. emedicine website. http://emedicine.medscape.com/article/261913-overview click to view disclaimer page. Updated March 8, 2012. Accessed February 11, 2013.
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How is hypothyroidism diagnosed?

Many symptoms of hypothyroidism are the same as those of other diseases, so hypothyroidism usually cannot be diagnosed based on symptoms alone. With suspected hypothyroidism, health care providers take a medical history and perform a thorough physical examination. Health care providers may then use several blood tests to confirm a diagnosis of hypothyroidism and find its cause:
TSH test. The ultrasensitive TSH test is usually the first test a health care provider performs. This test detects even tiny amounts of TSH in the blood and is the most accurate measure of thyroid activity available. Generally, a TSH reading above normal means a person has hypothyroidism and a reading below normal means a person has hyperthyroidism.
Mildly elevated TSH without symptoms indicates subclinical hypothyroidism. Some health care providers treat subclinical hypothyroidism immediately. Others prefer to leave it untreated but monitor their patients for signs that the condition is worsening.
Health care providers may conduct additional tests to help confirm the diagnosis or determine the cause of hypothyroidism.
T4 test. This test measures the actual amount of circulating thyroid hormone in the blood. In hypothyroidism, the level of T4 in the blood is lower than normal.
Thyroid autoantibody test. This test looks for the presence of thyroid autoantibodies. Most people with Hashimoto’s disease have these antibodies, but people whose hypothyroidism is caused by other conditions do not.
More information about testing for thyroid problems can be found in the NEMDIS fact sheet Thyroid Function Tests at www.endocrine.niddk.nih.gov.
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How is hypothyroidism treated?

Health care providers treat hypothyroidism with synthetic thyroxine, a medication that is identical to the hormone T4. The exact dose will depend on the patient’s age and weight, the severity of the hypothyroidism, the presence of other health problems, and whether the person is taking other drugs that might interfere with how well the body uses thyroid hormone.
Health care providers test TSH levels about 6 to 8 weeks after a patient begins taking thyroid hormone and make any necessary adjustments to the dose. Each time the dose is adjusted, the blood is tested again. Once a stable dose is reached, blood tests are normally repeated in 6 months and then once a year.
Hypothyroidism can almost always be completely controlled with synthetic thyroxine, as long as the recommended dose is taken every day as instructed.
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Eating, Diet, and Nutrition

Experts recommend that people eat a balanced diet to obtain most nutrients. More information about diet and nutrition can be found on the National Agricultural Library website at www.nutrition.gov.

Dietary Supplements

Iodine is an essential mineral for the thyroid. However, people with autoimmune thyroid disease may be sensitive to harmful side effects from iodine. Taking iodine drops or eating foods containing large amounts of iodine—such as seaweed, dulse, or kelp—may cause or worsen hypothyroidism or hyperthyroidism. More information about iodine can be found in the National Library of Medicine fact sheet Iodine in diet, available atwww.nlm.nih.gov/medlineplus/ency/article/002421.htm.
Women need more iodine when they are pregnant—about 250 micrograms a day— because the baby gets iodine from the mother’s diet. In the United States, about 7 percent of pregnant women may not get enough iodine in their diet or through prenatal vitamins.3 Choosing iodized salt— salt supplemented with iodine—over plain salt and prenatal vitamins containing iodine will ensure this need is met.
To help ensure coordinated and safe care, people should discuss their use of dietary supplements, such as iodine, with their health care provider. Tips for talking with health care providers can be found on the National Center for Complementary and Alternative Medicine’s Time to Talk campaign website atwww.nccam.nih.gov/timetotalk.
3Zimmerman MB. Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review. American Journal of Clinical Nutrition. 2009;89(2):668S–672S.
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Points to Remember

  • Hypothyroidism is a disorder that occurs when the thyroid gland does not make enough thyroid hormone to meet the body’s needs. Thyroid hormone regulates metabolism. Without enough thyroid hormone, many of the body’s functions slow down.
  • Hypothyroidism has several causes, including
    • Hashimoto’s disease
    • thyroiditis
    • congenital hypothyroidism
    • surgical removal of part or all of the thyroid
    • radiation treatment of the thyroid
    • some medications
  • Hypothyroidism has many symptoms that can vary from person to person. Some common symptoms of hypothyroidism are fatigue, weight gain, cold intolerance, constipation, impaired fertility, and depression.
  • Women are much more likely than men to develop hypothyroidism.
  • Women with hypothyroidism should discuss their condition with their health care provider before becoming pregnant.
  • Hypothyroidism can almost always be completely controlled with synthetic thyroxine, as long as the recommended dose is taken every day as instructed.
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Hope through Research

The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) conducts and supports research into many kinds of disorders, including hypothyroidism. Researchers throughout the United States and the world are working to better understand, prevent, and treat this disease. Researchers are investigating the development, signs and symptoms, and genetics of thyroid function disorders to further understand thyroid diseases. Scientists continue to study treatment options for hypothyroidism and other thyroid disorders.
Clinical trials are research studies involving people. Clinical trials look at safe and effective new ways to prevent, detect, or treat disease. Researchers also use clinical trials to look at other aspects of care, such as improving the quality of life for people with chronic illnesses. To learn more about clinical trials, why they matter, and how to participate, visit the NIH Clinical Research Trials and You website at www.nih.gov/health/clinicaltrials. For information about current studies, visit www.ClinicalTrials.gov.

What is hyperthyroidism?
Hyperthyroidism means your thyroid makes too much thyroidhormone. Your thyroid is a gland in the front of your neck camera. It controls your metabolism, which is how your body turns food into energy. It also affects your heart, muscles, bones, and cholesterol.
Having too much thyroid hormone can make a lot of things in your body speed up. You may lose weight quickly, have a fast heartbeat, sweat a lot, or feel nervous and moody. Or you may have no symptoms at all. While your doctor is doing a test for another reason, he or she may discover that you have hyperthyroidism.
Hyperthyroidism is easily treated. With treatment, you can lead a healthy life. Without treatment, hyperthyroidism can lead to serious heart problems, bone problems, and a dangerous condition called thyroid storm.
What causes hyperthyroidism?
Graves' disease causes most hyperthyroidism. In Graves? disease, the body's natural defense (immune) system attacks the thyroid gland. The thyroid fights back by making too much thyroid hormone. Like many thyroid problems, it often runs in families.
Sometimes hyperthyroidism is caused by a swollen thyroid or small growths in the thyroid called thyroid nodules.
This topic focuses on hyperthyroidism caused by Graves' disease.
What are the symptoms?
You may have no symptoms at all. Or:
  • You may feel nervous, moody, weak, or tired.
  • Your hands may shake, your heart may beat fast, or you may have problems breathing.
  • You may be hot and sweaty or have warm, red, itchy skin.
  • You may have more bowel movements than usual.
  • You may have fine, soft hair that is falling out.
  • You may lose weight even though you eat the same or more than usual.
If you have any of these symptoms, call your doctor. Without treatment, hyperthyroidism can lead to heart problems, bone problems, and a dangerous condition called thyroid storm.
How is hyperthyroidism diagnosed?
Your doctor will ask you about your symptoms and do a physical exam. Then he or she will order blood tests to see how much thyroid hormone your body is making.
Sometimes hyperthyroidism is found while you are having a test for another reason. You may be surprised to find out that you have this problem.
How is it treated?
If your symptoms bother you, your doctor may give you pills called beta-blockers. These can help you feel better while you and your doctor decide what your treatment should be. Hyperthyroidism can lead to more serious problems. So even if your symptoms do not bother you, you still need treatment.
Radioactive iodine and antithyroid medicine are the treatments doctors use most often. The best treatment for you will depend on a number of things, including your age. Some people need more than one kind of treatment.
  • Radioactive iodine is the most common treatment. Most people are cured after taking one dose. It destroys part of your thyroid gland, but it does not harm any other parts of your body.
  • Antithyroid medicine works best if your symptoms are mild. These pills do not damage your thyroid gland. But they do not always work, and you have to take them at the same time every day. If they stop working, you may need to try radioactive iodine.
  • After treatment, you will need regular blood tests. These tests check to see if your hyperthyroidism has come back. They also check to see if you are making enough thyroid hormone. Sometimes treatment cures hyperthyroidism but causes the opposite problem-too little thyroid hormone. If this happens, you may need to take thyroid hormone pills for the rest of your life.
Thyroid storm is a life-threatening condition that develops in cases of untreated thyrotoxicosis (hyperthyroidism, or overactive thyroid).

Causes

Thyroid storm results from untreated hyperthyroidism. It is usually brought on by a stress such as trauma or infection.

Symptoms

Symptoms are severe and may include:

Exams and Tests

  • The top number in a blood pressure reading may be high
  • Heart rate is increased
Blood tests are done to evaluate thyroid function.
  • TSH is usually too low to detect.
  • Thyroid hormone levels such as free T4 and total T3 are high.

Possible Complications

Congestive heart failure and pulmonary edema can develop rapidly and lead to death.

When to Contact a Medical Professional

This is an emergency condition. Call 911 or another emergency number if you have hyperthyroidism and experience symptoms of thyroid storm.

Alternative Names

Thyrotoxic storm; Hyperthyroid storm; Accelerated hyperthyroidism

Radioactive Iodine for Hyperthyroidism

Radioactive iodine is a medicine that you take one time. After you swallow it, it is taken up by your thyroid gland. Depending on the dosage used, the radioactivity in the iodine destroys most or all of the tissue in your thyroid gland, but it does not harm any other parts of your body.
Radioactive iodine treatment has been safely used on millions of people for more than 60 years.

Recommended Related to Thyroid Disorders

Also called Hashimoto's disease, Hashimoto's thyroiditis is an autoimmune disease, a disorder in which the immune system turns against the body's own tissues. In people with Hashimoto's, the immune system attacks the thyroid. This can lead to hypothyroidism, a condition in which the thyroid does not make enough hormones for the body's needs. Located in the front of your neck, the thyroid gland makes hormones that control metabolism. This includes your heart rate and how quickly your body uses calories...

What To Expect After Treatment

Within a few days after treatment, the radioactive iodine will leave your body in your urine. Drinking plenty of fluids during this time will help your body get rid of the radioactivity. To avoid exposing other people to radioactivity, it is important to take the following precautions for the first 5 days after your treatment:
  • Keep your distance from other people, especially children and pregnant women.
  • Do not sit next to someone in a motor vehicle for more than 1 hour.
  • Avoid close contact, kissing, or sexual intercourse.
  • Sleep alone in a separate room.
  • Use separate towels, washcloths, and sheets. Wash these and your personal clothing separately for 1 week.
To further reduce the chance of exposing other people to radioactivity:
  • Wash your hands with soap and lots of water each time you use the toilet.
  • Keep the toilet very clean. Men should urinate sitting down to avoid splashing. Also, flush the toilet two or three times after each use.
  • Rinse the bathroom sink and tub thoroughly after you use them.
  • Use separate (or disposable) eating utensils for the first few days. And wash them separately.
After you take your treatment, you may have follow-up exams every 4 to 6 weeks until your thyroid hormone levels return to normal.

Why It Is Done

Radioactive iodine has the best chance of permanently curing hyperthyroidism. Doctors often use it if your hyperthyroidism comes back after you have been treated with antithyroid medicine. It can also be used if your hyperthyroidism comes back after you have surgery to remove part of your thyroid gland.

How Well It Works

For most people, one dose of radioactive iodine treatment will cure hyperthyroidism. Usually, thyroid hormone levels return to normal in 8 to 12 weeks. In rare cases, the person needs a second or third dose of radioactive iodine.

Risks

For some people, radioactive iodine treatment causes the thyroid gland to become swollen and inflamed (radiation thyroiditis). If this happens, you may feel pain in your neck. Or your hyperthyroidism may temporarily get worse. If you get radiation thyroiditis, it usually does not last more than a few days. And you can take medicines that will help you feel better.
Radioactive iodine treatment may cause hypothyroidism, which means your body makes too little thyroid hormone. Most people will have hypothyroidism within a year after treatment. If you have hypothyroidism, you will need to take thyroid hormone medicine for the rest of your life. For more information, see the topicHypothyroidism.
If you have Graves' ophthalmopathy, it may get worse temporarily after radioactive iodine therapy.

What To Think About

Most people-depending on their ages, how much thyroid hormone their bodies make, and other health conditions they have-are treated first with radioactive iodine.
Radioactive iodine is often recommended if you have Graves' disease and are older than 50, or if you have thyroid nodules (toxic multinodular goiter) that are releasing too much thyroid hormone. Radioactive iodine is not used if:
  • You are pregnant or you want to become pregnant within 6 months of treatment.
  • You are breast-feeding.
  • You have thyroiditis or another kind of hyperthyroidism that is often temporary.
You may take antithyroid medicine for several weeks or months before treatment with radioactive iodine. The antithyroid medicine will lower thyroid hormone levels in your body and will also lower your chances of having a more serious problem calledthyroid storm. You may also take additional medicines that can make you feel better and help your thyroid return to normal before you are given radioactive iodine.
Radioactive iodine has been used to treat hyperthyroidism for more than 60 years. There is no evidence that radioactive iodine causes cancerinfertility, or birth defects.
If you have had radioactive iodine treatment and you want to travel within a few days after treatment, prepare for any problems you may have at airport security. People who have had radioactive iodine treatment can set off the radiation detection machines in airports.
If you plan to travel within 5 to 7 days of your radioactive treatment:
  • Check with local authorities about special procedures or considerations.
  • Ask your doctor to write a letter describing the radiation isotope used, the date and time of treatment, the dose, and its biological half-life (how long it takes for half of the radioactive iodine to be eliminated from the body). The letter should include your doctor's 24-hour telephone numbers so that authorities can call your doctor if they need to verify the information in the letter.
  • Keep in mind that you will have to wait for permission to travel.












The Thyroid-Lupus Relationship
  • Prevalence of thyroid dysfunction in systemic lupus erythematosus
    Journal of Clinical Rheumatology, Volume 15, Number 3, April 2009, pp. 117 – 119
What is the topic?
The thyroid gland makes hormones that act on many functions in the body, from how quickly cells use energy to bone development and nerve cell growth. The thyroid’s production of hormones is regulated by TSH (thyroid-stimulating hormone), which is made in the pituitary gland.
Autoimmune thyroid disease occurs when the body makes antibodies to thyroid cells. Different antibodies to the thyroid can have different effects. Some can inhibit the thyroid cells, causing an underactive thyroid (thyroiditis); others can stimulate the thyroid cells, leading to an overactive thyroid (Graves’ disease). Many of the symptoms of autoimmune thyroid disease -- fatigue, muscle pain and weakness, specific antibodies -- are also symptoms of lupus. Several studies have suggested that thyroid disease occurs more often in people with lupus than the general population, and this study was designed to learn more about this possibility.
What did the researchers hope to learn?
The researchers wanted to compare the rate of thyroid disease in people with lupus patients versus healthy people, and to see whether thyroid disease is associated with any specific types of lupus.
Who was studied?
Five hundred twenty-four patients at a rheumatology clinic in Sao Paulo, Brazil, were followed over a 4 ½ year period (January 1999 – July 2003). The individuals with lupus were mostly Caucasian women, with an average age of 28.8 years. The length of time since their lupus diagnosis ranged from 1 month to 28 years, and on average was 6.2 years. In addition to the lupus patients, 50 women (average age, 32.3 years) with no history of either lupus or thyroid conditions were looked at as a comparison.
How was the study conducted?
The patients had clinical and laboratory exams when they were first diagnosed and every three months after that. The initial exam at diagnosis included blood tests for thyroid function (FT4 and TSH) and thyroid antibodies. The researchers looked at four different types of thyroid conditions: (1) underactive thyroid with low FT4 and high TSH; (2) overactive thyroid with high FT4 and low TSH; (3) slightly underactive (sub-clinical) low thyroid without any symptoms, with high TSH and normal FT4; and (4) slightly overactive (sub-clinical) high thyroid without symptoms, with low TSH and normal FT4.
What did the researchers find?
Thirty-two of the lupus patients (6.1%) had autoimmune thyroid disease, 28 of whom had underactive thyroid and 4 of whom had overactive thyroid. Fifteen of these 32 patients had autoimmune thyroid disease at the time of their diagnosis of lupus, and seventeen developed their thyroid disease after the lupus. Twelve of the 17 patients (70.6%) who developed thyroid disease after being diagnosed with lupus had tested positive for thyroid antibodies more than once prior to the onset of detectable thyroid disease. Sixty other patients (11.5%) were identified as having sub-clinical hypothyroidism, and another 89 patients (17.0%) tested positive for thyroid antibodies but did not have clinical or subclinical thyroid disease.
Among the women without lupus, only one person (2%) had underactive thyroid disease, none had subclinical thyroid conditions, and two (4%) tested positive for thyroid antibodies in the absence of thyroid disease. The difference in the amount of thyroid disease between the lupus patients and the comparison group did not reach statistical significance even though the trend seemed to be more thyroid disease in the lupus patients. What this means is that it still could be true that there is increased thyroid disease in lupus, but this study cannot prove this, since the small increased percentage seen in the lupus patients could be a random difference.
Among the lupus patients, those with autoimmune thyroid disease were more likely to have Sjogren’s syndrome (an autoimmune condition in which tears and saliva can be decreased among other symptoms) and more tested positive for rheumatoid factor than the patients without thyroid disease. There was a significant correlation between clinical symptoms of overactive thyroid and lupus disease activity, but not for underactive thyroid. The researchers found no relationship between thyroid antibody levels and lupus disease activity.
What were the limitations of the study?
This study was conducted in Brazil, so it might not reflect what would be found in patients from other areas of the world who might have different genetic risk factors for thyroid disease and lupus and where thyroid disease might be more or less common in general.
What do the results mean for you?
Though the researchers did not find a statistically higher prevalence of thyroid disease among lupus patients, they did see a higher level of subclinical hypothyroidism and thyroid antibodies. All of these factors suggest that lupus patients should be tested for signs of abnormal thyroid activity, including thyroid antibody levels, which may show up earlier than other features of thyroid disease. This may be important since the symptoms of thyroid gland impairment may be overlooked or attributed to lupus but might require very different types of treatment.



Systemic Lupus Erythematous and Graves Disease

Izzedine, Hassane MD*; Roura, Raoul MD†; Bourry, Edward MD*; Georgin-Lavialle, Sophie MD‡; Cacoub, Patrice MD‡; Deray, Gilbert MD* http://journals.lww.com/theendocrinologist/Abstract/2005/09000/Systemic_Lupus_Erythematous_and_Graves_Disease.6.aspx

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Abstract

Despite the common genetic predisposition and autoimmune features of both disorders, Graves disease (GD) has been described quite infrequently in patients with systemic lupus erythematous (SLE; average incidence of 2.8% vs. 1.9% in general population). We present a patient with SLE who developed hyperthyroidism. A 57-year-old woman, followed since 1998 for lupus nephritis, was admitted for clinical evaluation of hyperthyroidism 5 years after the diagnosis of SLE. Her symptoms included heat intolerance, tremor, and irritability. Clinical examination showed diffuse thyroid gland enlargement with a vascular murmur on auscultation. Hormonal assays showed markedly increased free T3 and T4 levels and suppressed thyroid-stimulating hormone levels with circulating thyroid-stimulating hormone receptor antibodies. Graves disease responded well to carbimazole treatment and beta-blockers. The patient had a subtotal thyroidectomy, later. The patient was on 10 mg of prednisolone maintenance therapy when hyperthyroidism was discovered. Concomitantly, a slight increase in serum creatinine and serum levels of anti-DNA antibodies and complement activation without other abnormalities were found. A third renal biopsy showed mononuclear interstitial infiltration but no glomerular signs of lupus activity. Patients with SLE are likely to be at increased risk for thyroid disease.

Thyroid Disorder in Systemic Lupus Erythematosus Patients in Southeast Iran.

Zakeri Z*, Sandooghi M*.

* Assistant Professor, Department of Internal Medicine, Zahedan University of Medical Sciences, Zahedan, Iran.



Correspondence: Dr. M. Sandooghi, Department of Internal Medicine, Zahedan University of Medical Sciences, Zahedan, Iran, Telephone: +98(915) 161-3472, Fax: +98(541) 2442- 185, E-mail: mahnazsandooghi@yahoo.com


 Received for Publication: February 29, 2008, Accepted for Publication: November 3, 2009.

Abstract:

Background: We conducted this study to clarify the prevalence of thyroid dysfunction in patients with Systemic Lupus Erythematosus (SLE) and compared it to a matched healthy controls group.
Material and methods: Eighty-three SLE and 166 matched healthy controls underwent clinical examination and laboratory evaluation for serum T3, T4, TSH and Thyroid peroxides antibody (TPO AB).
Results: 24.1% of SLE patients and 13.3% of control group had thyroid dysfunction (p value = 0.04). Clinical thyroid dysfunction was seen neither in SLE patients nor in the control group. Elevated TSH levels were the most common dysfunction (19.3%) of the SLE, compared with control group (5.4%). Positive TPO antibody was detected in 16.9% of SLE and 16.3% of the control group. Mean level of TPO antibody was higher in SLE patients with thyroid dysfunction (137.05) than SLE patients without the disorder (30.8) (p value=0.007).
Conclusion: We concluded thyroid dysfunction was more frequent in SLE patients than in healthy controls. Moreover, SLE patients with anti TPO were more likely to have thyroid dysfunction than the control group. 

Keywords: SLE, thyroid dysfunction, hypothyroidism, hyperthyroidism, anti TPO antibody.

Introduction:
Many SLE patients are initially treated for thyroid dysfunction before the diagnosis of lupus is made or vice versa. Symptoms of thyroid disease can be confused with those of lupus. To identify the thyroid function in lupus patients many studies have been conducted. Although the relationship between autoimmune thyroid disease and SLE has been revealed, the prevalence of thyroid disease in lupus patients is controversial. Reported prevalence of autoimmune thyroid disease (3.9_24%) and anti thyroid antibodies (11-51%) in SLE patients varied considerably.(1) A study by Weetmen  et al has shown that 51% of SLE patients had thyroid antibodies compared to 27% of controls, and elevated TSH were detected in 25% of SLE patients and 12.5% in the control group.(2) In China, prevalence of thyroid antibodies and thyroid dysfunction in SLE patients was 46.7% and 22.2% respectively.(3) The prevalence of antimicrosomal and antithyroglobulin antibodies was 32.2% in SLE patients in Singapore.(4) In Korean patients with SLE, prevalence of Hashimotos  'thyroiditis, euthyroid sick syndrome, and graves' disease were 9.5% ,14.3%  and 4.8%  respectively, while antithyroid antibodies were 27%.(5)The study by Chan et al has shown that 13% of SLE patients had subclinical hypothyroidism and 4.3% had hypothyroidism and positive anti TPO were detected in 23.2% of SLE patients.(6) In Egypt, ElSharif et al revealed that thyroid disorders in SLE patients were 50% and TPO antibody was found in15% of SLE patients.(7) The aim of this study was to assess the prevalence of thyroid dysfunction and thyroid antibody in lupus patients in the southeast of Iran compared with a control group. Moreover, in this study we excluded other autoimmune diseases in both SLE patients and the healthy control group to better clarify the association between SLE and thyroid disease.

Method and Materials:
A case control study was conducted. Eighty-three patients with lupus (without other autoimmune diseases) were selected according to ACR criteria in rheumatologic clinic of Ali- ebn-Abitaleb hospital in Zahedan, Iran. The history for thyroid disorder and drug history for thyroid disease were asked and then participants underwent clinical examination for determination of thyroid size (WHO scoring) and laboratory evaluation for serum T3, T4, TSH and anti TPO antibody. The control group consisted of 166 subjects without SLE being matched in sex and age and were selected from a similar population. Individuals who did not cooperate and those who had other autoimmune diseases (diabetes, rheumatic disease, vetiligo, autoimmune hepatitis) or a history of any thyroid disease were excluded from the study. The included subjects were checked for clinical findings, thyroid hormones and anti TPO antibody. Finally, demographic data and type of thyroid dysfunction was recorded. However, disease activity score, duration of disease, medical therapy, T3RU and free thyroxin level were not detected in SLE patients. The study was approved by the ethical Committee of our institution, and all study participants signed a written informed consent.  


Statistical Analysis:
A t-test was used to compare means of variables. The Chi-Square test and Fisher exact test were also used to compare the frequency of the variables for the two groups. The Mann-Whitney-test was used when necessary. Elevated TSH and suppressed TSH levels were defined by TSH level ≥ 5 and TSH ≤ 0.1 mic IU / ml, respectively.

Results:
In the eighty-three SLE patients, mean age was 30.21 ± 10.83 ages (2-63y), seventy-five of whom were female (90.5%) and eight were male (9.5%). In the control group the mean age was 30.21 ± 10.83, 150 were female (91.0%) and 16 were male (9%). 24.1 % of SLE patients and 13.3% of the control group had thyroid dysfunction (p value = 0.04). Clinical thyroid dysfunction was seen neither in SLE patients nor in the control group.  Elevated TSH levels were the most common dysfunction in SLE patients (19.3%) and suppressed TSH was the next most common dysfunction in 4.8% of patients. The prevalence of subclinical hyperthyroidism was 7.8% and subclinical hypothyroidism was 5.4% in the control group. Elevated TSH levels were more common in SLE patients (19.3) compared to the control group (5.4%) (P value = 0.002). Positive TPO antibody was detected in 16.9% of SLE and 16.3% of the control group. Positive anti TPO in SLE patients and the control group with abnormal function was 35% and 22.7% respectively. In other words, a higher frequency of thyroid dysfunction was seen in SLE patients with thyroid antibody (50.0%) compared with the control group with thyroid antibody (18.5%). Mean level of TPO antibody was higher in SLE patients with thyroid dysfunctions (137.05 IU/mL) than SLE patients without the disorders (30.18 IU/mL) (p value = 0.007). Mean level of TPO antibody in the control group with and without thyroid dysfunctions was 41 IU/mL and 43 IU/mL respectively, which were not statistically significant (p value = 0.95). The distribution of sex and age was similar in both groups. In SLE patients, the size of thyroid was normal in patients with suppressed TSH but it was Grad 1(WHO scoring) in 31.3% of patients with elevated TSH levels and 1.6% of patients with normal TSH. In the control group, abnormal size of thyroid (grad 1 WHO scoring) was seen only in subjects with elevated TSH levels (11.1% of control group).

Discussion:
In our study 24.1% of SLE patients and 13.3% of the control group had thyroid dysfunction and anti TPO antibody was similar in both SLE patients (16.9%) and in the control group (16.3%). To clarify the association of thyroid disorder and SLE, we excluded other autoimmune disease in both SLE patients and the control group. Unfortunately in this study, serology of free T4 (FTI) and T3RU were not performed, thus the differentiation of subclinical hypothyroidism and euthyroid sick syndrome was not possible. Moreover, this study was short in duration and had a relatively small sample size. In previous studies, reported prevalence of autoimmune thyroid disease (3.9-24%) and anti-thyroid antibodies (11-51%) in SLE patients varied considerably.(1)  Early reports were mainly based on short term studies of small cohorts.(2-6)However, in our study which was similar to those short term and small cohorts, the prevalence of thyroid dysfunction was in the upper limits of reported prevalence. Two studies have reviewed SLE patients for longer periods of time. In the first study by Miller et al. the prevalence of diagnosed hypothyroidism (6.6%) was unexpectedly high and 18% had high antimicrosomal antibody.(7) In the second study by Pyne et al, the prevalence of hypothyroidism in SLE patients (5.7%) was higher than the normal population (1%) while that of hyperthyroidism (1.7%) was not significantly different. Also, 14% had thyroid antibody, rising to 68% in the subgroup who also had thyroid disease.(1) In our study the prevalence of thyroid antibody was comparable with these two studies, but we could not find clinical thyroid disease both in patients with SLE and those in the control group. Moreover, our findings contrasted to the study by Chane et al. in which 4.3% of SLE patients had clinical hypothyroidism.(6) Also, hypothyroidism was detected in 11.6% of SLE patients compared to 1.9% in the control group in study by Mader et al. However, a statistically significant difference was not observed in the levels of thyroid antibody between the SLE patients and the control group (8), which was compatible with our study. In a recent study by Biro et al. that determined the association of Hashimoto¢s thyroiditis (HT) and Grave¢s disease (GD) with systemic autoimmune disease, prevalence of HT in SLE was 90 fold higher than in the general population.(9) Maybe the reason for low prevalence of clinical hypothyroidism in the population of our study was the exclusion of patients with clinical autoimmune diseases from the control group. Furthermore, there were no coexisting autoimmune diseases in the group of SLE patients. Also, thyroid disease may be less common in southeast Iran, but larger controlled common longitudinal studies are necessary to confirm this. If other autoimmune diseases were not excluded from the group of SLE patients, we would likely find more frequent abnormal thyroid function tests and more severe symptomatic thyroid disease.
In our study, higher frequency of thyroid dysfunction was seen in SLE patients with positive thyroid antibody. Moreover, the level of TPO antibody was higher in SLE patients with thyroid disorder than SLE patients without thyroid disorder which was compatible with some other studies.(10-12) This was not seen in the control group. We concluded that thyroid abnormalities were more associated with autoimmune diseases like hypothyroidism (subclinical and overt) or euthyroid sick syndrome in SLE patients. In addition, this finding suggests that detection of high level TPO antibody in SLE patients may help in early detection of associated thyroid disorder. This finding is compatible with a study by Kausman et al. that reviewed the thyroid serology of 150 new cases of SLE patients who were followed up for 7.9 years. On average, 21% were thyroid autoantibody positive. Out of all antibody positive patients, 60% remained persistently thyroid antibody positive. All five cases of clinical thyroid disease, and two out of three cases of subclinical hypothyroidism, occurred in the group with persistently positive thyroid serology.(12) In some studies, older age and longer duration of SLE were related to thyroid disorder.(2, 5, 11) In our study, mean age was similar in all groups.
     
We concluded that thyroid disorder was more frequent in SLE patients than the healthy control group, although, we excluded other autoimmune diseases. Moreover, SLE patients with anti TPO were more likely to have thyroid dysfunction than the control group. For clarifying the relationship between SLE and thyroid dysfunction, we strongly recommend the following: the study of thyroid dysfunction in the onset of the disease in new cases of SLE patients without other autoimmune diseases; taking history for thyroid disorder and medication for thyroid; and regular follow-up for long periods of time. We also suggest further studies to evaluate prevalence of thyroid disorder in southeast Iran.