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Graves Disease:
An autoimmune disease which results from type II hypersensitivity in which there is stimulation of the thyroid by autoantibodies directed against the TSH receptor.

Type II Hypersensitivity:

Antibodies that attack antigens on the surface of specific cells or tissues (thyroid-stimulating immunoglobulins attack thyroid tissue)

The reaction is organ-specific (thyroid for Graves disease)

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-Postpartum
-Infections
-Iodine Excess (over iodized salt; animal milk; iodine-containing supplements)
-Emotional Stress
-Smoking
-Interferon Induced Thyroiditis (IIT) (Interferon-alpha used as treatment for may conditions most notably Hep C)

(Pokhrel & Bhusal, 2023)

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The end goal of treatment is to stop the production of Thyroid hormones. Some therapies manage symptoms only. The options are as follows:

1) Radioactive iodine therapy destroys cells over time due to accumulative radiation effects on cells.
2) Anti-thyroid medications interfere with iodine usage to create hormones.
3) Beta-blockers are used to block the effects of thyroid hormones on the body.
4) Surgical excision of the thyroid (total or partial) reduces or eliminates hormone production. Post-surgical therapies replace normal levels of thyroid hormones.
5) Management of Grave's ophthalmopathy done via corticosteroids, further surgeries and radiation, or infusion therapies.

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How TEPEZZA works to treat Thyroid Eye Disease, or T-E-D.

Thyroid Eye Disease, or T-E-D, is a serious, vision-threatening condition.

You may have heard Thyroid Eye Disease called Graves' eye disease.

To understand what causes T-E-D, you have to go behind the eye.

In the tissue behind the eye are cells which have receptors on their surface that act like switches.

But when you have T-E-D, your body's immune system attacks this tissue, which causes molecules-known as autoantibodies-to turn these switches on.

This leads to swelling of the muscle and fat.

This swelling can cause a number of symptoms like eye pain, redness in and around your eyes, and swollen eyelids.

The swollen muscle and fat tissue behind the eye can also make the eyes bulge, which your doctor may call proptosis.

And cause double vision, which your doctor may call diplopia.

TEPEZZA is the first and only FDA-approved treatment for Thyroid Eye Disease.

Unlike other medicines, TEPEZZA treats the cause of T-E-D, not just the symptoms.

TEPEZZA is designed to bind to the switch and block it from turning on.

Since TEPEZZA blocks the switches so they cannot turn on, swelling of the muscle and fat tissue goes down.

This leads to reduced bulging and less redness, pain, and swelling of the eyes.

TEPEZZA can also improve double vision and, in some cases, make it completely go away.

TEPEZZA has also been proven to improve visual ability and physical appearance.

So, ask your doctor if TEPEZZA is right for you.

Please keep watching to hear Important Safety Information about TEPEZZA.
INDICATION AND IMPORTANT SAFETY INFORMATION USE
TEPEZZA is a prescription medicine used to treat Thyroid Eye Disease.
IMPORTANT SAFETY INFORMATION What is the most important information I should know about TEPEZZA?
Infusion reactions can happen during or within 24 hours after your infusion of TEPEZZA. If you have a reaction while receiving TEPEZZA, your doctor or nurse will slow or stop your infusion and treat your reaction. If you have a severe infusion reaction, your doctor may stop your treatment completely.
Tell your doctor or nurse right away if you have any of these symptoms during or after your treatment with TEPEZZA:
If you have inflammatory bowel disease (IBD), such as Crohn's disease or ulcerative colitis, TEPEZZA may make your IBD symptoms worse. Symptoms of worsening IBD may include: an increased number of loose stools with stomach pain or cramps, and blood in your stools. After each TEPEZZA infusion, tell your doctor right away if you have worsening IBD symptoms.

TEPEZZA may cause an increase in your blood sugar. Before starting treatment with TEPEZZA, tell your doctor if you are currently being treated for diabetes, know your blood sugar is high, or have been diagnosed with diabetes. It is important for you to take your treatments and follow an appropriate diet for glucose control as prescribed by your doctor.
Before receiving TEPEZZA, tell your doctor if you:

Have inflammatory bowel disease (Crohn's disease or ulcerative colitis).

Are currently being treated for diabetes, have been diagnosed with diabetes, or know your blood sugar is high.

Are pregnant or plan to become pregnant. TEPEZZA may harm your unborn baby. Tell your doctor if you become pregnant or suspect you are pregnant during treatment with TEPEZZA.
Women who are able to become pregnant should use an effective form of birth control (contraception) prior to starting treatment, during treatment and for at least 6 months after the final dose of TEPEZZA.

Are breastfeeding or plan to breastfeed. It is not known if TEPEZZA passes into your breast milk. Talk to your doctor about the best ways to feed your baby during treatment with TEPEZZA.

Tell your doctor about all the medicines you take, including prescription and over-the-counter medicines, vitamins, dietary and herbal supplements. Know the medicines you take. Keep a list of them to show your doctor and pharmacist when you get a new medicine.

What are the possible side effects of TEPEZZA?
The most common side effects of TEPEZZA include muscle cramps or spasms, nausea, hair loss, diarrhea, feeling tired, high blood sugar, hearing problems, taste changes, headache, dry skin, weight loss, nail problems, and changes in menstruation.

This is not a complete list of all possible side effects. Tell your doctor or treatment team about any side effect you may have.
You are encouraged to report negative side effects of prescription drugs to the FDA. Visit www.fda.gov/safety/medwatch, or call 1-800-FDA-1088. Please visit TEPEZZA.com for more information.

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This is a unique kind of treatment for a debilitating disease.

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Watch a video to see how TEPEZZA works to treat Thyroid Eye Disease (TED) at the source, and not just the symptoms of TED. See safety info.

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Immune cells are created called thyroid-stimulating immunoglobulin (TSI) that serve as analogs of Thyroid Stimulating Hormone (TSH). Grave's Disease has a specific TSI known as Thyrotropin Receptor Antibody (TRAb) that performs this feat.

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The thyroid gland normally enlarges in response to the increase demand for TH. When the condition resulting in increase TH resolves, TSH secretion normally subsides, and the thyroid gland returns to its original size.

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Type II Hypersensitivity: Tissue specific; cytotoxic; antigens on cell-surface receptors are altered and bind to antibodies (IgG, IgM) complementing the self-antigen. Tissue destruction results from macrophages, natural killer cells, and neutrophils that complement. A decreased number of receptors available results from antibodies binding to hormones or neurotransmitters.

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-Fast/Irregular Heartbeat
-Weight Loss
-Insomnia
-Bulging Eyes
-Change in Menstrual Cycle/Reduced Libido
-Trembling Hands
-Goiter
-Heat Intolerance
-Muscle Weakness

https://www.thyroidcancer.com/blog/how-to-treat-graves-disease-top-3-options

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Pokhrel B, Bhusal K. Graves Disease. [Updated 2023 Jun 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448195/#

Walsh, Dr. N., How to treat graves’ disease: Top 3 options. https://www.thyroidcancer.com/blog/how-to-treat-graves-disease-top-3-options

Rogers, J. (2024). McCance & Huether’s pathophysiology: the biologic basis for disease in adults and children. (9th ed.). Elsevier.

Pokhrel, B., Bhusal, K. (June 2023). Grave’s Disease. National Library of Medicine. https://www.ncbi.nlm.nih.gov/books/NBK448195/

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Continuing Education Activity

Graves' disease is the most common cause of hyperthyroidism. It is a disorder with systemic manifestations that primarily affect heart, skeletal muscle, eyes, skin, bone, and liver. Failure to diagnose Graves' disease in a timely manner can predispose thyroid storm which carries high morbidity and mortality. Clinicians ought to be aware of systemic manifestations of Graves' disease and the different modalities available for treatment. Early diagnosis and management of Graves' disease can also prevent severe cardiac complications such as atrial flutter, atrial fibrillation, and high output cardiac failure. This activity reviews the evaluation and treatment of Graves' disease and highlights the role of the interprofessional team in reducing morbidity and improving care for affected patients.

Objectives:

Identify the etiology of Graves' disease.

Describe the proper evaluation of Graves' disease.

Summarize the treatment options for Graves' disease.

Review interprofessional team strategies for improving care coordination to improve outcomes for patients with Graves' disease.

Access free multiple choice questions on this topic.
Introduction

Graves' disease is an autoimmune disease which primarily affects the thyroid gland. It may also affect multiple other organs including eyes and skin. It is the most common cause of hyperthyroidism.[1] In this chapter, we attempt to review different aspects of Graves' disease.

Etiology

Like all autoimmune diseases, it occurs more commonly in patients with a positive family history. It is more common in monozygotic twins than in dizygotic twins. It is precipitated by environmental factors like stress, smoking, infection, iodine exposure, and postpartum, as well as after highly active antiretroviral therapy (HAART) due to immune reconstitution.[2]

Epidemiology

Graves' disease is the most common cause of hyperthyroidism accounting for 60% to 80% of hyperthyroid cases. The overall prevalence of hyperthyroidism in the United States is 1.2% with an incidence of 20/100,000 to 50/100,000. It is most common in people ages 20 to 50 years. Graves' disease is more common in women than men. Some data suggest its lifetime risk in women and men are 3% and 0.5%, respectively. As per the data from Nurses' Health Study II (NHSII), the 12-year incidence among women ages 25 to 42 years was as high as 4.6/1000.[2]

Pathophysiology

Graves' disease is caused by thyroid stimulating immunoglobulin (TSI), also known as thyroid stimulating antibody (TSAb). B lymphocytes primarily synthesize Thyroid stimulating immunoglobulin within the thyroid cells, but it can also be synthesized in lymph nodes and bone marrow. B lymphocytes are stimulated by T lymphocytes which get sensitized by antigen in the thyroid gland. Thyroid stimulating immunoglobulin binds with thyroid-stimulating hormone (TSH) receptor on the thyroid cell membrane and stimulates the action of the thyroid-stimulating hormone. It stimulates both, thyroid hormone synthesis and thyroid gland growth, causing hyperthyroidism and thyromegaly.[3]

Several environmental factors including pregnancy (mainly postpartum), iodine excess, infections, emotional stress, smoking, and interferon alfa trigger immune responses on susceptible genes to eventually cause Graves' disease.

Graves' orbitopathy (ophthalmopathy) is caused by inflammation, cellular proliferation and increased growth of extraocular muscles and retro-orbital connective and adipose tissues due to the actions of thyroid stimulating antibodies and cytokines released by cytotoxic T lymphocytes (killer cells). These cytokines and thyroid stimulating antibodies activate periorbital fibroblasts and preadipocytes, causing synthesis of excess hydrophilic glycosaminoglycans (GAG) and retro-orbital fat growth. Glycosaminoglycans cause muscle swelling by trapping water. These changes give rise to proptosis, diplopia, congestion, and periorbital edema. If left untreated, it eventually leads to irreversible fibrosis of the muscles.[4]

Pathogenesis of other rare manifestations of Graves disease like pretibial myxedema and thyroid acropachy are poorly understood and are believed to be due to cytokines mediated stimulation of fibroblasts. Many symptoms of hyperthyroidism like tachycardia, sweating, tremors, lid lag, and stare are thought to be related to increased sensitivity to catecholamine.

History and Physical

Most patients with Graves disease present with classic signs and symptoms of hyperthyroidism. Initial presentation of Graves disease with only Graves orbitopathy or pretibial myxedema is rare. Presentation depends on the age of onset, severity, and duration of hyperthyroidism. In the elderly population, symptoms may be subtle or masked, and they may present with non-specific signs and symptoms like fatigue, weight loss, and new onset atrial fibrillation. Atypical presentation of hyperthyroidism in elderly is also referred as apathetic thyrotoxicosis.

In younger patients, common presentations include heat intolerance, sweating, fatigue, weight loss, palpitation, hyper defecation, and tremors. Other features include insomnia, anxiety, nervousness, hyperkinesia, dyspnea, muscle weakness, pruritus, polyuria, oligomenorrhea or amenorrhea in the female, loss of libido, and neck fullness. Eye symptoms include lids swelling, ocular pain, conjunctival redness, double vision. Palpable goiter is more common in the younger population, age younger than 60 years. Up to 10 % of patients may have weight gain.[1]

Physical signs of hyperthyroidism include tachycardia, systolic hypertension with increased pulse pressure, signs of heart failure (like edema, rales, jugular venous distension, tachypnea), atrial fibrillation, fine tremors, hyperkinesia, hyperreflexia, warm and moist skin, palmar erythema and onycholysis, hair loss, diffuse palpable goiter with thyroid bruit and altered mental status.

Signs of extrathyroidal manifestations of Graves' disease include ophthalmopathy like eyelid retraction, proptosis, periorbital edema, chemosis, scleral injection, exposure keratitis. Thyroid dermopathy causes marked thickening of the skin, mainly over tibia which is rare, seen in 2% to 3% of cases.[1] The thickened skin has peau d'orange appearance and is difficult to pinch. Bone involvement includes subperiosteal bone formation and swelling in the metacarpal bones which is called osteopathy or thyroid acropachy. Onycholysis (Plummer nails) and clubbing are very rare.

Evaluation

Diagnosis of Graves disease starts with a thorough history and physical examination. History should include a family history of Graves' disease. [5][6]

Thyroid function tests to diagnose hyperthyroidism:

The initial test for diagnosis of hyperthyroidism is the thyroid-stimulating hormone (TSH) test. If TSH is suppressed, one needs to order Free T4 (FT4) and Free T3 (FT3). If free hormone assays are not available, total T4 (Thyroxine) and total T3 (Triiodothyronine) can be ordered. Suppressed TSH with high FT4 or FT3 or both will confirm the diagnosis of hyperthyroidism. In subclinical hyperthyroidism, only TSH is suppressed, but FT4 and FT3 are normal.

Tests to differentiate Graves from other causes of hyperthyroidism:

Graves diagnosis can be obvious with a careful history and physical examination. Features suggestive of Graves disease include a positive family history of Graves disease, the presence of orbitopathy, diffusely enlarged thyroid with or without bruit and pretibial myxedema. However, if the diagnosis is in question due to lack of one or more of these features, following tests can be ordered:

1. Measurement of TSH receptor antibody (TRAb): There are two available assays, the thyroid stimulating immunoglobulin (TSI) and thyrotropin-binding inhibiting (TBI) immunoglobulin or thyrotropin-binding inhibitory immunoglobulin (TBII). Measurement of TRAb with third generation assay has sensitivity and specificity of 97% and 99% for the diagnosis of Graves disease.[7] TRAb measurement is indicated in following conditions:

Hyperthyroidism during pregnancy when thyroid uptake scan is contraindicated

Pregnant women with h/o Graves disease to determine possible fetal and neonatal hyperthyroidism as these antibodies cross placenta

Patients with possible Graves' orbitopathy without biochemical hyperthyroidism

Patients with recent h/o large iodine load where thyroid uptake scan cannot be reliable, e.g., recent amiodarone use, recent imaging studies with iodinated contrast

To determine the prognosis of hyperthyroidism who are being treated.

2. Radioactive iodine uptake scan with I-123 or I-131: In Graves disease, the uptake will be high and diffuse whereas, in a toxic nodule, the uptake will be focal known as a hot nodule. Toxic multinodular goiter will have heterogeneous uptake. The radioactive iodine uptake in subacute or silent thyroiditis, factitious hyperthyroidism, and recent iodine load will be low.

3. Thyroid Ultrasonogram with Doppler: The thyroid gland in Graves disease is usually hypervascular.

4. T3/T4 ratio greater than20 (ng/mcg) or FT3/FT4 ratio greater than 0.3 (SI unit) suggests Graves disease and can be used to differentiate Graves' disease from thyroiditis induced thyrotoxicosis.

Other Tests:

CT or MRI of orbits can be performed to diagnose Graves orbitopathy in patients who present with orbitopathy without hyperthyroidism.

Patient with hyperthyroidism can have microcytic anemia, thrombocytopenia, bilirubinemia, high transaminases, hypercalcemia, high alkaline phosphatase, low LDL and HDL cholesterol.

Treatment / Management

Treatment for Graves' disease depends on its presentation. Treatment consists of rapid symptoms control and reduction of thyroid hormone secretion.

A beta-adrenergic blocker should be started for symptomatic patients, specifically for patients with heart rate more than 90 beats/min, patients with a history of cardiovascular disease, and elderly patients. Atenolol 25 mg to 50 mg orally once daily may be considered the preferred beta blocker due to its convenience of daily dosing, and it is cardioselective (beta-1 selective). Some prescribers recommend Propranolol 10 mg to 40 mg orally every six to eight hours, due to its potential effect to block peripheral conversion of T4 to T3. If a beta blocker after that, calcium channel blockers like diltiazem and verapamil can be used to control heart rate.[6][8][9]

There are three options to reduce thyroid hormone synthesis. These options are:

1. Antithyroid drugs which block thyroid hormone synthesis and release

2. Radioactive iodine (RAI) treatment of the thyroid gland

3. Total or subtotal thyroidectomy.

All three options have pros and cons, and there is no consensus on which one is the best option. It is very important to discuss all three options in detail with the patients and make an individualized decision.

Anti-thyroid Drugs (Thionamides)

Methimazole (MMI) and propylthiouracil (PTU) are two anti-thyroid drugs available in the USA. Outside USA, carbimazole, a derivative of methimazole which is rapidly metabolized to methimazole, is also available. These thioamides inhibit Thyroid Peroxidase (TPO) mediated iodination of thyroglobulin in the thyroid gland, blocking the synthesis of T4 and T3. To some extent, Propylthiouracil also blocks peripheral conversion of T4 to T3.

In nonpregnant patients, methimazole is the drug of choice due to its less frequent side effects (especially hepatotoxicity), once-daily dosing, and more rapid achievement of normal thyroid function. During the first trimester of pregnancy, propylthiouracil must be used due to its less teratogenic side effects. We can start methimazole from the second trimester of pregnancy. American Thyroid Association (ATA) recommends propylthiouracil for patients with thyroid storm and for patients with minor reactions to methimazole therapy who refuses surgery or RAIA.

Before starting thionamide treatment, patients should be informed about possible side effects including allergic reactions, neutropenia, and hepatotoxicity. A complete blood count with differentials and liver function test should be obtained. Thionamide should not be started if baseline transaminase level is more than five times the upper limit of normal or if absolute neutrophil count (ANC) is less than 1000/ml.

Dosage: Initiate methimazole 5 mg to 10 mg oral daily if FT4 is 1 to 1.5 times the upper limit of normal (ULN), 10 mg to 20 mg oral daily if FT4 is 1.5 to 2 times ULN, 30 mg to 40 mg oral daily if FT4 is more than two to three times ULN. Start PTU 50 mg t0 150 mg oral three times daily based on the severity of hyperthyroidism. Once thyroid function improves, the thioamide dose can be tapered and continued at maintenance doses once TFTs become euthyroid. Methimazole is usually maintained at 5 mg to 10 mg daily, and propylthiouracil is maintained at 50 mg two to three times a day.

Adverse effects: Minor side-effects include pruritus and rash (3% to 6%), and major side effects include hepatocellular injury (2.7% propylthiouracil, 0.4% Methimazole), agranulocytosis (0.7%, ANC less than 500/ml) and vasculitis (rarely lupus and pANCA-positive small vessel vasculitis; more with propylthiouracil than methimazole). Rarely hypoglycemia has been reported with methimazole therapy.

Follow-up and monitoring: Monitor thyroid function tests (TFTs) every four to six weeks for the thionamide dose adjustment. Once TFTs improve, we can reduce the thionamide dose by 30% to 50% until a maintenance dose is achieved. Once on a maintenance dose, TFTs can be checked every three months for up to 18 months, thereafter every six months is acceptable. Monitor for adverse effects and perform blood tests as needed based on clinical information. Stop the thionamide if transaminase level is more than three times of ULN. Routine monitoring of liver function tests and complete blood count is not necessary. Thionamides can be continued for minor cutaneous reactions with or without concurrent use of antihistamines, but if the problem persists, alternative treatment options including surgery or RAI therapy should be considered.

Duration of treatment: For patients on long-term, thionamide therapy who are on maintenance doses, we can consider stopping the therapy after 12 to 8 months, if TSH and TRAb levels normalize during follow-up. If patients remain clinically and biochemically euthyroid, we can repeat TFTs every two to three months during the first six months after stopping the treatment, then every four to six months for another six months, then every six to 12 months. If TSH remains normal for one year without treatment, annual monitoring with TSH is enough.

RAI Therapy

It is preferred for non-pregnant adult patients older than 21 years, patients not planning to get pregnant within the next six to 12 months after treatment, patients with risky comorbid conditions for surgery, and patients with contraindications for thioamides. It is contraindicated during pregnancy, lactation, coexisting thyroid cancer, in patients with moderate to severe Graves orbitopathy, and for individuals who cannot follow radiation safety guidelines.

Preparation: Beta-adrenergic blockade and pretreatment with methimazole (propylthiouracil pretreatment has a high failure rate for RAI treatment) should be considered for patients with an increased risk of complications from hyperthyroidism and patients with very high thyroid hormone levels. If methimazole is started, it should be stopped three to five days before RAI treatment. It can be restarted for high-risk patients three to seven days after treatment. A pregnancy test is required before RAI treatment.

Dosage: I-131 is administered as a capsule or liquid. The I-131 dose can be calculated or one may use a fixed dose. Calculated dose is based on thyroid volume, uptake of RAI and local factors. A fixed dose can be 10 to 25 mCi of I-131. The patient should be provided with a written radiation safety precautions after RAI treatment to avoid exposure to household members or community members, especially children, and pregnant women.

Follow-up and monitoring: TFTs should be monitored every four to six weeks for six months or until the patient becomes hypothyroid. Once the patient is on a stable levothyroxine dose, TFTs can be repeated every six to 12 months. If hyperthyroidism persists after six months of RAI therapy, it can be considered as treatment failure, and a repeat treatment with RAI may be needed.[10]

Thyroidectomy

Thyroidectomy is preferred for patients with very large goiter (more than 80 grams), anterior neck compressive symptoms, co-existing suspicious thyroid cancer, large thyroid nodules (greater than 4 cm), cold nodules, co-existing parathyroid adenoma, very high TRAb, and moderate to severe Graves orbitopathy.

Preparation:

Use thionamides to achieve near or complete euthyroid state before surgery

Use Beta-blockers as needed

Use potassium iodide, five to seven drops of Lugol's solution or one to two drops of SSKI, mixed in water or juices three times a day, starting seven to ten days before surgery to reduce vascularity

Assess calcium and Vitamin D levels and replace if needed

Post-op follow-up:

Thionamides should be stopped after surgery and beta-blocker should be weaned off. Levothyroxine is started at 1.6 micrograms per kg body weight, and the dose is adjusted based on TSH level every six to eight weeks.[11][12]

Other Adjunct Treatment for Graves Hyperthyroidism

Iodinated contrast agents, sodium ipodate, and iopanoic acid inhibit peripheral conversion of T4 to T3. They are used with methimazole but not as a solo agent as they can cause resistant hyperthyroidism. They are not available in the United States. Iodide (SSKI drops) can be used for mild hyperthyroidism especially after RAI treatment. Glucocorticoid, cholestyramine, lithium, carnitine are other agents have also been tried. Rituximab may induce remission in patients with Graves disease, but it is costly.

Treatment of Graves Orbitopathy (GO)

Rapid achievement of euthyroid level should be sought in patients with Graves orbitopathy. Patients should be advised to quit smoking if they do. Treatment depends on the severity of orbitopathy. For patients with mild orbitopathy who undergo RAI treatment, prednisone 0.4 mg/kg/day to 0.5 mg/kg/day should be started one to three days after treatment and continued for one month. It should be tapered slowly over two months. Mild active Graves orbitopathy should be treated with artificial tears, and glucocorticoid therapy can be considered. Elevation of the head during sleep reduces orbital congestion. Selenium treatment has doubtful benefits. Prompt ophthalmology referral should be considered for all cases of Graves orbitopathy.

Treatment of moderate to severe active Graves orbitopathy requires up to 100 mg of oral prednisone daily for one to two weeks, then tapered over six to 12 weeks or intravenous (IV) methylprednisolone 500 mg/wk for six weeks followed by 250 mg/wk for six weeks. If glucocorticoids is in effective, tepretumumab is FDA approved for use in moderate to severe active graves orbitopathy. [13]Other options include orbital irradiation, rituximab, and emergency orbital decompression.[14]

Treatment of inactive Graves orbitopathy involves interval close clinical monitoring, elective orbital decompression, strabismus repair and eyelid repair depending upon severity.

Treatment of Dermopathy and Acropachy

Graves dermopathy usually does not need treatment. If treatment is considered, topical high potency glucocorticoid with occlusive dressing can be considered. Rituximab treatment to reduce B-cell may be beneficial, but it remains experimental. There is no treatment available for acropachy.

Differential Diagnosis

Complications

Enhancing Healthcare Team Outcomes

Graves disease is a systemic disorder that affects numerous organs; it's presentations are diverse and hence the disorder is best managed by an interprofessional team. The natural history of Graves disease is well documented and eventually, all patients become hypothyroid and require hormone replacement therapy. Similarly, the ocular features of the disorder also become quiescent with time. Some patients may develop recurrence of hyperthyroidism after ablation and further therapy with radioactive iodine is needed. While the antithyroid drugs do control the symptoms, they do not cure the disease and hence relapses are common. The condition is best addressed with radioactive iodine. All patients need to be educated about the symptoms and signs of hyper-and hypothyroidism, as well as the side effects of the medications. More importantly, the patient should be urged to avoid over-the-counter medications that contain pseudoephedrine or ephedrine during treatment.

References

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Graves' disease is an autoimmune disease which primarily affects the thyroid gland. It may also affect multiple other organs including eyes and skin. It is the most common cause of hyperthyroidism.[1] In this chapter, we attempt to review different aspects of Graves' disease.