Even though some patients undergo spontaneous remission of symptoms within a year, many need treatment. The first step is the regulation of thyroid hormone levels by a physician.

There is some published evidence that a total or sub-total thyroidectomy may assist in reducing levels of TSH receptor antibodies (TRAbs) and as a consequence reduce the eye symptoms, perhaps after a 12-month lag. However, a 2015 meta review found no such benefits, and there is some evidence that suggests that surgery is no better than medication; and there are risks associated with a Thyroidectomy, as there are with long-term use of anti-thyroid medication.

Topical lubrication of the ocular surface is used to avoid corneal damage caused by exposure. Tarsorrhaphy is an alternative option when the complications of ocular exposure can't be avoided solely with the drops.

Corticosteroids are efficient in reducing orbital inflammation, but the benefits cease after discontinuation. Corticosteroids treatment is also limited because of their many side effects. Radiotherapy is an alternative option to reduce acute orbital inflammation. However, there is still controversy surrounding its efficacy. A simple way of reducing inflammation is to stop smoking, as pro-inflammatory substances are found in cigarettes.

Surgery may be done to decompress the orbit, to improve the proptosis, and to address the strabismus causing diplopia. Surgery is performed once the patient's disease has been stable for at least six months. In severe cases, however, the surgery becomes urgent to prevent blindness from optic nerve compression. Because the eye socket is bone, there is nowhere for eye muscle swelling to be accommodated, and, as a result, the eye is pushed forward into a protruded position. In some patients, this is very pronounced. Orbital decompression involves removing some bone from the eye socket to open up one or more sinuses and so make space for the swollen tissue and allowing the eye to move back into normal position and also relieving compression of the optic nerve that can threaten sight.

Eyelid surgery is the most common surgery performed on Graves ophthalmopathy patients. Lid-lengthening surgeries can be done on upper and lower eyelid to correct the patient's appearance and the ocular surface exposure symptoms. Marginal myotomy of levator palpebrae muscle can reduce the palpebral fissure height by 2–3 mm. When there is a more severe upper lid retraction or exposure keratitis, marginal myotomy of levator palpebrae associated with lateral tarsal canthoplasty is recommended. This procedure can lower the upper eyelid by as much as 8 mm. Other approaches include müllerectomy (resection of the Müller muscle), eyelid spacer grafts, and recession of the lower eyelid retractors. Blepharoplasty can also be done to debulk the excess fat in the lower eyelid.

An article in the New England Journal of Medicine reports that treatment with selenium is effective in mild cases.

A large European study performed by the European Group On Graves' Orbitopathy (EUGOGO) has recently shown that the trace element selenium had a significant effect in patients with mild, active thyroid eye disease. Six months of selenium supplements had a beneficial effect on thyroid eye disease and were associated with improvement in the quality of life of participants. These positive effects persisted at 12 months. There were no side effects.

A summary of treatment recommendations was published in 2015 by an Italian taskforce, which largely supports the other studies.

Treatment of Graves' disease includes antithyroid drugs which reduce the production of thyroid hormone; radioiodine (radioactive iodine I-131); and thyroidectomy (surgical excision of the gland). As operating on a frankly hyperthyroid patient is dangerous, prior to thyroidectomy, preoperative treatment with antithyroid drugs is given to render the patient "euthyroid" ("i.e." normothyroid). Each of these treatments has advantages and disadvantages. No one treatment approach is considered the best for everyone.

Treatment with antithyroid medications must be given for six months to two years to be effective. Even then, upon cessation of the drugs, the hyperthyroid state may recur. The risk of recurrence is about 40–50%, and lifelong treatment with antithyroid drugs carries some side effects such as agranulocytosis and liver disease. Side effects of the antithyroid medications include a potentially fatal reduction in the level of white blood cells. Therapy with radioiodine is the most common treatment in the United States, while antithyroid drugs and/or thyroidectomy are used more often in Europe, Japan, and most of the rest of the world.

β-Blockers (such as propranolol) may be used to inhibit the sympathetic nervous system symptoms of tachycardia and nausea until such time as antithyroid treatments start to take effect. Pure β-blockers do not inhibit lid-retraction in the eyes, which is mediated by alpha adrenergic receptors.

The main antithyroid drugs are carbimazole (in the UK), methimazole (in the US), and propylthiouracil/PTU. These drugs block the binding of iodine and coupling of iodotyrosines. The most dangerous side effect is agranulocytosis (1/250, more in PTU). Others include granulocytopenia (dose-dependent, which improves on cessation of the drug) and aplastic anemia. Patients on these medications should see a doctor if they develop sore throat or fever. The most common side effects are rash and peripheral neuritis. These drugs also cross the placenta and are secreted in breast milk. Lugol's iodine may be used to block hormone synthesis before surgery.

A randomized control trial testing single-dose treatment for Graves' found methimazole achieved euthyroid state more effectively after 12 weeks than did propylthyouracil (77.1% on methimazole 15 mg vs 19.4% in the propylthiouracil 150 mg groups).

No difference in outcome was shown for adding thyroxine to antithyroid medication and continuing thyroxine versus placebo after antithyroid medication withdrawal. However, two markers were found that can help predict the risk of recurrence. These two markers are a positive TSHr antibody (TSHR-Ab) and smoking. A positive TSHR-Ab at the end of antithyroid drug treatment increases the risk of recurrence to 90% (sensitivity 39%, specificity 98%), a negative TSHR-Ab at the end of antithyroid drug treatment is associated with a 78% chance of remaining in remission. Smoking was shown to have an impact independent to a positive TSHR-Ab.

Many of the common symptoms of hyperthyroidism such as palpitations, trembling, and anxiety are mediated by increases in beta-adrenergic receptors on cell surfaces. Beta blockers, typically used to treat high blood pressure, are a class of drugs that offset this effect, reducing rapid pulse associated with the sensation of palpitations, and decreasing tremor and anxiety. Thus, a patient suffering from hyperthyroidism can often obtain immediate temporary relief until the hyperthyroidism can be characterized with the Radioiodine test noted above and more permanent treatment take place. Note that these drugs do not treat hyperthyroidism or any of its long-term effects if left untreated, but, rather, they treat or reduce only symptoms of the condition.

Some minimal effect on thyroid hormone production however also comes with Propranolol - which has two roles in the treatment of hyperthyroidism, determined by the different isomers of propranolol. L-propranolol causes beta-blockade, thus treating the symptoms associated with hyperthyroidism such as tremor, palpitations, anxiety, and heat intolerance. D-propranolol inhibits thyroxine deiodinase, thereby blocking the conversion of T to T, providing some though minimal therapeutic effect. Other beta-blockers are used to treat only the symptoms associated with hyperthyroidism. Propranolol in the UK, and metoprolol in the US, are most frequently used to augment treatment for hyperthyroid patients.

Surgery (thyroidectomy to remove the whole thyroid or a part of it) is not extensively used because most common forms of hyperthyroidism are quite effectively treated by the radioactive iodine method, and because there is a risk of also removing the parathyroid glands, and of cutting the recurrent laryngeal nerve, making swallowing difficult, and even simply generalized staphylococcal infection as with any major surgery. Some people with Graves' may opt for surgical intervention. This includes those that cannot tolerate medicines for one reason or another, people that are allergic to iodine, or people that refuse radioiodine.

If people have toxic nodules treatments typically include either removal or injection of the nodule with alcohol.

Risk factors of progressive and severe thyroid-associated orbitopathy are:

- Age greater than 50 years

- Rapid onset of symptoms under 3 months

- Cigarette smoking

- Diabetes

- Severe or uncontrolled hyperthyroidism

- Presence of pretibial myxedema

- High cholesterol levels (hyperlipidemia)

- Peripheral vascular disease

Hypothyroidism caused by Hashimoto's thyroiditis is treated with thyroid hormone replacement agents such as levothyroxine, triiodothyronine or desiccated thyroid extract. A tablet taken once a day generally keeps the thyroid hormone levels normal. In most cases, the treatment needs to be taken for the rest of the person's life. In the event that hypothyroidism is caused by Hashimoto's thyroiditis, it may be recommended that the TSH levels be kept under 3.0 mIU/L.

Treatment for TM is typically done with the collaboration of many medical specialists. Usually a neuromuscular specialist, an endocrinologist, a surgeon, and an ophthalmologist will combine their efforts to successfully treat patients with TM. If a patient develops significant to severe muscle degradation as a result of TM, a physical therapist may be consulted for rehabilitation.

Since excess thyroxine leads to onset of TM, the overall goal of treatment is to reduce to overproduction of thyroxine from the thyroid gland and restore normal thyroid homeostasis. This can be accomplished three ways including using medication, radiation, and surgery.

The first choice involves using medications to alleviate the symptoms and reverse the damage by blocking the production of thyroxine from the thyroid gland. Beta-blockers are used to alleviate the symptoms associated with TM. But beta-blockers do not reduce the damage done by excess thyroxine. Medications such as propylthiouracil and methimazole are administered to block the release of thyroxine from the thyroid and to block the damage thyroxine inflicts on muscle fiber tissue.

One treatment option is the use of radioactive iodine which directly destroys the overactive thyroid gland. The thyroid gland naturally uses iodine to produce thyroxine and other hormones. It cannot distinguish between normal iodine and the radioactive version. Administering the radioactive isotope causes the thyroid to take in the lethal iodine and quickly radiation destroys it. Typically overproduction of thyroxine using radio-iodine is blocked with one dose. The drawback to this treatment is the thyroid gland is completely destroyed and patients often develop hypothyroidism. Some do so only a few months after treatment while others may not be affected for 20–30 years. Hypothyroidism patients must begin a lifelong regimen of thyroid replacement hormones. While the onset of hypothyroidism is most common with radio-iodine treatment, the condition has been observed in patients treated with medication series and surgery.

The last option for TM treatment includes surgical removal of portions of the thyroid which can also be performed to restore thyroid homeostasis. This treatment option usually is done when overproduction of TM is caused by multinodular goiters. Since these goiters enlarge the thyroid and can cause the patient to become physically disfigured surgical treatment can alleviate both the aesthetic and physiological effects simultaneously.

Toxic multinodular goiter can be treated with antithyroid medications such as propylthiouracil or methimazole, radioactive iodine, or with surgery.

Another treatment option is injection of ethanol into the nodules.

Thyroid surgery is performed for a variety of reasons. A nodule or lobe of the thyroid is sometimes removed for biopsy or because of the presence of an autonomously functioning adenoma causing hyperthyroidism. A large majority of the thyroid may be removed ("subtotal thyroidectomy)" to treat the hyperthyroidism of Graves' disease, or to remove a goiter that is unsightly or impinges on vital structures.

A complete thyroidectomy of the entire thyroid, including associated lymph nodes, is the preferred treatment for thyroid cancer. Removal of the bulk of the thyroid gland usually produces hypothyroidism unless the person takes thyroid hormone replacement. Consequently, individuals who have undergone a total thyroidectomy are typically placed on thyroid hormone replacement (e.g. Levothyroxine) for the remainder of their lives. Higher than normal doses are often administered to prevent recurrence.

If the thyroid gland must be removed surgically, care must be taken to avoid damage to adjacent structures, the parathyroid glands and the recurrent laryngeal nerve. Both are susceptible to accidental removal and/or injury during thyroid surgery.

The parathyroid glands produce parathyroid hormone (PTH), a hormone needed to maintain adequate amounts of calcium in the blood. Removal results in hypoparathyroidism and a need for supplemental calcium and vitamin D each day. In the event that the blood supply to any one of the parathyroid glands is endangered through surgery, the parathyroid gland(s) involved may be re-implanted in surrounding muscle tissue.

The recurrent laryngeal nerves provide motor control for all external muscles of the larynx except for the cricothyroid muscle, which also runs along the posterior thyroid. Accidental laceration of either of the two or both recurrent laryngeal nerves may cause paralysis of the vocal cords and their associated muscles, changing the voice quality.

Radioiodine therapy with iodine-131 can be used to shrink the thyroid gland (for instance, in the case of large goiters that cause symptoms but do not harbor cancer—after evaluation and biopsy of suspicious nodules has been done), or to destroy hyperactive thyroid cells (for example, in cases of thyroid cancer). The iodine uptake can be high in countries with iodine deficiency, but low in iodine sufficient countries. To enhance iodine-131 uptake by the thyroid and allow for more successful treatment, TSH is raised prior to therapy in order to stimulate the existing thyroid cells. This is done either by withdrawal of thyroid hormone medication or injections of recombinant human TSH (Thyrogen), released in the United States in 1999. Thyrogen injections can reportedly boost uptake up to 50-60%. Radioiodine treatment can also cause hypothyroidism (which is sometimes the end goal of treatment) and, although rare, a pain syndrome (due to radiation thyroiditis).

Goitre is treated according to the cause. If the thyroid gland is producing too much T3 and T4, radioactive iodine is given to the patient to shrink the gland. If goitre is caused by iodine deficiency, small doses of iodide in the form of Lugol's Iodine or KI solution are given. If the goitre is associated with an underactive thyroid, thyroid supplements are used as treatment. In extreme cases, a partial or complete thyroidectomy is required.

The prognosis tends to be good for patients with MG. It is often best not to treat mild cases of MG. Management necessitates avoidance of medications that can worsen neuromuscular transmission, such as aminoglycoside antibiotics, quinolone antibiotics, beta-blockers, chloroquine, anti-arrhythmics, calcium channel blockers, some anticonvulsants and intravenous iodinated contrast should be avoided.

MG is characteristically variable in course, with the frequency of diplopia and ptosis affected by environmental, emotional and physical factors such as bright sunlight, stress, viral illness, menstruation, pregnancy, etc. Spontaneous remission can occur in any patient and remain for years. In a study of the natural history of generalized MG among 168 patients (with an average follow-up of 12 years), 14% experienced complete remission.

Patients with mild-to-moderate ocular myasthenia are usually treated initially with oral anticholinesterase agents, Mestinon (pyridostigmine) being the most commonly employed. There have not been any randomized clinical trials conducted with these agents, and this treatment is often unsuccessful, particularly in resolving diplopia. Immunosuppressive therapy is then started and the agent of choice is usually prednisone. In a small controlled study this drug demonstrated greater efficacy than pyridostigmine. Steroid therapy is controversial, but in another study the results suggested that prednisone does decrease progression to generalized MG. There is no single recommended dosing regimen in light of the side effects commonly associated with chronic corticosteroid therapy, and the difficulty in weaning patients from steroids without exacerbation of symptoms. Response to prednisone therapy is variable.

Additionally, MG patients should be examined for thymomas, and if found, should undergo surgery to address this condition. A prophylactic thymectomy is controversial, but has been shown to be helpful in young MG patients with acute disease within 3 years of disease onset, in patients with enlarged thymus glands and for whom surgery is low-risk, and patients with generalized MG who are unresponsive to medical treatment.

The symptoms of ocular MG can also be addressed by non-medicinal means. Ptosis can be corrected with placement of crutches on eyeglasses and with ptosis tape to elevate eyelid droop. Diplopia can be addressed by occlusion with eye patching, frosted lens, occluding contact lens, or by simply placing opaque tape over a portion of eyeglasses. Also, plastic prisms (Fresnel prisms) can be attached to eyeglasses of a diplopic patient, allowing for alignment of vision from both eyes in the affected direction, but are often problematic if the degree of muscle weakness, and therefore ocular misalignment, fluctuates frequently.

Treatment is beta blockers, ASA, and NSAIDs (or corticosteroids if NSAIDs are ineffective).

The main strategies for the management of thyroid storm are reducing production and release of thyroid hormone, reducing the effects of thyroid hormone on tissues, replacing fluid losses, and controlling temperature. Thyroid storm requires prompt treatment and hospitalization. Often, admission to the intensive care unit is needed.

Iodine

Guidelines recommend the administration of inorganic iodide (potassium iodide or Lugol's iodine) to reduce the synthesis and release of thyroid hormone. Iodine reduces the synthesis of thyroid hormone via the Wolf-Chaikoff effect. Some guidelines recommend that iodine be administered after antithyroid medications are started, because iodine is also a substrate for the synthesis of thyroid hormone, and may worsen hyperthyroidism if administered without antithyroid medications.

Antithyroid Medications

Antithyroid drugs (propylthiouracil or methimazole) are used to reduce the synthesis and release of thyroid hormone. Propylthiouracil is preferred over methimazole due to its additional effects on reducing peripheral conversion of T4 to T3, however both are commonly used.

Beta Blockers

The administration of beta-1-selective beta blockers (e.g. propranolol) is recommended to reduce the effect of circulating thyroid hormone on end organs. In addition, propanolol at high doses also reduces peripheral conversion of T4 to T3, which is the more active form of thyroid hormone. Although previously unselective beta blockers (e.g., propranolol) have been suggested to be beneficial due to their inhibitory effects on peripheral deiodinases recent research suggests them to be associated with increased mortality. Therefore, cardioselective beta blockers may be favourable.

Corticosteroids

High levels of thyroid hormone result in a hypermetabolic state, which can result in increased breakdown of cortisol, a hormone produced by the adrenal gland. This results in a state of relative adrenal insufficiency, in which the amount of cortisol is not sufficient. Guidelines recommend that corticosteroids (hydrocortisone and dexamethasone are preferred over prednisolone or methylprednisolone) be administered to all patients with thyroid storm. However, doses should be altered for each individual patient to ensure that the relative adrenal insufficiency is adequately treated while minimizing the risk of side effects.

Supportive Measures

In high fever, temperature control is achieved with fever reducers such as paracetamol/acetaminophen and external cooling measures (cool blankets, ice packs). Dehydration, which occurs due to fluid loss from sweating, diarrhea, and vomiting, is treated with frequent fluid replacement. In severe cases, mechanical ventilation may be necessary. Any suspected underlying cause is also addressed.

Ideally a woman who is known to have hyperthyroidism should seek pre-pregnancy advice, although as yet there is no evidence for its benefit. Appropriate education should allay fears that are commonly present in these women. She should be referred for specialist care for frequent checking of her thyroid status, thyroid antibody evaluation and close monitoring of her medication needs. Medical therapy with anti-thyroid medications is the treatment of choice for hyperthyroidism in pregnancy.Methimazole and propylthiouracil (PTU) are effective in preventing pregnancy complications by hyperthyroidism. Surgery is considered for patients who suffer severe adverse reactions to anti-thyroid drugs and this is best performed in the second trimester of pregnancy. Radioactive iodine is absolutely contraindicated in pregnancy and the puerperium. If a woman is already receiving carbimazole, a change to propylthiouracil (PTU) is recommended but this should be changed back to carbimazole after the first trimester. This is because carbimazole can rarely be associated with skin and also mid line defects in the fetus but PTU long term also can cause liver side effects in the adult. Carbimazole and PTU are both secreted in breast milk but evidence suggests that antithyroid drugs are safe during lactation. There are no adverse effects on IQ or psychomotor development in children whose mothers have received antithyroid drugs in pregnancy.

Current guidelines suggest that a pregnant patient should be on PTU during the first trimester of pregnancy due to lower tetragenic effect and then be switched to methimazole during the second and third trimester due to lower liver dysfunction side effects.

Primary treatment is prompted by the administration of adequate doses of either the thyroid hormone l-throxine given intravenously or by giving L-triiodothyronine via a nasogastric tube. It is essential to identify and treat the condition precipitating the coma.

Myxedema coma is rare but often fatal. It occurs most often in elderly women and may be mistaken for one of the chronic debilitating diseases common to this age group.

Though the exact cause of myxedema is still unclear, a wealth of skillful research has demonstrated the importance of iodine. In an important study the researchers showed that in the myxedematous type of cretinism treatment with iodine normalizes thyroid function provided that the treatment is begun early in the postnatal period. If not, the prognosis remains dismal.

Treatment is based on symptoms. Beta-blockers relieve rapid heart rate and excessive sweating during the hyperthyroid phase.

For most women, the hyperthyroid phase presents with very mild symptoms or is asypmtomatic; intervention is usually not required. If symptomatic cases require treatment, a short course of beta-blockers would be effective.

Assessing treatment for the hypothyroid is more complex. Women with symptoms or a very high TSH level, or both, are usually prescribed a course of levothyroxine. Asymptomatic women with slightly elevated TSH levels who are planning subsequent pregnancies, should consider a course of treatment until completion of the family to avoid possible developmental complications in future children. Otherwise, treatment could be discontinued after 1 year postpartum.

Corticosteroids remain the main treatment modality for IOI. There is usually a dramatic response to this treatment and is often viewed as pathognomonic for this disease. Although response is usually quick, many agree that corticosteroids should be continued on a tapering basis to avoid breakthrough inflammation.

Although many respond to corticosteroid treatment alone, there are several cases in which adjuvant therapy is needed. While many alternatives are available, there is no particular well-established protocol to guide adjuvant therapy. Among the available options there is: surgery, alternative corticosteroid delivery, radiation therapy, non-steroidal anti-inflammatory drugs, cytotoxic agents (chlorambucil, cyclophosphamide), corticosteroid sparing immunosuppressants (methotrexate, cyclosporine, azathioprine), IV immune-globin, plasmapheresis, and biologic treatments (such as TNF-α inhibitors).

Levofloxacin does pass through breast milk. It is not likely to cause problems for the baby. In some cases, an underactive thyroid may inhibit the production of breast milk.

During pregnancy, women may want to see both an OB/GYN and an endocrinologist, a doctor who treats people with hormone problems. Levothyroxine is safe to use during pregnancy and necessary for the health of the baby. Women with Hashimoto's disease or an underactive thyroid who are taking levothyroxine before pregnancy may need a higher dose to maintain normal thyroid function. Clinicians may check thyroid function every 6 to 8 weeks during pregnancy. After delivery, hormone levels usually go back to the pre-pregnancy level.

Overt, symptomatic thyroid dysfunction is the most common complication, with about 5% of persons with subclinical hypothyroidism and chronic autoimmune thyroiditis progressing to thyroid failure every year. Transient periods of thyrotoxicosis (over-activity of the thyroid) sometimes occur, and rarely the illness may progress to full hyperthyroid Graves' disease with active orbitopathy (bulging, inflamed eyes). Rare cases of fibrous autoimmune thyroiditis present with severe dyspnea (shortness of breath) and dysphagia (difficulty swallowing), resembling aggressive thyroid tumors – but such symptoms always improve with surgery or corticosteroid therapy. Primary thyroid B cell lymphoma affects fewer than one in a thousand persons, and it is more likely to affect those with long-standing autoimmune thyroiditis.

TM, with proper diagnosis and effective treatment, can be beaten. Patients who are diagnosed have a normal life expectancy and can ultimately lead healthy lives if proper treatment is administered. Typically, once the over-production of thyroxine is corrected and thyroid function adequately reaches a level of homeostasis, patients begin to regain muscle strength in two to four months. Depending on the severity of the TM progression symptoms may take up to a year to completely reverse the damage done by TM. Untreated TM can eventually cause severe respiratory distress or arrest possible leading to death, yet this is very rarely seen.

Infiltrative ophthalmopathy is found in 5-10% of patients with Graves disease and resembles exophthalmos, except that the blurry or double vision is acquired because of weakness in the ocular muscles of the eye. In addition, there is no known correlation with the patient's thyroid levels. Exophthalmos associated with Grave's disease disappears when the thyrotoxicosis is corrected. Infiltrative ophthalmopathy at times may not be cured. Treatments consist of high dose glucocorticoids and low dose radiotherapy. The current hypothesis is that infiltrative ophthalmopathy may be autoimmune in nature targeting retrobulbar tissue. Smoking may also have a causative effect.