Hyperthyroidism

Hyperthyroidism occurs when your thyroid gland produces more hormone than your body needs. It can cause weight loss, heat intolerance, palpitations, tremor, sweating, anxiety, diarrhoea and muscle weakness. Treatment depends on whether the cause is Graves' disease, toxic nodules, thyroiditis, medicine exposure or another process.

What hyperthyroidism is Hyperthyroidism means that the thyroid gland is producing and releasing more thyroid hormone than your body needs. The excess hormones speed up many body processes. Your heart, muscles, digestive system, temperature regulation and nervous system can all be affected. Symptoms can be mild and gradual or severe and rapidly progressive. Some people notice palpitations and weight loss, while others mainly experience anxiety, weakness or heat intolerance. Hyperthyroidism is usually treatable. The best treatment depends on the cause, severity, pregnancy plans, eye disease, other health conditions and your preferences. Hyperthyroidism and thyrotoxicosis are related but different Thyrotoxicosis means that too much thyroid hormone is circulating and acting on body tissues, whatever the source. Hyperthyroidism is a type of thyrotoxicosis in which the thyroid actively makes and releases too much hormone. Graves' disease and toxic thyroid nodules are examples. Thyroiditis can cause thyrotoxicosis without true hyperthyroidism. Stored hormone leaks from damaged thyroid cells, but new hormone production may not be increased. Excess levothyroxine can also cause thyrotoxicosis without an overactive gland. The distinction matters because antithyroid medicines only block new hormone production. The thyroid hormones T4 and T3 The thyroid produces mainly thyroxine, called T4, and a smaller amount of triiodothyronine, called T3. Body tissues convert part of the circulating T4 into T3. T3 binds more strongly to thyroid hormone receptors and produces many of the biological effects. When thyroid hormone is excessive, the body's use of energy and sensitivity to adrenaline like signals increase. This contributes to tremor, sweating, anxiety and a rapid heartbeat. Some people have T3 predominant hyperthyroidism, where free T3 is raised before free T4. Measuring both hormones can therefore be important when TSH is suppressed. The TSH feedback loop The pituitary gland releases thyroid stimulating hormone, usually shortened to TSH. TSH tells the thyroid to make and release T4 and T3. As circulating thyroid hormone rises, the pituitary reduces TSH through a negative feedback loop. In most hyperthyroidism, TSH becomes very low or undetectable while free T4, free T3 or both become raised. A suppressed TSH is a sensitive clue but is not the complete diagnosis. Pregnancy, acute illness, medicines and pituitary disease can alter the result. What Graves' disease is Graves' disease is an autoimmune disorder and the commonest cause of hyperthyroidism in the UK. The immune system produces TSH receptor antibodies, often shortened to TRAb. These antibodies stimulate the thyroid receptor as though they were TSH. The whole gland is usually activated, producing a diffuse goitre and excess thyroid hormone. Graves' disease can also affect tissues around the eyes and, rarely, the skin over the shins. These features arise from the autoimmune process rather than hormone excess alone. Why Graves' disease develops Graves' disease results from a combination of genetic susceptibility and immune system dysregulation. It can run in families and may occur alongside type 1 diabetes, coeliac disease, pernicious anaemia or other autoimmune disorders. Smoking strongly affects the risk and severity of thyroid eye disease. Stress, infection, pregnancy and the postpartum period may influence onset in some people. No one causes Graves' disease through personality, diet or failure to manage stress. Often there is no single identifiable trigger. A diffuse goitre and thyroid bruit A goitre is an enlarged thyroid gland. Graves' disease commonly produces smooth enlargement of both lobes. The gland may feel soft or firm and can sometimes be visible at the lower front of the neck. Increased blood flow through an active Graves' thyroid can produce a sound called a bruit, heard with a stethoscope. A diffuse goitre with a bruit supports Graves' disease but is not present in every case. A hard, irregular or rapidly enlarging lump requires separate assessment. Toxic multinodular goitre A toxic multinodular goitre contains several thyroid nodules that produce hormone without normal TSH control. It is more common with increasing age and often develops within a longstanding nodular thyroid. Symptoms may be less dramatic than in younger people with Graves' disease. Atrial fibrillation, weight loss, breathlessness or weakness may be the main presentation. Toxic nodules do not usually enter lasting remission after a short antithyroid drug course. Radioiodine, surgery or long term medicine may therefore be needed. Toxic adenoma A toxic adenoma is a single autonomously functioning thyroid nodule. The nodule produces thyroid hormone independently, suppressing TSH and reducing activity in the surrounding thyroid tissue. A radionuclide scan may show one area of strong uptake with suppression of the rest of the gland. Definitive treatment commonly involves radioiodine or removal of the affected thyroid lobe. Lifelong antithyroid medicine can be considered when definitive treatment is unsuitable. Thyroiditis and transient thyrotoxicosis Thyroiditis is inflammation or injury of the thyroid. Damaged cells can release hormone that was made and stored before the inflammation began. This can produce a temporary thyrotoxic phase even though the gland is not actively overproducing hormone. The thyrotoxic phase may be followed by temporary hypothyroidism before recovery. Some people develop permanent hypothyroidism. Because new hormone synthesis is not the main problem, carbimazole and propylthiouracil usually do not help uncomplicated destructive thyroiditis. Subacute thyroiditis Subacute thyroiditis often follows a viral type illness and can cause a painful, tender thyroid. Pain may radiate to the jaw or ears. Fever, malaise and raised inflammatory markers can occur. The condition often passes through hyperthyroid, hypothyroid and recovery phases over several months. Treatment usually focuses on pain and inflammation, with beta blockers when thyrotoxic symptoms are troublesome. Severe or persistent pain requires clinical assessment because infection and other neck disorders can resemble it. Painless and postpartum thyroiditis Painless thyroiditis is usually autoimmune and causes temporary hormone leakage without marked neck pain. Postpartum thyroiditis develops within the first year after pregnancy. It can cause a hyperthyroid phase, a hypothyroid phase or either phase alone. The hyperthyroid phase can resemble postpartum anxiety or Graves' disease. TRAb testing and the clinical pattern help distinguish them. Postpartum thyroiditis often improves, but future thyroid dysfunction is more likely. Follow up is needed even when symptoms settle. Excess thyroid hormone medicine Too much levothyroxine or liothyronine can cause thyrotoxicosis. This may result from an excessive prescribed dose, a change in body weight or absorption, accidental duplication or use of thyroid hormone for weight loss. The thyroid gland itself may be appropriately suppressed rather than overactive. Treatment involves a supervised dose review. Abrupt changes can be unsafe in some circumstances, and intentional TSH suppression after thyroid cancer follows a different specialist plan. Amiodarone induced thyrotoxicosis Amiodarone is an anti arrhythmic medicine containing a large iodine load. It can cause hypothyroidism or thyrotoxicosis. Type 1 amiodarone induced thyrotoxicosis involves increased hormone production, often in a thyroid with Graves' disease or nodules. Type 2 involves destructive thyroiditis and release of stored hormone. Mixed patterns also occur. The distinction affects treatment and can be difficult. Amiodarone should not be stopped independently because it may be controlling a dangerous rhythm. Endocrinology and cardiology teams usually coordinate care. Other iodine related causes A large iodine exposure can trigger hyperthyroidism in a susceptible gland with autonomous nodules or Graves' disease. Possible sources include iodinated contrast, iodine containing medicines and high dose supplements. Ordinary dietary iodine does not usually cause hyperthyroidism in a healthy thyroid. Seaweed and kelp supplements can contain unpredictable iodine amounts. They should not be used to treat thyroid symptoms without professional advice. Weight loss and appetite Weight loss is common because excessive thyroid hormone increases energy use. You may lose weight despite a normal or increased appetite. Some people eat substantially more but continue losing weight. Older adults may instead develop poor appetite and muscle loss. Rapid or unexplained weight loss still requires broader assessment. Cancer, diabetes, gastrointestinal disease and other conditions can coexist with thyroid dysfunction. Heat intolerance and sweating Excess thyroid hormone increases heat production and skin blood flow. You may feel hot when other people are comfortable, sweat excessively or prefer cooler rooms and lighter clothing. Warm, moist skin and red palms can be examination clues. Heat intolerance also occurs during menopause, fever, medicines and anxiety. Blood testing distinguishes thyroid excess from symptom overlap. Palpitations and fast heart rate Hyperthyroidism increases heart rate and the heart's sensitivity to adrenaline like stimulation. You may notice pounding, racing, skipped beats or an irregular pulse. A persistently fast resting heart rate can reduce exercise tolerance and contribute to breathlessness. Chest pain, collapse, severe breathlessness or a sustained very rapid or irregular rhythm requires urgent assessment rather than waiting for a routine thyroid appointment. Atrial fibrillation Atrial fibrillation is an irregular heart rhythm associated with hyperthyroidism, particularly in older adults. It may cause palpitations, dizziness, fatigue or breathlessness, but it can also be silent. Atrial fibrillation increases stroke risk. Management includes rhythm or rate assessment and consideration of anticoagulation according to standard cardiovascular guidance. Treating the thyroid disorder helps, but the rhythm and stroke risk still require direct management. Tremor and nervous system symptoms A fine tremor is commonly visible when you hold your hands out. You may feel restless, overactive, unable to relax or unusually sensitive to noise and stimulation. Reflexes can become brisk, and sleep may be disrupted. These features overlap with anxiety, caffeine effects, medicines and neurological disorders. A tremor alone does not diagnose hyperthyroidism. Anxiety, irritability and mood change Hyperthyroidism can cause nervousness, irritability, emotional lability and panic like symptoms. You may feel physically driven, unable to switch off or unlike your usual self. A primary anxiety disorder can produce similar palpitations, sweating and tremor. The conditions can coexist. Severe agitation, psychosis, suicidal thoughts or inability to remain safe requires urgent mental health and medical assessment. Muscle weakness Excess thyroid hormone increases muscle protein breakdown and can cause proximal muscle weakness. You may struggle to rise from a chair, climb stairs or lift objects above shoulder height. Muscle wasting can develop when disease is prolonged, particularly with significant weight loss. Focal weakness, one sided symptoms or loss of sensation is not typical and requires neurological assessment. Bowel and bladder symptoms Hyperthyroidism can speed intestinal movement, causing frequent stools or diarrhoea. Some people develop abdominal discomfort or urgency rather than watery diarrhoea. Increased thirst and urination can occur, particularly when heat and sweating increase fluid needs. Persistent diarrhoea, blood in the stool, severe abdominal pain or dehydration should not be attributed automatically to thyroid disease. Menstrual and fertility changes Periods may become lighter, less frequent or stop temporarily. This is called oligomenorrhoea or amenorrhoea. Ovulation can become irregular, reducing fertility while the thyroid remains uncontrolled. Hyperthyroidism can also affect libido and sexual function in people of any sex. Pregnancy can still occur, so reproductive planning and effective contraception matter during treatments that could harm a fetus. Hair, skin and nail changes Hair may become fine, soft or diffusely thin. Nails can loosen from the nail bed, and the skin may feel warm, moist or itchy. These changes develop gradually and may take months to recover after thyroid control improves. Iron deficiency, skin disease, menopause and many other conditions cause similar changes and may need separate assessment. Older adults may present differently Older adults can have fewer obvious adrenergic symptoms. Instead of marked tremor and agitation, they may develop weight loss, low mood, weakness, atrial fibrillation or heart failure. This quieter presentation is sometimes called apathetic hyperthyroidism. New functional decline in an older adult should not be assumed to be ageing, depression or dementia without considering physical causes. Graves' thyroid eye disease Thyroid eye disease is an autoimmune inflammation of tissues within the eye socket. It is strongly associated with Graves' disease but can occur when thyroid hormone levels are normal or low. Symptoms include gritty or dry eyes, watering, redness, swelling, pressure, eyelid retraction and a staring appearance. Eye disease can follow a different course from thyroid hormone levels. Treating hyperthyroidism is important but does not guarantee that the eye disease will resolve immediately. Bulging eyes and double vision Inflammation can enlarge eye muscles and fatty tissue behind the eye, pushing the eye forwards. This is called proptosis or exophthalmos. Swollen eye muscles can restrict movement and cause double vision. Eyelids may not close completely, exposing the cornea and worsening dryness. New double vision, pain with eye movement or a clear change in eye position requires prompt ophthalmic assessment. Sight threatening eye disease Severe swelling can compress the optic nerve or damage the exposed cornea. Warning features include reduced visual sharpness, altered colour vision, loss of part of the visual field and inability to close the eye. Sight threatening disease is uncommon but needs urgent specialist treatment. Do not wait for the next routine endocrine appointment if vision changes suddenly or progressively. Smoking and thyroid eye disease Smoking increases the risk, severity and progression of thyroid eye disease. It also reduces the likelihood of a good response to treatment and increases the risk that radioiodine will worsen eye disease. Stopping smoking is one of the most effective modifiable actions for eye health. NHS behavioural support and licensed smoking cessation treatment improve the chance of quitting. Advice should be practical rather than judgemental. Pretibial myxoedema Pretibial myxoedema is a rare skin manifestation of Graves' disease. The skin over the shins or tops of the feet becomes thickened, raised or waxy and may have an orange peel texture. Despite the name, this is associated with Graves' disease rather than hypothyroid myxoedema. It usually occurs with high antibody activity and often with thyroid eye disease. Other causes of leg swelling and skin change still require assessment. Thyroid acropachy Thyroid acropachy is an extremely rare Graves' manifestation involving swelling of fingers or toes, clubbing and new bone formation. It almost always occurs with severe eye disease and pretibial myxoedema. Routine finger clubbing should not be assumed to be caused by Graves' disease. Lung, heart, liver, bowel and malignant causes of clubbing need appropriate investigation. The usual blood test pattern Overt primary hyperthyroidism usually produces a TSH below the reference range with raised free T4, free T3 or both. TSH may remain suppressed for some time after hormone levels improve, so early treatment monitoring also uses free hormone measurements. A low TSH with normal FT4 and FT3 is called subclinical hyperthyroidism. Laboratory results must be interpreted with pregnancy, illness, medicines and the clinical picture. T3 thyrotoxicosis Some people have a suppressed TSH and raised FT3 while FT4 remains within the reference range. This pattern is called T3 thyrotoxicosis and can occur early in Graves' disease or toxic nodular disease. Measuring only TSH and FT4 could therefore miss a clinically important pattern. T3 measurement is less useful in hypothyroidism but can be important when TSH is low. Subclinical hyperthyroidism Subclinical hyperthyroidism means that TSH is below the reference range while FT4 and FT3 remain normal. The pattern may be temporary and should often be confirmed before treatment decisions. Persistent marked TSH suppression can increase atrial fibrillation and bone risks, especially in older adults. NICE advises seeking specialist advice when TSH is below 0.1 milliunits per litre on two tests at least three months apart and there are symptoms or evidence of thyroid disease. Testing during acute illness Acute illness can alter TSH and thyroid hormones without a primary thyroid disorder. This non thyroidal illness pattern can complicate interpretation in hospital. NICE advises avoiding thyroid testing during acute illness unless thyroid dysfunction is a possible cause of the illness. Thyroid storm is an exception because urgent diagnosis and treatment cannot wait for recovery. Biotin and assay interference High dose biotin in hair, skin and nail supplements can interfere with some thyroid assays. It may create a falsely low TSH and falsely high thyroid hormone result that resembles hyperthyroidism. Tell your clinician about supplements and specialist vitamin treatments before testing. Unexpected results that do not match symptoms should prompt review for assay interference rather than immediate lifelong treatment. Confirming the cause with TRAb Once thyrotoxicosis is confirmed, NICE recommends measuring TSH receptor antibodies to confirm Graves' disease. A positive TRAb result strongly supports autoimmune stimulation of the thyroid. TRAb can also help assess pregnancy related fetal risk because stimulating antibodies can cross the placenta. A negative result does not end the investigation when the biochemical pattern clearly shows thyrotoxicosis. Radionuclide uptake scanning When TRAb is negative or the cause remains uncertain, a radionuclide scan can show how thyroid tissue is taking up tracer. Graves' disease usually produces diffuse increased uptake across the gland. A toxic adenoma produces one focal hot area, while toxic multinodular goitre produces a patchy pattern. Destructive thyroiditis and excess external thyroid hormone usually produce low uptake because the gland is not actively synthesising new hormone. Why ultrasound is not the main functional test Ultrasound shows thyroid structure, including nodules, cysts and tissue appearance. It does not directly show whether the gland is producing excess hormone. NICE advises considering ultrasound in adults with thyrotoxicosis only when a thyroid nodule is palpable. Unnecessary ultrasound can reveal incidental nodules that create anxiety without explaining the hormone abnormality. Other initial investigations An ECG helps identify atrial fibrillation or another rhythm problem when palpitations or tachycardia are present. Blood tests may assess full blood count, liver function, kidney function, calcium and other abnormalities according to the presentation. A baseline full blood count and liver function tests are recommended before antithyroid medicines begin. Pregnancy testing is essential before radioiodine and may affect antithyroid drug choice. Differential diagnosis from anxiety Anxiety can cause palpitations, sweating, tremor, diarrhoea and weight change. Hyperthyroidism can also trigger anxiety symptoms, so the two conditions cannot be distinguished reliably from feelings alone. A thyroid examination and blood tests clarify whether hormone excess is present. Normal thyroid tests should redirect care towards anxiety, cardiac, medicine related or other causes rather than repeated antithyroid treatment. Differential diagnosis from menopause Menopause and hyperthyroidism can both cause sweating, sleep disturbance, palpitations, anxiety and menstrual change. Hot flushes often occur in episodes, while thyroid heat intolerance may be more persistent, but this distinction is not absolute. Weight loss despite increased appetite, tremor and a persistent fast pulse strengthen thyroid suspicion. NICE warns that thyroid dysfunction can be mistaken for menopause, so appropriate blood testing is important. Other conditions that can mimic thyrotoxicosis Anaemia, infection, stimulant use, phaeochromocytoma, arrhythmia and uncontrolled diabetes can cause overlapping symptoms. Cancer and gastrointestinal disease can cause weight loss, weakness and altered bowel habits. Medicine effects from salbutamol, decongestants, caffeine, prescribed stimulants or recreational drugs may produce tremor and tachycardia. A suppressed TSH with raised free hormones confirms thyrotoxicosis, but another condition can still coexist and contribute to severity. Beta blockers for symptom control Beta blockers such as propranolol can reduce tremor, palpitations and adrenergic symptoms while the cause is treated. They do not stop the thyroid from producing hormone and do not cure Graves' disease or toxic nodules. They can act quickly, making them useful while antithyroid drugs take effect. Asthma, slow heart rate, low blood pressure and some heart conditions can make a beta blocker unsuitable. Another rate control option may be chosen. Antithyroid medicines Carbimazole and propylthiouracil reduce new thyroid hormone synthesis. They help in Graves' disease and toxic nodular hyperthyroidism because these conditions involve active hormone production. They do not remove stored hormone immediately, so symptom improvement takes time. They usually do not help transient destructive thyroiditis, where supportive treatment is more appropriate. Carbimazole Carbimazole is the antithyroid medicine used most commonly in the UK. The body converts it into the active drug thiamazole, also known internationally as methimazole. Carbimazole blocks steps in thyroid hormone production. It does not directly remove hormone already circulating. For adults with Graves' disease receiving drug treatment as a definitive approach, NICE recommends a 12 to 18 month course before the need for further treatment is reviewed. Titration treatment In a titration regimen, the carbimazole dose is adjusted according to FT4, FT3 and later TSH results. A higher initial dose controls hormone production, then the dose reduces as levels normalise. This approach aims to use the lowest dose that maintains control. It avoids routine levothyroxine addition but requires regular blood tests and careful dose changes. Block and replace treatment In block and replace treatment, a higher carbimazole dose suppresses thyroid production and levothyroxine is added to replace a controlled amount of hormone. NICE permits either titration or block and replace for adults receiving first line antithyroid treatment for Graves' disease. Block and replace can simplify some fluctuations but exposes the person to a higher antithyroid drug dose. It is not used routinely in pregnancy because excessive antithyroid exposure can suppress the fetal thyroid. Monitoring antithyroid treatment NICE advises measuring TSH, FT4 and FT3 about every six weeks until TSH returns to the reference range. After that, TSH with additional hormones when indicated is measured about every three months until treatment stops. TSH can remain suppressed after FT4 and FT3 normalise, so dose changes should not rely on TSH alone early in treatment. After antithyroid drugs stop, thyroid function is checked within eight weeks, every three months for a year and then annually. Baseline blood count and liver tests A full blood count and liver function tests should be checked before carbimazole or propylthiouracil begins. Mild abnormalities can result from untreated thyrotoxicosis itself and require clinical interpretation. Routine repeated blood counts and liver tests are not recommended without symptoms suggesting toxicity. A normal previous blood count cannot predict or exclude later agranulocytosis, which can develop suddenly. Agranulocytosis Agranulocytosis is a rare, severe reduction in neutrophils, the white blood cells that fight bacterial and fungal infection. It can occur with carbimazole or propylthiouracil, often early in treatment but potentially at any time. Fever, a sore throat, mouth ulcers, severe flu like illness or an unexplained infection can be the first warning. The antithyroid medicine must be stopped immediately and an urgent same day full blood count with neutrophil count arranged. What happens if agranulocytosis is confirmed Confirmed agranulocytosis requires urgent specialist management and protection from severe infection. NICE advises stopping and never restarting any antithyroid drug after agranulocytosis. The person may need hospital treatment, antibiotics and supportive haematology care according to severity. Future hyperthyroidism treatment usually requires radioiodine or surgery because switching casually to another antithyroid drug is unsafe. Liver injury and carbimazole Carbimazole can rarely cause liver injury, often with a cholestatic pattern. Warning symptoms include jaundice, dark urine, pale stools, itching, abdominal pain and marked unexplained fatigue. These symptoms require prompt medical review and liver testing. A mild change in liver results during untreated hyperthyroidism is not automatically a medicine reaction, but it must be interpreted carefully. Propylthiouracil and hepatotoxicity Propylthiouracil, usually shortened to PTU, can cause severe liver injury. Rare cases have led to liver failure, transplantation or death. Seek urgent medical advice for jaundice, dark urine, severe nausea, loss of appetite, abdominal pain, itching or unusual fatigue. PTU is therefore reserved for situations where its benefits outweigh this risk, including selected pregnancy circumstances and intolerance of carbimazole. Other important carbimazole adverse effects Mild rash, itching, nausea, headache and joint discomfort can occur. Sudden severe abdominal pain can indicate acute pancreatitis and needs urgent assessment. Carbimazole should not be restarted after confirmed carbimazole related pancreatitis. Easy bruising, bleeding or severe malaise can indicate blood cell toxicity. A severe allergic reaction with facial swelling or breathing difficulty requires emergency treatment. Pregnancy prevention with carbimazole Carbimazole can cause congenital malformations, particularly when used in the first trimester and at higher doses. People who could become pregnant should receive contraceptive and preconception advice while taking it. An unexpected pregnancy requires immediate contact with the endocrine and maternity team. Do not simply stop treatment because uncontrolled hyperthyroidism also harms pregnancy. The safest plan balances maternal control against fetal medicine exposure using the lowest effective dose. Why PTU is often used early in pregnancy PTU is often preferred during the first trimester because the characteristic birth defect risk associated with carbimazole is lower. After the first trimester, clinicians commonly consider switching from PTU to carbimazole because of PTU's rare severe liver risk. The exact plan is individual and should be made by clinicians experienced in thyroid disease during pregnancy. Both medicines cross the placenta and can suppress the fetal thyroid if the dose is too high. Antithyroid remission and relapse A 12 to 18 month drug course can lead to remission in some people with Graves' disease. Remission means that thyroid function remains normal after the medicine stops. It does not mean the autoimmune tendency has been erased permanently. Relapse is more likely with a large goitre, high TRAb, severe disease or previous relapse, although prediction is imperfect. Persistent or relapsed hyperthyroidism can be treated with another medicine course in selected cases, radioiodine or surgery. Radioiodine treatment Radioiodine uses iodine 131, which is taken up by thyroid cells and emits radiation that gradually reduces their function. It is given by mouth as a capsule or liquid and usually avoids an operation. The full effect takes weeks or months, so antithyroid drugs and beta blockers may be needed around treatment according to specialist instructions. NICE recommends radioiodine as first line definitive treatment for many adults with Graves' disease and toxic nodular hyperthyroidism when it is suitable. Benefits and limitations of radioiodine Radioiodine is effective, non invasive and often requires one treatment. It does not provide immediate control and some people need a second treatment. Hypothyroidism is a common and often expected long term outcome. Lifelong levothyroxine is straightforward for most people but still requires monitoring. Radiation safety precautions temporarily limit close contact with other people, particularly pregnant people and young children. When radioiodine is unsuitable Radioiodine must not be used during pregnancy or breastfeeding. It is unsuitable when someone plans conception within the specified post treatment interval given by the nuclear medicine service. NICE also lists active thyroid eye disease, suspected malignancy and significant compression as reasons it may be unsuitable. Severe uncontrolled thyrotoxicosis usually needs stabilisation before definitive treatment. Radioiodine and eye disease Radioiodine can worsen thyroid eye disease in susceptible people, particularly smokers and those with active disease. Active eye disease is therefore an important reason to select another treatment. In selected mild cases, steroid protection may be considered by specialists when radioiodine remains appropriate. Smoking cessation and stable thyroid control reduce, but do not eliminate, eye risk. Monitoring after radioiodine NICE advises checking TSH, FT4 and FT3 every six weeks for the first six months after radioiodine until TSH is within range. Thyroid function is then checked at nine and twelve months when it remains normal, followed by regular long term monitoring. Hypothyroidism may develop early or years later. Persistent hyperthyroidism at six months prompts consideration of further treatment. Thyroid surgery Surgery provides rapid definitive treatment once thyroid hormone levels have been controlled adequately. Total thyroidectomy removes the whole gland and is commonly used for Graves' disease when surgery is selected. Hemithyroidectomy removes one lobe and can treat a single toxic adenoma. An experienced high volume thyroid surgeon reduces, but cannot remove, surgical risk. When surgery is favoured Surgery is considered with a large goitre causing pressure, suspected cancer, active eye disease or when radioiodine and medicines are unsuitable. It may suit someone who wants rapid definitive treatment or is planning pregnancy after recovery. It is also used after relapse or poor control with antithyroid drugs. The decision considers anaesthetic risk, neck anatomy, access to expert surgery and willingness to take lifelong replacement after total thyroidectomy. Risks of thyroidectomy Bleeding into the neck can compress the airway and requires emergency treatment. The recurrent laryngeal nerves control the vocal cords. Injury can cause hoarseness or, rarely, breathing difficulty. The parathyroid glands regulate calcium and can be temporarily or permanently impaired, causing tingling, cramps or low calcium. Total thyroidectomy causes permanent hypothyroidism and requires lifelong levothyroxine. Preparing for surgery Hyperthyroidism is usually controlled before surgery to reduce cardiac and thyroid storm risk. Antithyroid medicine, beta blockade and sometimes iodine preparations are used according to the surgical plan. The surgeon and anaesthetist assess airway, heart rhythm, calcium risk and other health conditions. Stopping antithyroid treatment without instructions before surgery can be dangerous. Managing mild thyroid eye disease Stable thyroid function and smoking cessation are fundamental. Lubricating eye drops or ointment can reduce dryness and exposure symptoms. Sunglasses, elevating the head during sleep and prisms for double vision may help selected people. Selenium is used in some specialist pathways for mild active disease, but it should not be taken at high doses without advice because excess can be harmful. Managing moderate or severe eye disease Active moderate or severe disease may require intravenous corticosteroids or other immune modifying treatment. Specialist eye and endocrine teams assess activity, severity, optic nerve function and corneal exposure. Orbital radiotherapy or newer targeted treatments may be considered in selected pathways. Decompression, eye muscle and eyelid surgery are generally timed according to whether disease is active or stable, except when vision is threatened. Thyroid storm Thyroid storm is a rare, life threatening escalation of thyrotoxicosis with failure of several body systems. Features can include high fever, severe tachycardia, atrial fibrillation, heart failure, vomiting, diarrhoea, jaundice, agitation, delirium or reduced consciousness. The diagnosis is clinical. Hormone results may not be dramatically higher than in uncomplicated hyperthyroidism. Call 999 immediately when the pattern is suspected. Triggers for thyroid storm Infection is a common trigger. Surgery, trauma, childbirth, acute heart disease, diabetic emergencies and abrupt interruption of antithyroid treatment can also precipitate storm. Radioiodine or thyroid surgery performed without adequate preparation can increase risk. A trigger may be the main reason a previously compensated person becomes critically unwell. Hospital treatment of thyroid storm Treatment occurs in hospital, often in a high dependency or intensive care setting. Care includes rapid control of adrenergic symptoms, antithyroid medicine, appropriately timed iodine, corticosteroids and treatment of the precipitating illness. Cooling, fluids, oxygen, cardiac monitoring and organ support may be required. This combination should never be attempted at home or delayed while waiting for routine test confirmation. Long term complications of uncontrolled hyperthyroidism Persistent thyroid excess can cause atrial fibrillation, heart failure, muscle wasting and reduced quality of life. Accelerated bone turnover can reduce bone mineral density and increase fragility fracture risk. Menstrual disruption, reduced fertility and pregnancy complications can occur. Early diagnosis and sustained biochemical control reduce these risks. Hyperthyroidism in pregnancy Pregnancy changes thyroid physiology and requires pregnancy specific interpretation of blood tests. Poorly controlled hyperthyroidism increases maternal and fetal risks, including pre eclampsia, preterm birth, low birthweight and stillbirth. Well controlled disease has a much lower risk of complications. Care should be planned with clinicians experienced in obstetric and endocrine medicine. How Graves' disease changes during and after pregnancy Graves' activity often improves during later pregnancy as immune activity changes, so antithyroid doses may fall. Disease can worsen or relapse after birth when immune activity rebounds. Postpartum thyroiditis is a separate autoimmune condition and can be mistaken for Graves' recurrence. TRAb testing, examination and the pattern of hormone change help distinguish them. Fetal and neonatal thyrotoxicosis TRAb can cross the placenta and stimulate the fetal thyroid. High maternal antibody levels can cause fetal or neonatal hyperthyroidism even when the mother previously had radioiodine or thyroidectomy and now takes levothyroxine. Possible clues include fetal tachycardia, poor growth, fetal goitre and advanced bone maturation. High risk pregnancies require maternal antibody testing, fetal surveillance and neonatal thyroid testing. Avoiding fetal hypothyroidism Antithyroid medicines also cross the placenta and can suppress fetal hormone production. The lowest dose that adequately controls maternal disease is therefore used. Block and replace treatment is generally avoided because the fetus receives the antithyroid drug but little protective levothyroxine from the mother. Frequent maternal testing guides careful balance between under treatment and over treatment. Radioiodine and surgery in pregnancy Radioiodine is absolutely contraindicated during pregnancy because fetal thyroid tissue can absorb it and be damaged. It is also unsuitable during breastfeeding. When medicine cannot control severe disease or causes serious toxicity, surgery may be considered, usually during the second trimester. The decision requires specialist maternal, fetal, endocrine, surgical and anaesthetic planning. Breastfeeding Antithyroid treatment can be compatible with breastfeeding at appropriately selected doses. The maternity and endocrine team chooses the lowest effective dose and advises timing and infant monitoring where needed. Radioiodine is not compatible with breastfeeding for the treated pregnancy and requires specialist advice about stopping breastfeeding. Do not stop necessary antithyroid treatment solely because you wish to breastfeed. Monitoring after antithyroid drugs stop Relapse is most likely during the first year but can occur later. NICE advises thyroid testing within eight weeks of stopping, then every three months for a year and annually thereafter. Return of palpitations, weight loss, tremor or heat intolerance should prompt earlier testing. Long term follow up also detects later hypothyroidism, particularly after autoimmune thyroid disease. Monitoring after surgery After total thyroidectomy, levothyroxine begins and is monitored according to hypothyroidism guidance. Calcium is checked because temporary parathyroid dysfunction is common after total thyroid removal. After hemithyroidectomy, NICE advises TSH and FT4 at two and six months, followed by annual TSH. Voice change, neck swelling, breathing difficulty or tingling after surgery requires prompt clinical assessment. Living with treatment uncertainty Each treatment has trade offs. Antithyroid drugs avoid permanent gland destruction but require monitoring and can relapse or cause rare serious toxicity. Radioiodine avoids surgery but acts slowly, often causes hypothyroidism and can worsen eye disease. Surgery provides rapid definitive control but carries operative risks and usually creates lifelong replacement needs after total thyroidectomy. The aim of care Good hyperthyroidism care confirms that hormone excess is present and identifies whether the gland is overproducing hormone. It controls immediate cardiovascular and neurological symptoms while choosing a cause specific treatment. It protects you from antithyroid drug toxicity, eye complications, pregnancy risks and thyroid storm. It also provides long term monitoring because relapse, hypothyroidism and treatment complications can appear after symptoms improve.

Thyrotoxicosis must first be confirmed and then separated into active thyroid overproduction or release from another source. Treatment is cause specific, and urgent recognition of antithyroid drug toxicity, sight threatening eye disease and thyroid storm prevents avoidable harm.