Hyperthyroidism — Symptoms, Causes & Treatment | MyMedicPlus

Hyperthyroidism is the overproduction of thyroid hormones (thyroxine T4 and triiodothyronine T3), causing a hypermetabolic state characterized by accelerated body functions. It affects approximately 1.2% of the population and is significantly more common in women. The most common cause is Graves' disease (an autoimmune thyroid disorder) accounting for 70–80% of cases. Elevated free T4 and free T3 with suppressed TSH (thyroid-stimulating hormone) — the key diagnostic hallmark — confirm thyrotoxicosis, with TSH the most sensitive marker of thyroid function. Thyrotoxicosis refers to the clinical syndrome of excess thyroid hormone action from any cause, while hyperthyroidism specifically describes overproduction by the thyroid gland. Sub-clinical hyperthyroidism (suppressed TSH below 0.1 mIU/L with normal free T4 and T3) affects 0.7% of adults and, in older patients, carries increased risks of atrial fibrillation, osteoporosis, and dementia even without overt symptoms — treatment decisions are individualized based on cardiovascular and fracture risk.

Graves' disease — an autoimmune disorder where TSH receptor-stimulating antibodies (TRAb) continuously activate thyroid hormone production — is the most common cause, strongly associated with female sex, family history, and smoking. Toxic multinodular goitre (Plummer's disease) and toxic adenoma are autonomously functioning thyroid nodules causing hormone overproduction independent of TSH. Transient thyrotoxicosis occurs with viral thyroiditis (de Quervain's), postpartum thyroiditis, and silent thyroiditis. Drug-induced causes include amiodarone (contains 37% iodine) and interferon. Excess iodine intake can precipitate the Jod-Basedow phenomenon in susceptible individuals. TSH receptor antibodies (TRAb) — stimulating antibodies characteristic of Graves' disease — can cross the placenta and cause transient neonatal hyperthyroidism, which resolves as maternal antibodies are cleared over 6–12 weeks. Struma ovarii — ectopic thyroid tissue in an ovarian dermoid tumour — is an extremely rare cause of thyrotoxicosis from an extracervical source. Factitious thyrotoxicosis from surreptitious thyroid hormone ingestion shows low thyroglobulin alongside elevated T4/T3 — useful diagnostic clue.

Classic symptoms reflect the hypermetabolic state: heat intolerance, excessive sweating, palpitations and fast heart rate (tachycardia), fine tremor of hands, weight loss despite increased appetite, anxiety, nervousness, irritability, diarrhoea, oligomenorrhoea, muscle weakness (proximal myopathy — difficulty climbing stairs), and fatigue. Graves' disease specifically causes ophthalmopathy (proptosis, periorbital oedema, diplopia, visual loss in 25–50%), pretibial myxedema, and thyroid acropachy. Thyroid storm (thyrotoxic crisis) is a rare life-threatening emergency with extreme tachycardia, fever, altered consciousness, and multiorgan failure. Gynaecomastia occurs in hyperthyroid men from increased conversion of androgens to oestrogens in peripheral adipose tissue. Pretibial myxoedema (thyroid dermopathy) — raised, indurated, orange-peel-textured skin on the anterior tibiae — affects 1–5% of Graves' disease patients and may persist or worsen after treatment of hyperthyroidism. Thyroid acropachy — clubbing of the fingers and periosteal new bone formation — is a rare manifestation specific to Graves' disease.

TSH is the single most sensitive test — a suppressed TSH (below 0.1 mIU/L) prompts further testing. Free T4 and free T3 levels confirm the diagnosis and severity: both are elevated in overt hyperthyroidism; elevated T3 alone with normal T4 indicates T3 toxicosis. TSH receptor antibodies (TRAb) confirm Graves' disease with high specificity. Thyroid scintigraphy distinguishes Graves' disease (diffusely increased uptake) from destructive thyroiditis (absent uptake) and toxic nodules (focal uptake) — critical for treatment planning. Thyroid ultrasound assesses gland size and blood flow. ECG may show atrial fibrillation, a common complication. The Thyroid Imaging Reporting and Data System (TI-RADS) grades ultrasound nodules by malignancy risk — important in Graves' disease with coexisting nodules. Scintigraphy with technetium-99m (Tc-99m) pertechnetate or iodine-123 (I-123) is preferred over iodine-131 for diagnostic scanning due to lower radiation dose. Radioiodine uptake (RAIU) at 4 and 24 hours quantifies iodine uptake — high uptake in Graves' and toxic nodular goitre, low uptake in thyroiditis and factitious thyrotoxicosis.

Three definitive treatment options exist. Antithyroid drugs (ATDs) — carbimazole or methimazole (preferred); propylthiouracil (PTU) in first trimester pregnancy — block thyroid hormone synthesis. An 18-month course achieves remission in approximately 50% of Graves' disease patients. Beta-blockers (propranolol) provide rapid symptomatic relief of tachycardia, tremor, and anxiety while awaiting ATD effect. Radioactive iodine (RAI, I-131) ablation is the most widely used definitive treatment in adults (not in pregnancy or severe ophthalmopathy) — destroys thyroid tissue; most patients develop hypothyroidism requiring lifelong levothyroxine. Total thyroidectomy offers immediate cure and is preferred in large goiters or significant ophthalmopathy. Carbimazole must never be given in the first trimester — embryopathy (choanal atresia, aplasia cutis, carbimazole embryopathy syndrome) has been documented at doses above 20 mg/day. Thyroid storm management requires a multi-drug approach: high-dose propylthiouracil (PTU — also blocks peripheral T4 to T3 conversion), Lugol's iodine (given 1 hour after PTU to block thyroid hormone release), dexamethasone (reduces T4-T3 conversion and addresses potential adrenal insufficiency), and propranolol (high-dose IV — rate control and symptom relief).

Atrial fibrillation develops in 10–15% of patients with hyperthyroidism, increasing stroke risk and requiring anticoagulation. Osteoporosis from accelerated bone resorption increases fracture risk, particularly in postmenopausal women. Thyroid storm (thyrotoxic crisis) — a life-threatening emergency precipitated by infection, surgery, or iodine load — carries 10–30% mortality and requires emergency ICU treatment. Graves' ophthalmopathy can cause corneal exposure, optic nerve compression, and permanent visual loss — requires specialist ophthalmology management independent of thyroid disease treatment. Graves' ophthalmopathy treatment: mild-moderate — selenium supplementation (200 mcg daily for 6 months, EUGOGO-recommended) and smoking cessation; moderate-severe — IV methylprednisolone pulse therapy (EUGOGO protocol: 4.5–16.6 g total dose over 12 weeks); sight-threatening — emergency orbital decompression surgery or high-dose IV methylprednisolone. Teprotumumab (an IGF-1 receptor inhibitor) has shown dramatic efficacy in reducing proptosis in Graves' ophthalmopathy in clinical trials and received FDA approval in 2020.

Graves' disease cannot currently be prevented. Avoid smoking — smoking worsens Graves' ophthalmopathy severity and outcomes significantly. Monitor TRAb levels during pregnancy — elevated levels can cross the placenta and cause neonatal hyperthyroidism. After RAI treatment, monitor thyroid function tests every 4–6 weeks until stable, then every 6 months long-term. Ensure adequate calcium and vitamin D intake to mitigate osteoporosis risk from thyrotoxicosis. Selenium supplementation (200 mcg daily for 6 months) has modest evidence for reducing mild-moderate Graves' ophthalmopathy in early disease.

Seek emergency care immediately for suspected thyroid storm (thyrotoxic crisis): extreme rapid heart rate (above 150 bpm), high fever, confusion or agitation, vomiting, diarrhoea, and severe tremor — especially if triggered by infection, surgery, or iodine load in a known hyperthyroid patient. Thyroid storm is a life-threatening emergency with 10–30% mortality; call emergency services (999/112) immediately. Seek same-day medical assessment for: new atrial fibrillation in a hyperthyroid patient (5-fold increased stroke risk — requires urgent anticoagulation review); sudden severe eye pain, double vision, or visual loss in Graves' disease (optic neuropathy from orbital compression — sight-threatening, requires emergency ophthalmology); and signs of severe cardiac compromise (severe breathlessness, chest pain, palpitations causing near-fainting). See your endocrinologist urgently if: thyroid function has been difficult to control on current medication; you develop a rash or significant low white cell count on antithyroid drugs (agranulocytosis — a rare but serious side effect of carbimazole — stop the drug immediately and seek urgent medical review); or pregnancy is planned or confirmed while receiving RAI treatment.