Hyperthyroidism — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Hyperthyroidism is the clinical state resulting from excess thyroid hormone (thyroxine/T4 and triiodothyronine/T3) production, causing acceleration of virtually all body metabolic processes. It affects approximately 1-2% of women and 0.1-0.2% of men in iodine-sufficient countries. The most common cause is Graves' disease (70-80% of cases) — an autoimmune condition in which thyroid-stimulating immunoglobulins (TSI/TRAb — stimulatory antibodies to the TSH receptor) continuously drive thyroid hormone overproduction. Other causes include toxic multinodular goitre (elderly patients), toxic adenoma (autonomously functioning single nodule), subacute (de Quervain's) thyroiditis (viral inflammation — transient, self-limiting), and iodine excess (amiodarone, iodine contrast agents). Subclinical hyperthyroidism (suppressed TSH, normal free T4) is more common and particularly risks atrial fibrillation and osteoporosis in older patients. Thyroid storm — extreme hyperthyroidism precipitated by illness or surgery — carries up to 20% mortality without immediate treatment with thionamides, beta-blockers, iodine, and corticosteroids in an intensive care setting.

Graves' disease: TSH receptor antibodies (TRAb) act as TSH agonists, continuously stimulating thyroid hormone synthesis and thyroid growth (goitre). Triggers include postpartum immune rebound, stress, smoking (strongly associated with Graves' ophthalmopathy), and recent viral illness. Genetic predisposition (HLA-DR3, PTPN22 variants). Toxic multinodular goitre (Plummer's disease): autonomously functioning thyroid nodules develop TSH-independent hormone production; most common cause of hyperthyroidism in elderly patients and iodine-deficient regions. Toxic adenoma: a single autonomous hot nodule (follicular adenoma) with TSH receptor activating mutation produces excess hormone. Thyroiditis: subacute thyroiditis (de Quervain's — painful, viral, self-limiting); painless (silent) thyroiditis (lymphocytic — postpartum thyroiditis); drug-induced (amiodarone, interferon, checkpoint inhibitors). Factitious hyperthyroidism: excess exogenous thyroxine intake (accidental or intentional). Rare: TSH-secreting pituitary adenoma, struma ovarii.

Weight loss despite increased appetite (hypermetabolism), heat intolerance and excessive sweating, palpitations and tachycardia (persistent resting heart rate above 100 bpm), atrial fibrillation (new-onset AF in an older patient — always check TFTs), tremor (fine resting hand tremor), anxiety, irritability, emotional lability, difficulty concentrating, fatigue despite hyperactivity, muscle weakness (proximal myopathy — difficulty climbing stairs), diarrhoea and increased stool frequency, menstrual irregularity or amenorrhoea in women, and oligospermia in men. Diffuse goitre with thyroid bruit (Graves' disease); nodular goitre (toxic multinodular goitre or toxic adenoma); painful thyroid (subacute thyroiditis). Graves'-specific features: exophthalmos (bulging eyes — proptosis), periorbital oedema, lid lag, restricted eye movements (diplopia), pretibial myxoedema (skin infiltration on shins — orange-peel texture). Thyroid storm (crisis): extreme hyperthyroidism — fever above 40°C, extreme tachycardia/AF, agitation, confusion, vomiting, and cardiovascular collapse — life-threatening.

Thyroid function tests (TFTs): suppressed TSH (below 0.1 mIU/L — the most sensitive test) with elevated free T4 and/or elevated free T3 confirms overt hyperthyroidism. Subclinical hyperthyroidism: suppressed TSH with normal free T4 and T3. TSH receptor antibodies (TRAb): positive in 95% of Graves' disease — the most specific diagnostic test, particularly useful in pregnancy and when radioiodine uptake scan is not available. Thyroid peroxidase antibodies (TPO-Ab): positive in 70% of Graves' but non-specific. Thyroid ultrasound: Graves' — diffusely enlarged heterogeneous gland with markedly increased Doppler vascularity ('thyroid inferno'); toxic multinodular goitre — multiple nodules; toxic adenoma — single hypervascular nodule. Radioiodine uptake scan (RAIU/thyroid scintigraphy): Graves' — diffuse increased uptake; toxic multinodular goitre — patchy increased uptake; toxic adenoma — single hot nodule with suppressed background; thyroiditis — near-zero uptake (distinguishes from Graves'). ECG: assess for atrial fibrillation and rate. Bone density (DXA) for subclinical/overt hyperthyroidism — osteoporosis risk. Ophthalmology review for Graves' eye disease.

Beta-blockers (propranolol 40 mg three times daily, or atenolol): rapid symptom control — reduces tachycardia, tremor, anxiety, and palpitations while awaiting thyroid-specific treatment; does not treat the underlying disease. Antithyroid drugs (ATDs): Carbimazole (UK) or Methimazole (USA) — inhibit thyroid hormone synthesis; 80-90% symptom response within 4-8 weeks; given for 12-18 months (40-50% remission in Graves' after completing ATD course). Propylthiouracil (PTU): alternative, used in first trimester pregnancy (carbimazole is teratogenic in first trimester — PTU is preferred). Block-and-replace regimen: carbimazole at high dose plus T4 — reduces fluctuations and monitoring requirements. Weekly FBC for the first month (rare but life-threatening agranulocytosis in 0.1-0.5% — sore throat/fever must be evaluated immediately). Definitive treatments for Graves' and toxic goitre: Radioiodine (I-131): oral single dose; causes progressive thyroid ablation over 3-6 months; most patients become hypothyroid (requiring lifelong levothyroxine); avoid if pregnant, breastfeeding, or significant Graves' ophthalmopathy (may worsen eye disease). Total thyroidectomy: definitive immediate cure; risks include post-operative hypoparathyroidism (hypocalcaemia) and recurrent laryngeal nerve injury (hoarseness); preferred for large goitre, active eye disease, or coexisting thyroid nodule requiring histology. Toxic adenoma: radioiodine or hemithyroidectomy. Subacute thyroiditis: NSAIDs or corticosteroids for pain; beta-blockers for transient hyperthyroid phase (no ATDs needed — hormone release not synthesis).

Thyroid storm (thyrotoxic crisis) is the most life-threatening complication — extreme thyroid hormone excess precipitated by acute stress (infection, surgery, acute MI, trauma, radioiodine in poorly prepared patients) causes fever above 41°C, tachycardia above 140 bpm, agitation, confusion, cardiovascular collapse, and multi-organ failure; mortality is 10–20% even with optimal intensive care treatment. The Burch-Wartofsky scoring system aids diagnosis. Treatment requires propylthiouracil (PTU) to block both synthesis and peripheral T4-to-T3 conversion (preferred over carbimazole in thyroid storm), Lugol's iodine (given 1 hour after PTU to block hormone release), IV beta-blocker (propranolol), IV hydrocortisone (to prevent relative adrenal insufficiency and reduce T4-to-T3 conversion), and ICU supportive care. Atrial fibrillation complicates hyperthyroidism in 10–15% of cases — thyroid hormone directly increases atrial ectopy and reduces the atrial fibrillation threshold; AF in hyperthyroidism is associated with elevated thromboembolic stroke risk and requires anticoagulation. Osteoporosis: chronic hyperthyroidism accelerates bone resorption, reducing bone mineral density by up to 10% within 1 year — particularly problematic in postmenopausal women. Graves' ophthalmopathy (thyroid eye disease — TED) develops in 25–50% of Graves' patients — exophthalmos (proptosis), diplopia, periorbital oedema, and in severe cases compressive optic neuropathy requiring urgent high-dose methylprednisolone, orbital radiotherapy, or orbital decompression surgery. Thyrotoxic periodic paralysis — sudden muscle paralysis from hypokalaemia — occurs predominantly in East Asian males. Heart failure from tachycardia-induced cardiomyopathy in sustained untreated hyperthyroidism.

Graves' disease cannot be prevented, but several lifestyle modifications reduce recurrence risk and severity. Smoking cessation is critical — smoking increases Graves' disease risk, worsens eye disease, and reduces response to radioiodine. Stress management: significant life stressors are known triggers for Graves' relapse. Avoid iodine excess during active hyperthyroidism — iodinated contrast agents, amiodarone, and high-dose iodine supplements can worsen hyperthyroidism and should be used cautiously. Selenium supplementation (200 mcg/day) in mild-moderate Graves' ophthalmopathy reduces eye disease progression. Adequate calcium and vitamin D intake is important as hyperthyroidism causes bone density loss — particularly relevant for older women with longstanding disease. Bone density monitoring (DXA scan) is recommended after treatment of overt hyperthyroidism. Regular TFT monitoring after radioiodine or thyroidectomy ensures timely identification of hypothyroidism requiring levothyroxine.

See a GP if you have unexplained weight loss, persistent palpitations or rapid heartbeat, excessive sweating, anxiety, or a visible neck swelling — particularly if you have a family history of thyroid disease. Seek urgent care for: new-onset atrial fibrillation (palpitations, irregular heartbeat — may be precipitated by undiagnosed hyperthyroidism); symptoms of thyroid storm — extremely rapid heart rate, fever above 39°C, confusion, vomiting, and agitation in a known hyperthyroid patient — this is a life-threatening emergency requiring immediate hospital admission. If taking carbimazole or methimazole, seek same-day blood count testing (FBC) if you develop sore throat, fever, or mouth ulcers — these may indicate agranulocytosis (life-threatening low white cell count). Women planning pregnancy who have Graves' disease must see an endocrinologist before conception to optimise thyroid control.