Hyperthyroidism in the elderly — presentation, investigation and treatment

Definition and causes. Overt hyperthyroidism is characterised by high levels of thyroid hormones with a low TSH. The most common causes in old age are Graves' disease in iodine-sufficient areas and nodular goitre (Plummer's disease or multinodular toxic goitre) and functioning follicular adenoma in iodine-deficient areas. Toxic multinodular goitre is more frequent in older persons than in the young. Transient thyrotoxicosis occurs in subacute thyroiditis and during treatment with amiodarone (particularly in iodine-deficient areas), which may represent a major therapeutic challenge; thyrotoxicosis during levothyroxine or interferon treatment is self-limited and remits on drug withdrawal.

Presentation is paucisymptomatic and atypical — the highest-yield point. Whereas younger patients have multiple emblematic symptoms, the older patient may have few symptoms and they are frequently atypical. Patients lack the hyperdynamic symptomatology — tremor, heat intolerance, ocular signs, nervousness or tachycardia — and instead have a more sedated, apathetic presentation. However, the frequency of atrial fibrillation is higher. Weight loss and cardiac symptoms frequently predominate, and goitre is frequently absent, making the diagnosis less obvious. Approximately one-third have no goitre. Depression and mania can be manifestations of hyperthyroidism in older adults.

Apathetic thyrotoxicosis and the masked presentation. Apathetic thyrotoxicosis is due in part to the decreased post-receptor responsiveness of β-adrenergic receptors that occurs with ageing. Its classical features are depression, weight loss, atrial fibrillation, heart failure, blepharoptosis and proximal myopathy, and it occurs in about 7% of older people with hyperthyroidism. Severe non-thyroidal disease may disguise thyrotoxicosis; congestive heart failure, stroke and infection are common disorders associated with masked hyperthyroidism. Suspect it in unexplained heart failure or tachyarrhythmia, recent-onset psychiatric disorder, or profound myopathy. The triad of weight loss, anorexia and constipation — which may raise the possibility of neoplastic disease — occurs in 15% of older thyrotoxic patients.

Investigation. Ultrasensitive TSH assays can differentiate hyperthyroidism from normal, and in the absence of acute non-thyroidal disease this test alone may confirm the clinical diagnosis. In the presence of acute illness, concomitant determination of TSH and free T4 is more appropriate. Then free T3 (for T3 toxicosis), TRAb for Graves' disease, and a radioisotope uptake scan to separate Graves' (diffuse uptake), toxic nodular goitre (patchy or focal) and thyroiditis or exogenous hormone (low uptake). Also ECG for atrial fibrillation, liver function and full blood count before antithyroid drugs, and bone densitometry where relevant. A T3 suppression test should not be done in older adults because of the risk of angina or myocardial infarction.

Treatment — radioiodine is the treatment of choice. Treatment of older patients with hyperthyroidism includes antithyroid drugs and radioactive iodine. 131I is the treatment of choice, especially when concomitant cardiovascular diseases are present, while surgery may be considered if obstructive symptoms caused by large goitres are present, even though it is rarely indicated owing to the high operative risk in older patients with comorbidity — though radioiodine may also be successfully used in large compressive goitres. Antithyroid drugs (methimazole/carbimazole or propylthiouracil) may be the treatment of choice for controlling hyperfunction before definitive treatment with 131I. A crucial closing line: treatment of an underactive thyroid after definitive treatment with 131I may be simpler than a recurrence of hyperthyroidism in an older patient — that is, accept hypothyroidism as a planned outcome.

Adjunctive treatment and the special situations. Beta-adrenergic blockers (propranolol, metoprolol) may be used with prudence, and when needed the dosage should be the lowest possible; treatment with beta blockers may prevent symptoms of thyrotoxicosis following 131I treatment. In general, atrial fibrillation reverts to sinus rhythm within a few months after the restoration of euthyroidism — so do not rush to cardiovert, but do anticoagulate according to stroke risk. For severe thyrotoxicosis or thyroid storm: antithyroid drugs, preferably propylthiouracil because it blocks peripheral conversion of T4 to T3, plus iodides to block thyroid hormone secretion (given after the thionamide) and beta blockers. Where beta blockers are contraindicated or the patient is allergic to antithyroid drugs, calcium ipodate 3 g every 3 days inhibits peripheral T4-to-T3 conversion, and dexamethasone 2 mg every 6 hours does the same and may be added to any of these regimens.

Long-term low-dose antithyroid drug therapy has become an accepted alternative to definitive treatment, and a large network meta-analysis has now compared the three modalities head to head. Revised American Thyroid Association guidance reflects less of a push towards definitive therapy: whereas antithyroid drug duration was previously limited on safety grounds, it is now accepted to remain on antithyroid drugs long term, with methimazole at 2.5–10 mg/day continued for many years shown to be safe and effective, and prolonged low-dose therapy producing better outcomes and fewer side effects than radioiodine in relapsed Graves' disease. A 2025 systematic review and network meta-analysis in Thyroid examined the long-term mortality risks of antithyroid drugs, radioiodine and surgery. Practical relevance for geriatrics: in a frail older patient with toxic multinodular goitre, radioiodine remains preferable because the disease does not remit; but in Graves' disease, continuing low-dose carbimazole with six-monthly thyroid function tests is a legitimate, low-burden option that avoids radiation precautions, the risk of transient post-radioiodine thyrotoxic exacerbation, and the near-certain need for lifelong levothyroxine. Always warn about agranulocytosis — stop the drug and check a full blood count urgently for fever or sore throat — and about hepatotoxicity.