Hyperthyroidism

Descriptive text is not available for this image BASICS

  • Hyperthyroidism or thyrotoxicosis is due to thyroid hormone excess. The former describes excess from the thyroid gland, the latter can also be produced from another source.
  • Patients could also suffer thyrotoxicosis from subacute thyroiditis, exogenous thyrotoxicosis, and radiation-induced thyroiditis.

DESCRIPTION

  • Graves disease (GD) is the most common cause with autoantibodies directed at the thyroid-stimulating hormone (TSH) receptors.
  • Toxic multinodular goiter (TMNG) is the most common cause of hyperthyroidism in patients >65 years of age; often an insidious onset, frequent in iodine-deficient areas
  • Toxic adenoma (Plummer disease) is seen in younger patients—autonomously functioning nodules.
  • TSH-producing adenoma, not to be confused with a resistance to thyroid hormone
  • Iodine-induced hyperthyroidism
  • Subacute thyroiditis/de Quervain: granulomatous giant cell thyroiditis, benign course; viral infections have been involved.
  • Postpartum thyroiditis
  • Drug-induced thyroiditis: amiodarone, interferon-α, interleukin-2, lithium
  • Subclinical hyperthyroidism: suppressed TSH with normal thyroxine (T4)
  • Thyroid storm: fever, tachycardia, gastrointestinal (GI) symptoms, CNS dysfunction (e.g., coma); up to 50% mortality

Geriatric Considerations

  • Classic symptoms and signs may be absent.
  • Atrial fibrillation can be seen when TSH is <0.1 mIU/L (1)[A].

Pediatric Considerations

  • Neonates and children are treated with antithyroid medications for 12 to 24 months.

Pregnancy Considerations

Propylthiouracil (PTU) is currently the drug of choice during 1st trimester of pregnancy, and methimazole is preferred in the 2nd and 3rd trimester (2)[A]. Treat with lowest effective dose because PTU can cross the placenta and put the fetus at risk for goiter. Radioiodine therapy is contraindicated.

EPIDEMIOLOGY

  • Predominant age: autoimmune thyroid disease (GD) in 2nd and 3rd decades; TMNG is more common in patients aged >40 years.

Prevalence

The global prevalence is 2% among women and 0.5% among men

ETIOLOGY AND PATHOPHYSIOLOGY

  • GD: autoimmune disease
  • TMNG: 60% TSH receptor gene abnormality; 40% unknown
  • Toxic adenoma: point mutation in TSH receptor gene with increased hormone production
  • Hashitoxicosis: autoimmune destruction of the thyroid; antimicrosomal antibodies present
  • Subacute/de Quervain thyroiditis: Granulomatous reaction viruses, such as coxsackievirus, adenovirus, echovirus, and influenza virus, have been implicated.
  • Postpartum thyroiditis: Autoimmune thyroiditis that lasts up to 8 weeks, and in 60% of patients, hypothyroidism manifests in the future.

Genetics

Concordance rate of GD among monozygotic twins is 35%.

RISK FACTORS

  • Positive family history, especially in maternal relatives
  • Other autoimmune disorders
  • Iodide repletion after iodide deprivation, especially in TMNG

COMMONLY ASSOCIATED CONDITIONS

  • Autoimmune diseases
  • Down syndrome

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