graves'%20disease
GRAVES' DISEASE
Graves' disease is an autoimmune disorder that results into overproduction of thyroid hormones.
Thyrotoxicosis signs and symptoms include hyperactivity, irritability, insomnia, dysphoria, sweating, heat intolerance, palpitations, weakness, fatigue, weight loss despite increased appetite, diarrhea, steatorrhea polyuria, decreased libido, tachycardia, tremor, goiter, alopecia, gynecomastia, eyelid lag or retraction and rarely periodic paralysis.
Clinical features in thyrotoxic patient that suggests Graves's disease are ophthalmopathy, thyroid dermopathy, thyroid acropachy, diffuse goiter, antibodies to thyroid peroxidase or thyroglobulin and thyroid radionuclide scan demonstrating a diffuse goiter.

Principles of Therapy

Treatment methods will depend on:
  • Clinical presentation
  • Age of patient
    • Elderly without cardiac problems and children: Antithyroid agents - first-line agent
    • Elderly with cardiac problems: Radioactive iodine
  • Regional preferences
    • Europe and Asia: Antithyroid agents - first-line agent
    • North America: Radioactive iodine - first-line agent
  • Clinician preference
    • Patient’s input

Pharmacotherapy

Antithyroid Agents
  • Usually first-line agent for patients in Europe and Asia
  • Preferred therapy in pregnant women and children, patients with high likelihood of remission, elderly, or others with comorbidities increasing surgical risk or with limited life expectancy
  • May also be a treatment option for patients with previously operated or irradiated necks or lack access to an experienced/high-volume thyroid surgeon, patients with moderate-severe active Graves' orbitopathy and those needing rapid biochemical disease control
  • 30-40% of patients remain euthyroid 10 years after antithyroid treatment
    • Remission is most likely to occur in patients with mild hyperthyroidism and small goiters
    • Patients unable to attain remission after 12-18 months of antithyroid therapy can continue antithyroid therapy for another 12 months or opt for radioactive Iodine (RAI) or thyroidectomy
    • 10-15% of patients become hypothyroid 15 years after treatment
  • Usually takes 4-8 weeks to control symptoms
    • May use beta-blockers to control symptoms during this period, but not always needed
  • Contraindicated in patients with previous known major adverse reactions to antithyroid drugs
Carbimazole and Methimazole
  • Inhibit thyroid peroxidase and hence the synthesis of thyroid hormone
  • Fewer tablets are needed for initial treatment compared with Propylthiouracil (PTU)
  • In most circumstances, preferred thionamide antithyroid agent than PTU
Propylthiouracil (PTU)
  • Inhibits thyroid peroxidase and hence the synthesis of thyroid hormone, and blocks the extrathyroidal deiodination of thyroxine (T4) to triiodothyronine (T3)
    • Preferred over Methimazole during first trimester of pregnancy, thyrotoxic crises and in patients with adverse reactions with Methimazole that are not candidate for radioiodine therapy or surgery 
Beta-blockers
  • Eg Atenolol, Bisoprolol, Metoprolol, Propranolol
  • Should be given to elderly patients with symptomatic thyrotoxicosis and to other thyrotoxic patients with heart rate >90 beats/min or coexistent cardiovascular disease
    • Should be considered in all patients with symptomatic thyrotoxicosis
  • Decreases heart rate, systolic blood pressure, muscle weakness and tremor
  • Shows improvement in the degree of irritability, emotional lability and exercise tolerance
  • Helps prevent episodes of hypokalemic periodic paralysis
  • High-dose Propranolol inhibits peripheral conversion of T4 to T3
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