Goiter medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2] Mehrian Jafarizade, M.D [3]

Overview

Pharmacologic medical therapy for goiter involves normalizing thyroid hormone levels and treating the inflammation. Treatment regimen involves Lugol's iodine, antithyroid drugs and β-adrenergic blockers. In some cases, radioactive iodine may be used to treat an overactive thyroid gland.

Medical Therapy

• Pharmacologic medical therapy is recommended for patients with goiter.

Hypothyroidism:

• In cases of hypothyroidism, thyroid hormone replacement with levothyroxine may help resolve symptoms of hypothyroidism and also help with the slow release of thyroid stimulating hormone (TSH) from pituitary which would result in the decrease in the size of the goiter.
• The drug used in the treatment of hypothyroidism is:
  1. Levothyroxine:
     • Lifelong synthetic levothyroxine (L-T4) is used to treat the hypothyroidism.
     • Main goals of levothyroxine replacement therapy are:
       • Resolution of the hypothyroid symptoms and signs including biological and physiologic markers of hypothyroidism,
       • Normalization of serum thyrotropin with improvement in thyroid hormone concentrations,
       • To avoid overtreatment (iatrogenic thyrotoxicosis).
     • Side effects include atrial fibrillation and osteoporosis. Drug Regimen:
  • Synthetic levothyroxine (L-T4) 1.6–1.8 μg/kg of body weight per day orally.

Hyperthyroidism:

• In hyperthyroidism, treatment targeted at normalizing thyroid hormone levels is considered.
• In cases of inflammation of thyroid gland, medication to treat the inflammation are generally prescribed. For goiters associated with hyperthyroidism, you may need medications to normalize thyroid hormone levels.
• Radioactive Iodine: In some cases, radioactive iodine may be used to treat an overactive thyroid gland. Radioactive iodine is prescribed as an oral medication which helps destroy thyroid cells resulting in the decreasing the size of the goiter. This therapy may also lead to under-activity of the thyroid gland.
• Lugol's iodine:
  • Decreases thyroid hormone synthesis,
  • Decreases vascularity.
• Antithyroid drugs such as carbimazole, methimazole:
  • Used to restore the patient to a euthyroid state
• β-adrenergic blockers such as propranolol:
  • Lowers tachycardia and palpitations,
  • Used to restore the patient to a euthyroid state,
  • It also decreases vascularity.

• The following table summarizes the medical therapy and surgical option for treatment.

Treatment	Mechanism	Route of administration	Advantages	Disadvantages	Special considerations
Beta-blockers	Block β-adrenergic receptors; propranolol may block conversion of T4 to T3	Oral; may be administered intravenously in acute cases	Ameliorates sweating, anxiety, tremulousness, palpitations, and tachycardia	Does not influence course of disease Use cautiously in patients with asthma, CHF , bradyarrhythmias or Raynaud’s phenomenon	Use cardioselective beta-blockers, especially in patients with COPD Use calcium-channel blockers as alternative
Antithyroid drugs (methimazole, carbimazole, and propylthiouracil)	Methimazole, carbimazole, and propylthiouracil block thyroid peroxidase and thyroid hormone synthesis propylthiouracil also blocks conversion of thyroxine to triiodothyronine	Given as either a single, high fixed dose (e.g., 10–30 mg of methimazole or 200–600 mg of propylthiouracil daily) and adjusted as euthyroidism is achieved or combined with thyroxine to prevent hypothyroidism (“block–replace” regimen)	Outpatient therapy Low risk of hypothyroidism No radiation hazard or surgical risk Remission rate 40–50%	High recurrence rate Frequent testing required unless block-replacement therapy is used Minor side effects in ≤5% of patients (rash, urticaria, arthralgia, fever, nausea, abnormalities of taste and smell)	Major side effect usually within first 3 mo of therapy Agranulocytosis in <0.2% of patients Hepatotoxicity in ≤0.1% Cholestasis for the thionamides and hepatocellular necrosis for propylthiouracil Antineutrophil cytoplasmic antibody–associated vasculitis in ≤0.1% of patients
Radioactive iodine (iodine-131)	Irradiation causes thyroid cell damage and cell death	Oral; activity either fixed (e.g., 15 mCi [555 MBq]) or calculated on the basis of goiter size and uptake and turnover investigations	Normally outpatient procedure Definitive therapy Low cost Few side effects Effectively reduces goiter size	Potential radiation hazards Adherence to a country’s particular radiation regulations Radiation thyroiditis Decreasing efficacy with increasing goiter size Eventual hypothyroidism in most patients	Should not be used in patients with active thyroid ophthalmopathy Contraindicated in women who are pregnant or breast-feeding and for 6 wk after breast-feeding has stopped
Thyroidectomy	Most or all thyroid tissue is removed surgically	-----	Rapid euthyroidism Recurrence extremely rare No radiation hazard, Definitive histologic results Rapid relief of pressure symptoms	Most expensive therapy Hypothyroidism is the aim Risks associated with surgery and anesthesiology Minor complications in 1–2% of patients (bleeding, infection, scarring), Major complications in 1–4% (hypoparathyroidism, recurrent laryngeal-nerve damage)	Does not influence course of Graves’ ophthalmopathy during pregnancy Is best performed during the second trimester