Subacute Thyroiditis Medication
- Author: Stephanie L Lee, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP more...
Medical treatment for subacute thyroiditis is supportive in general. Thyrotoxicosis can be extreme but temporary (eg, 6-8 wk). The subsequent hypothyroid phase is usually mild and lasts 2-4 months. Therapy is directed toward reducing the signs and symptoms of the hyperthyroidism with beta blockers or iodine agents. Pain is treated with nonsteroidal anti-inflammatory agents (NSAIDs). Rarely, high-dose steroids and narcotic analgesic agents are used for extremely painful or recurrent life-threatening hyperthyroidism.
Salicylates are used for symptomatic treatment. They aid in the relief of mild to moderate pain by inhibiting inflammatory reactions and pain. Patients should avoid high-dose aspirin because it can increase free thyroid hormone levels by displacing thyroid hormone from its protein-binding sites.
Aspirin treats mild to moderate pain. It inhibits prostaglandin synthesis, which prevents the formation of platelet-aggregating thromboxane A2.
Nonsteroidal Anti-Inflammatory Drugs
Anti-inflammatory agents are administered to patients with subacute granulomatous thyroiditis. Narcotic analgesics can be administered if the pain is extreme and prevents oral hydration. In rare cases, high-dose steroids (eg, prednisone 40-60 mg/day PO for 4-6 wk) may be used to decrease the pain.
Ibuprofen is the drug of choice for patients with mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Naproxen is used for the relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing the activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.
Indomethacin, which is rapidly absorbed, inhibits prostaglandin synthesis. The drug is metabolized in the liver by demethylation, deacetylation, and glucuronide conjugation.
Iodinated Contrast Agents
High iodine levels inhibit the peripheral conversion of T4 to T3. The most effective agents are the iodinated contrast agents, but high levels of iodine provided by saturated solution of potassium iodide (SSKI; 2 drops in full glass of water PO tid) can be substituted.
Iopanoic acid (Telepaque)
This is an oral contrast agent used for the rapid and significant inhibition of the peripheral conversion of T4 to T3. Inorganic iodide also blocks the release of thyroid hormones. Reduction in the conversion of T4 to T3 can greatly reduce T3 levels and thyrotoxic symptoms.
Ipodate is one of the most effective inhibitors of deiodinase, which converts T4 to the more biologically active T3. Reduction in the conversion of T4 to T3 can greatly reduce T3 levels and thyrotoxic symptoms.
Most patients with subacute thyroiditis experience a hypothyroid phase following thyrotoxicosis. Asymptomatic patients do not need to be treated if the TSH level is mildly elevated (< 15 µIU/mL), but they should be tested every 4 weeks to confirm that hypothyroidism is not worsening or becoming permanent.
Thyroid hormone is generally administered (usually 50 mcg/day) to normalize TSH. After 6 months, when 90-95% of patients have returned to normal thyroid function, thyroid hormone is discontinued; the TSH level is checked 4 weeks after discontinuation of therapy. If the TSH level is within the reference range, no further treatment is necessary. If the level is elevated, however, the patient has permanent hypothyroidism, and therapy should be continued indefinitely.
Levothyroxine is used for supplementation during the hypothyroid phase of subacute thyroiditis. The goal of levothyroxine therapy is to keep the TSH level within the reference range for 6 months; therapy is then discontinued. The TSH level should be checked 4 weeks later; if the level is elevated, levothyroxine therapy must be reinstituted and continued indefinitely.
Tirosint is a preparation of T4 in a liquid form in a gelatin capsule. This form of thyroid hormone contains only T4, glycerol, and gelatin, with no other additives. This form may be preferred in patients on long-term proton pump inhibitors, a history of erratic T4 absorption, and reactions to the nonhormone content of other pills (eg, gluten, dyes).
Liothyronine is a synthetic form of natural thyroid hormone T3 converted from T4. Its duration of activity is short, which allows for quick dosage adjustments in the event of overdosage. Liothyronine may need to be administered as often as 4 times daily. In its active form, the drug influences the growth and maturation of tissues.
Thyroid hormone replacement with T3 alone is not recommended because of the need for dosing at 2-3 times daily. The short half-life means there is significant fluctuation between too low and too high levels during the course of the day.
Beta-Adrenergic Blocking Agents
Beta-blockers reduce many of the symptoms of thyrotoxicosis, including tachycardia, tremor, and anxiety. Propranolol is usually recommended because of its CNS penetration, but some patients prefer the longer-acting beta-blockers.
Propranolol is the drug of choice for treating cardiac arrhythmia resulting from hyperthyroidism. The drug effects cardiac and psychomotor manifestations within minutes.
Atenolol selectively blocks beta1 receptors, with little or no effect on beta2 types. This agent is useful for treating cardiac arrhythmias resulting from hyperthyroidism. It effects cardiac and psychomotor manifestations within minutes.
Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. It aids in the treatment of cardiac arrhythmias resulting from hyperthyroidism. The drug effects cardiac and psychomotor manifestations within minutes.
If thyroid pain is extreme, high-dose steroids rapidly reduce thyroid hormone levels and swelling. Generally, therapy must be continued for 4-6 weeks before tapering.
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects, modifying the body's immune response to diverse stimuli.
Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN) cell activity.
Corticosteroids act as potent inhibitors of inflammation. They may cause profound and varied metabolic effects, particularly in relation to salt, water, and glucose tolerance, in addition to their modification of the immune response of the body. Alternative corticosteroids may be used in equivalent dosages.
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|Parameters||Stage 1||Stage 2||Stage 3||Stage 4|
|T4 = thyroxine
T3 = triiodothyronine
TSH = thyroid-stimulating hormone