Several varieties of thyroiditis can present with thyrotoxicosis, including postpartum thyroiditis, painless thyroiditis, drug-induced thyroiditis, subacute thyroiditis, traumatic thyroiditis, and acute thyroiditis. In general, thyroid dysfunction caused by thyroiditis is less severe than that seen with other forms of endogenous thyrotoxicosis; RAIU is universally low during the thyrotoxic stage, owing to leaking of thyroid hormone with suppression of serum TSH concentrations.
[V1] Subacute thyroiditis
The diagnosis of subacute thyroiditis in a thyrotoxic patient should be made based on clinical history, physical examination, and RAIU. Subacute thyroiditis presents with moderate-to- severe pain in the thyroid, often radiating to the ears, jaw, or throat. The pain may begin focally and spread throughout the gland over several weeks. Patients may have malaise, low-grade fever, and fatigue in addition to the symptoms of thyrotoxicosis. The thyroid is firm and painful to palpation. In addition to laboratory evidence of thyrotoxicosis, the erythrocyte sedimentation rate or C-reactive protein is elevated, and mild anemia is common. RAIU is low, and thyroid ultrasonography shows diffuse heterogeneity and decreased or normal color-flow Doppler, rather than the enhanced flow characteristic of GD.
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Patients with mild symptomatic subacute thyroiditis should be treated initially with beta-adrenergic-blocking drugs and nonsteroidal anti-inflammatory agents. Those failing to respond or those with moderate-to-severe symptoms should be treated with corticosteroids. 1/+00
Subacute thyroiditis is treated with beta-blockers and antiinflammatory therapy. Nonsteroidal anti-inflammatory agents (NSAIDs) provide pain relief in patients with mild symptoms due to subacute thyroiditis, and should be considered first-line therapy in such patients. Patients who fail to respond to full doses of NSAIDs over several days should be treated instead with corticosteroid therapy, such as prednisone 40mg daily for 1–2 weeks followed by a gradual taper over 2–4 weeks or longer, depending upon clinical response. A retrospective review of patients receiving care for subacute thyroiditis found that patients treated with corticosteroids had more rapid resolution of pain (mean duration, 8 days) compared with those treated with NSAIDs (mean duration, 35 days). However, symptoms can recur as the dose of corticosteroid is reduced (19). As with painless and postpartum thyroiditis, levothyroxine may be employed during the hypothyroid stage, but should be withdrawn after 3–6months with recovery of normal function verified by thyroid function testing.
[V2] Painless thyroiditis
Painless or silent thyroiditis is an autoimmune disease manifested by positive anti-TPO antibodies in the majority of patients, and a triphasic pattern in some cases. The postpartum period is the most common time when painless thyroiditis is seen, but painless thyroiditis can also occur in nonpregnant patients and men. Painless thyroiditis has been described in some types of drug-induced thyroid dysfunction, including that associated with lithium or cytokine therapy. The latter includes IFN-α or interleukin-2 (discussed elsewhere), but not IFN-β therapy. Beta-adrenergic blockers can be used to treat thyrotoxic symptoms in patients with painless thyroiditis, but antithyroid drugs have no utility, since new hormone synthesis is already low in these patients. Rarely, corticosteroids have been used to ameliorate the severity and the time course of thyrotoxicosis due to painless thyroiditis (350), but they should be reserved only for more severe cases. Some patients may have recurrent episodes of painless thyroiditis, separated by years.
[V3] Acute thyroiditis
Patients with acute thyroiditis (also referred to as suppurative thyroiditis or thyroid abscess) are generally euthyroid. However, on occasion, the condition presents as destructive thyrotoxicosis (351). The etiology of acute thyroiditis is most frequently a bacterial infection affecting the thyroid, either through hematogenous spread or direct extension through a fistula from an infected pyriform sinus. Therapy involves systemic antibiotics as well as abscess drainage or removal, and excision or occlusion of the offending pyriform sinus. Thyrotoxicosis should be treated symptomatically with beta-blocking agents. As in other forms of destructive thyroiditis, there is no role for antithyroid drugs.