Subacute Thyroiditis Christa M

ENDOCRINECONSULT

Subacute Thyroiditis Christa M. Blose, MPAS, PA-C, Holly Jodon, MPAS, PA-C

erry, a 48-year-old white man, is referred to endocri- TABLE Jnology for abnormal results Lab Results for Case Patient of thyroid tests performed four Time after symptom onset weeks ago (see table for values). Two months ago, Jerry developed 1 mo 2 mo 4 mo 6 mo an upper respiratory infection TSH (0.40-4.50 mlU/mL) 0.03 0.14 8.23 3.54 (URI) with fever, odynophagia, and anterior neck discomfort. Free T4 (0.8-1.8 ng/dL) 2.58 1.74 0.72 1.66 His symptoms resolved after two weeks; however, he has since de- Free T3 (2.3-4.2 pg/mL) 4.12 1.7 3.0 veloped fatigue and nervousness. The remaining review of sys- TPO antibody (< 20) 11 tems is unremarkable. Medical ESR (0-22 mm/h) 55 history is negative. Jerry denies any factors that can affect thyroid Abbreviations: ESR, erythrocyte sedimentation rate; T3, triiodothyronine; T4, thyroxine; function: He does not take thyroid TPO, thyroid peroxidase antibody. medication, OTC thyroid supple- ments, amiodarone, lithium, or TSH, with normal free thyroxine except for a small, firm thyroid interferon-α, does not have high (T4) and free triiodothyronine gland without the tenderness iodine intake, and has not un- (T3) levels. His thyroid peroxidase elicited previously. Labwork re- dergone head/neck irradiation. antibody (Anti-TPO) is negative. veals an elevated TSH with low There is no personal or family Radioactive iodine uptake (RAIU) free T4 and free T3. He is again history of thyroid disease, organ- reveals a low 24-hour uptake of counseled regarding the natural specific autoimmune disease 4% (normal, 5% to 30%). history of SAT and reassured that (ie, vitiligo, myasthenia gravis, or Jerry is given the presumptive his symptoms will abate as his Sjögren syndrome) or systemic diagnosis of subacute thyroid- thyroid hormone levels normal- autoimmune disease (rheuma- itis (SAT). He is advised that the ize. He is advised to continue the toid arthritis, systemic lupus ery- condition will progress through plan of follow-up testing every thematosus, or progressive sys- multiple phases—from the initial four to six weeks. temic sclerosis). thyrotoxicosis to euthyroidism Approximately eight weeks lat- Vital signs are stable. On physi- to transient hypothyroid—before er, Jerry’s thyroid function studies cal examination, his thyroid gland resolution and is educated on the indicate normal levels, and he is is firm, with slight enlargement of symptoms and signs to watch for. notified of the results. Jerry com- the left lobe and mild tenderness. Since he presented in a euthyroid ments that his symptoms have There are no palpable nodules or phase, with only mild anterior completely resolved and he is cervical adenopathy. The remain- neck tenderness, no treatment is back to feeling like his usual self. der of the exam is unremarkable. indicated. He is instructed to fol- He is discharged to follow-up as Lab studies (see table) reveal low up for thyroid function test- needed. an elevated erythrocyte sedimen- ing in four to six weeks and to call tation rate (ESR) and suppressed with any symptomatic changes. WHAT IS Two months later, Jerry re- SUBACUTE THYROIDITIS? Christa Blose and Holly Jodon practice at turns with complaints of ongo- Subacute thyroiditis is also known Metabolic Disease Associates in Erie, Penn- ing fatigue, unintentional weight as de Quervain thyroiditis or gran- sylvania. Jodon is also Associate Director and 1,2 Associate Professor in the Department of PA gain, and “mental fog.” Physical ulomatous giant cell thyroiditis. Studies at Mercyhurst University in Erie. exam findings are unremarkable The most common cause of thy-

34 Clinician Reviews • AUGUST 2014 clinicianreviews.com ENDOCRINECONSULT

roid pain, it is a self-limited in- PRODROME transitory immunologic markers flammatory disorder in which a The precursor URI is followed in develop several weeks after the painful tender goiter is associated days or weeks by the clinical man- onset and appear to be a physi- with malaise, fever, and transient ifestations of SAT. These typically ologic response to the inflamma- thyroid dysfunction.2,3 As with include myalgia, pharyngitis, low- tory insult to the gland.2 In most other thyroid disorders, SAT oc- grade fever, and fatigue.2 patients, the antibody titer gradu- curs most frequently in women There may be pain of vary- ally decreases, then disappears as ages 40 to 50.2,3 Thought to be of ing degrees in part or all of one the disease resolves.2-4 viral origin, it usually occurs after or both lobes; the pain often mi- The 24-hour RAIU is low a URI and commonly correlates grates to the entire gland and may (< 5%) in the toxic phase of SAT, with the peak incidence of viral radiate to the angle of the jaw or and thyroid scan will reveal a infections (spring/fall).2,3 the ear of the affected side(s). patchy and irregular distribution The disruptive process begins Moving the head, swallowing, or of the tracer.2,3 The thyrotoxicosis with inflammatory destruction of coughing aggravates the pain.2 during this early phase is caused thyroid follicles.2 This causes leak- The hallmark of SAT is a mark- by the inflammatory release of age of stored colloid, which is bro- edly elevated ESR (often > 100 preformed thyroid hormones ken down, releasing unregulated mm/h).1-3 Leukocyte count is nor- (not hyperfunctioning in the T4 and T3 into the circulation and mal (50% of cases) or only slightly gland), resulting in a “low-uptake resulting in a thyrotoxicosis that elevated (50%).2 thyrotoxicosis.”2 This differenti- typically lasts six weeks.1,2,4 Thy- ates SAT from the elevated uptake roid cells are incapable of produc- THYROTOXIC PHASE seen in Graves disease (> 30% at ing new thyroid hormone during Fifty percent of patients have mild 24 hours).2 this time, so as excess circulating to moderate symptoms of hyper- hormone is utilized, T4 and T3 thyroidism, including nervous- TRANSIENT HYPOTHYROIDISM levels become normal, then defi- ness, weight loss, heat intoler- PHASE cient, and the patient transitions ance, or palpitations; hoarseness As circulating T4 and T3 are uti- through a period of euthyroidism or dysphagia may be present.2 lized but follicular function re- mains temporarily impaired, levels decline, resulting in a period Subacute thyroiditis will of euthyroidism followed by hypothyroidism. TSH levels, previ- progress through multiple phases before ously suppressed in the thyrotox- ‘‘ ic phase, now become elevated. resolution. This transient hypothyroidism occurs in two-thirds of patients, to transient hypothyroidism.1,2,4 Signs include tremors or tachy- and the presentation varies from As the disruption’’ of thyroid pa- cardia. The thyroid gland may subclinical to pronounced.2 renchyma abates, recovery en- reveal slight to moderate unilat- sues. The follicles regenerate, eral enlargement, usually firm in RECOVERY PHASE colloid is repleted, and normal the involved area, and tenderness After several weeks or months, all thyroid function is restored.1-4 may be mild, moderate, or se- thyroid function studies return to SAT typically lasts four to six vere.2 Cervical lymphadenopathy normal and complete recovery months, although painful thyro- is absent.2 Serum T4 and T3 lev- commonly ensues. SAT rarely re- megaly may persist for one year els are elevated, and TSH is sup- curs, most likely due to immunity after resolution of thyroid dys- pressed.1-4 to the precipitating virus.1,2,4 function.2 Throughout the course Thyroid antibodies (antithy- of SAT, thyroid test results can be roid peroxidase antibodies [An- MANAGEMENT confusing, and misdiagnosis of ti-TPO or TPOAb] or antithyro- Thyroid function should be moni- hyperthyroidism or hypothyroid- globulin antibodies [Anti-TG or tored by testing every two to four ism may occur unless each phase TgAb]) have been found in 42% to weeks, dependent on the sever- of SAT is recognized. 62% of patients with SAT.2 These ity of the patient’s symptoms and

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rate of progression.1 Often, no if the TSH level is markedly el- CONCLUSION treatment is required.1,2 evated or the phase refractory. Primary care providers may en- Symptomatic relief of mild thy- However, levothyroxine therapy counter SAT at some point, and roid pain can be achieved with should be low dose (< 100 mg) a level of clinical suspicion must NSAIDs or aspirin (2 to 3 g/d). and not be considered lifelong.2,3 be maintained. Referral to endo- Severe symptoms can be treat- crinology may be warranted in ed with short-term prednisone, DIFFERENTIAL DIAGNOSIS some cases; however, textbook which should be tapered and dis- During the prodrome, SAT is of- cases can often be followed in continued.1-3 Steroids suppress ten misdiagnosed as pharyngi- primary care. Patient education the inflammatory response, and tis. Acute suppurative thyroiditis is the foundation of SAT care. the dramatic relief of thyroid pain initially may mimic SAT, but the Symptomatic treatments may be within 24 hours can be diagnostic febrile and leukocytic responses employed as needed. Fortunate- of SAT.2 are greater, and localized edema, ly, for most patients, this self- During the thyrotoxic phase, erythema, and tenderness be- limited disease state rarely leads β-blockers (propranolol) can al- come more evident as the condi- to complications. CR leviate adrenergic symptoms, tion progresses. with the dose tapered once the Painless or silent thyroiditis REFERENCES 1-3 1. Cooper DS. The thyroid gland. In: Gardner patient is euthyroid. Antithy- is distinguished from SAT by the D, Shobeck D (eds). Greenspan’s Basic and roid medications that directly in- lack of pain or tenderness and a Clinical Endocrinology. 9th ed. China: hibit thyroid hormone synthesis normal ESR in the presence of McGraw-Hill; 2011:163-226. 2. Guimaraes VC. Subacute and Riedel’s thy- (eg, methimazole or propylthio- a similar pattern of thyroid dys- roiditis. In: Jameson JL, De Groot LJ (eds). uracil) are ineffective due to the function. Graves disease pres- Endocrinology Adult and Pediatric. 6th ed. lack of T4 and T3 production in ents with symptoms similar to Philadelphia: Saunders; 2010:1595-1600. 3. Jameson JL. Disorders of the thyroid gland. the follicular cells after the in- the thyrotoxic phase of SAT, but In: Jameson JL (ed). Harrison’s Endocrin flammatory response.2,3 T3 is usually disproportionately ology. 2nd ed. China: McGraw-Hill; 2010: During the transient hypo- elevated compared to T4, RAIU is 62-98. 4. Smallridge RC. Thyroiditis. In: McDermott thyroid phase, thyroid hormone elevated, and thyroid antibodies MT (ed). Endocrine Secrets. 6th ed. Philadel- replacement may be indicated are prevalent.2 phia, PA: Elsevier Saunders; 2013:289-293.

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