Subacute Thyroiditis

Subacute thyroiditis is a self limiting inflammatory condition of the thyroid gland, most commonly caused by a viral upper respiratory tract infection (subacute granulomatous, or de Quervain, thyroiditis).

It produces a characteristic triphasic course of transient hyperthyroidism followed by a transient hypothyroid phase. Thyroid function returns to normal in the great majority of patients.

It is distinguished from other causes of thyroiditis by striking thyroid pain and tenderness, which give it the alternative name of painful thyroiditis.

Recognising this self limiting pattern avoids unnecessary antithyroid medication during the initial hyperthyroid phase, since there is no genuine excess hormone synthesis.

Pathophysiology

• After a viral illness that is often mild or unremarked, a granulomatous inflammatory process develops within the thyroid gland. Follicular cell disruption releases preformed thyroid hormone into the circulation, which accounts for the initial, transient hyperthyroid phase.
• As the inflamed gland's hormone stores become depleted, and before normal synthetic function recovers, a transient hypothyroid phase follows.
• The great majority of patients return to normal thyroid function as the inflammation resolves and normal gland architecture and function are restored over subsequent weeks to months.
• The thyroid pain and tenderness reflect the acute inflammatory process itself. This distinguishes the condition clinically from painless thyroiditis, which is more typical of postpartum thyroiditis and the initial phase of Hashimoto thyroiditis in some patients.
• Both of those conditions can produce a broadly similar triphasic biochemical pattern, but without the pain and tenderness of subacute (de Quervain) thyroiditis.

• Thyroid pain and tenderness are the characteristic and defining presenting feature. The pain is often significant and sometimes radiates to the jaw or ears.
• Examination shows a firm, tender, diffusely or focally enlarged thyroid gland. A viral prodrome (fever, malaise, upper respiratory symptoms) frequently occurs in the weeks before.
• Systemic features including fever, malaise and fatigue frequently accompany the local thyroid symptoms.
• Symptoms also reflect the phase of thyroid dysfunction at assessment: hyperthyroid symptoms (palpitations, tremor, heat intolerance) during the initial phase, followed in the subsequent weeks by hypothyroid symptoms (fatigue, cold intolerance) during the second phase, before eventual resolution.
• The condition typically runs a course of several weeks to a few months from presentation to resolution and return to normal thyroid function.
• A small proportion of patients (generally estimated at around ten to fifteen percent) develop permanent hypothyroidism requiring long term levothyroxine replacement, reflecting more extensive, irreversible follicular cell damage in this subgroup.
• Recurrence, while uncommon, is recognised in a small proportion of patients and is sometimes associated with a further viral illness.
• In a patient with recurrent thyroid related symptoms, genuine recurrence must be distinguished from an evolving, separate autoimmune thyroid condition.

• Elevated inflammatory markers (erythrocyte sedimentation rate and C reactive protein), often markedly so, together with thyroid pain and tenderness, are important supportive features that help distinguish this condition from other causes of thyroid dysfunction.
• Thyroid function testing shows the biochemical pattern of the phase at assessment. The initial hyperthyroid phase shows suppressed thyroid stimulating hormone with elevated free thyroxine and triiodothyronine. The subsequent hypothyroid phase shows elevated thyroid stimulating hormone with reduced free thyroxine.
• Serial monitoring over subsequent weeks to months tracks this evolution.
• Radioactive iodine uptake scanning during the hyperthyroid phase characteristically shows low or absent uptake. This reflects release of preformed hormone from a damaged, inflamed gland rather than increased synthesis.
• That is a useful distinguishing feature from Graves disease, which shows diffusely increased uptake. The scan is not required in every case where the clinical picture (characteristic pain and tenderness, elevated inflammatory markers, appropriate biochemical pattern) is already sufficiently characteristic.
• Thyroid ultrasound may show hypoechoic areas within the gland corresponding to the inflamed regions.
• Thyroid peroxidase and thyroid stimulating hormone receptor antibodies are typically negative or only mildly positive. This supports distinction from Hashimoto thyroiditis and Graves disease respectively, which can occasionally present with overlapping clinical or biochemical features.

• Nonsteroidal anti inflammatory drugs are first line treatment for mild to moderate pain, given their combined analgesic and anti inflammatory action. Use a trial period of several days to a week to assess response before considering escalation to corticosteroid treatment.
• Oral corticosteroids (prednisolone, typically starting at 20 to 40 mg once daily) are highly effective for more significant pain not adequately controlled with nonsteroidal anti inflammatory drugs alone.
• The symptomatic response is characteristically rapid, often dramatic, within days, which is a further supportive clinical feature of this diagnosis. Taper gradually over several weeks according to clinical response.
• A proportion of patients have symptom recurrence during tapering and need temporary dose escalation before successful discontinuation.
• Beta blockade provides symptomatic relief during the transient hyperthyroid phase, following the same general principle as for thyroiditis related hyperthyroidism generally. Antithyroid medication is not indicated, since there is no genuine excess ongoing thyroid hormone synthesis in this transient phase.
• Manage the subsequent transient hypothyroid phase according to symptom severity and the biochemical degree of hypothyroidism. Mild, asymptomatic biochemical hypothyroidism is often managed with observation alone, given the anticipated spontaneous resolution.
• More significant symptomatic hypothyroidism may warrant temporary levothyroxine replacement. Consider a trial of dose reduction and eventual discontinuation after several months, once thyroid function has had adequate opportunity to recover.
• A small but real proportion of patients will prove to have permanent, rather than transient, hypothyroidism requiring continued long term treatment.
• Monitor thyroid function regularly throughout the expected triphasic course.
• Clear patient education on the expected, generally self limiting natural history and the sequential phases supports management. It also addresses the understandable concern that can arise from shifting between hyperthyroid and hypothyroid symptoms over a relatively short period.