Background
Subacute thyroiditis is a self-limited thyroid condition associated with a triphasic clinical course of hyperthyroidism, hypothyroidism, and return to normal thyroid function. Subacute thyroiditis may be responsible for 15-20% of patients presenting with thyrotoxicosis and 10% of patients presenting with hypothyroidism. Recognizing this condition is important, because it is self-limiting, and no specific therapy, such as antithyroid or thyroid hormone replacement therapy, is necessary in most patients.
In general, the following 3 forms of subacute thyroiditis are recognized:
- Subacute granulomatous (see the image below), subacute painful, or de Quervain thyroiditis.
Three multinucleated, giant cell granulomas observed in a fine-needle aspiration biopsy of the thyroid; from a patient with thyrotoxicosis from lymphocytic or subacute granulomatous thyroiditis. - Lymphocytic thyroiditis (also known as subacute painless thyroiditis)
- Subacute postpartum thyroiditis
Although the etiology appears to be different for the 3 subtypes, the clinical courses are the same.
The high thyroid hormone levels are a result of destruction of the thyroid follicle and release of preformed thyroid hormone into the circulation. The high thyroid hormone levels are not a function of new thyroid hormone synthesis and secretion. Conditions of excess thyroid hormone synthesis and secretion (eg, Graves disease, toxic multinodular goiter, toxic adenoma) are discussed in the eMedicine article Hyperthyroidism.
Eventually, thyroid hormone is depleted and the patient may become hypothyroid. Often, the hypothyroidism is mild, and no thyroid hormone therapy is required unless the patient has signs or symptoms of hypothyroidism. The hypothyroid phase may last up to 2 months.
Ninety to 95% of patients return to normal thyroid function.
Pathophysiology
The hypermetabolic effect of thyrotoxicosis is the same, regardless of cause. Thyrotoxicosis affects every organ system, because thyroid hormones made in the thyroid travel via the circulation to reach every cell in the body. Thyroid hormone is necessary for normal growth and development, and it regulates cellular metabolism. Excess thyroid hormone causes an increase in metabolic rate that is associated with increased total body heat production, increased cardiovascular activity (eg, increased heart contractility, heart rate, vasodilation) to remove heat to the periphery and remove metabolic wastes, and perspiration to cool the body.
The major symptoms of thyrotoxicosis include palpitations, nervousness, sweating, hyperdefecation, and heat intolerance. Women often note a reduction in menstrual flow or oligomenorrhea. Common signs of thyrotoxicosis include weight loss despite increased appetite, lid lag and stare, sinus tachycardia, atrial fibrillation or high-output failure (in elderly persons), fine tremor, and muscle weakness. Synergism occurs between thyrotoxicosis and the adrenergic system, with increases in nervousness, stare, tremor, and tachycardia.
The manifestations of thyrotoxicosis vary among patients. Younger patients tend to exhibit more sympathetic activations (eg, anxiety, hyperactivity, tremor), while older patients have more cardiovascular symptoms (eg, dyspnea, atrial fibrillation) and unexplained weight loss. The clinical manifestation of thyrotoxicosis does not always correlate with the extent of the biochemical abnormality.
Subacute thyroiditis is a destructive thyroiditis resulting in the release of preformed thyroid hormone and not in the new synthesis of thyroid hormone. A characteristic finding in this thyrotoxic condition is a very low radioactive iodine uptake by the thyroid, as seen in the images below.
The 3 types of subacute thyroiditis are subacute granulomatous thyroiditis, also referred to as subacute painful thyroiditis; lymphocytic thyroiditis, which is silent and is also referred to as subacute painless thyroiditis; and postpartum thyroiditis. The etiology of each of these conditions is different, but all of them follow the same clinical course, including 6-8 weeks of thyrotoxicosis, 2-4 months of mild hypothyroidism, and finally, a return to the euthyroid state in 90-95% or more of the patients. A patient may experience 1 or more of these phases. The course is illustrated in the second image below.
Absence of iodine-123 (123I) radioactive iodine uptake in a patient with thyrotoxicosis and lymphocytic (subacute painless) thyroiditis. Laboratory studies at the time of the scan demonstrated the following: thyroid-stimulating hormone (TSH), less than 0.06 mIU/mL; total thyroxine (T4), 21.2 mcg/dL (reference range, 4.5-11); total triiodothyronine (T3), 213 ng/dL (reference range, 90-180); T3-to-T4 ratio, 10; and erythrocyte sedimentation rate (ESR), 10 mm/h. The absence of thyroid uptake, the low T3-to-T4 ratio, and the low ESR confirm the diagnosis of lymphocytic thyroiditis. 
Example of laboratory values during subacute granulomatous thyroiditis. The entire episode may evolve through all 3 phases over a period of as long as 6 months. Thyroid biopsies in subacute granulomatous thyroiditis show characteristic multinucleated, giant cell granulomas and a mononuclear infiltration, as seen in the image below. Thyroid biopsy tissue from patients with postpartum and painless or lymphocytic thyroiditis shows a lymphocytic infiltration.
Three multinucleated, giant cell granulomas observed in a fine-needle aspiration biopsy of the thyroid; from a patient with thyrotoxicosis from lymphocytic or subacute granulomatous thyroiditis. A Japanese study derived from a medical records review of 852 patients with subacute thyroiditis found that most of the laboratory test–based indications for thyrotoxicosis and thyroiditis-associated inflammation peaked within a week after the onset of subacute thyroiditis.[1]
Epidemiology
Frequency
United States
The thyrotoxicosis caused by lymphocytic, subacute painful, or postpartum thyroiditis is more frequently recognized as a cause of transient thyrotoxicosis. Estimates indicate that 20-25% of thyrotoxicosis is caused by these destruction-induced forms.
International
No difference in the worldwide prevalence of subacute thyroiditis is apparent.
Mortality/Morbidity
Thyrotoxicosis from subacute thyroiditis is brief, usually lasting no longer than 6-8 weeks. Patients can be extremely thyrotoxic during this period and can appear extremely ill, but concerns regarding left ventricular hypertrophy and osteoporosis are not as great as those associated with conditions of permanent hyperthyroidism. However, sudden-onset thyrotoxicosis and severe thyrotoxicosis can be associated with atrial arrhythmia and congestive heart failure (CHF).
Race
Subacute thyroiditis appears to affect all races and ethnic groups equally.
Sex
- Subacute granulomatous thyroiditis has a female-to-male prevalence ratio of 5:1.
- Lymphocytic thyroiditis and postpartum thyroiditis are associated with autoimmune thyroiditis. Lymphocytic thyroiditis occurs 2 times more often in women than it does in men.
- Postpartum thyroiditis occurs 1-6 months after giving birth. If a woman has postpartum thyroiditis with one baby, all other pregnancies are likely to be associated with this condition.
Age
- Lymphocytic thyroiditis can occur in any age group, while granulomatous thyroiditis usually occurs in adults (ie, aged 20-60 y).
- Postpartum thyroiditis occurs in women of childbearing age.
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