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Subacute granulomatous thyroiditis



Endocrine system


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Subacute granulomatous thyroiditis


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Subacute granulomatous thyroiditis

6 flashcards

USMLE® Step 1 style questions USMLE

4 questions

An 18-year-old woman comes to the clinic due to upper neck and jaw pain that started gradually a week ago. The patient is generally healthy, and medical history is unremarkable other than dysmenorrhea, for which she takes acetaminophen. Two weeks ago, she had an upper respiratory infection that resolved without treatment. During the past week, she has noticed that she sweats more than usual and has difficulty sleeping. Temperature is 37.0°C (98.6°F), pulse is 110/min, and blood pressure is 125/85 mmHg. On physical examination, the thyroid gland is diffusely enlarged and very sensitive to touch. Laboratory tests are obtained and reveal the following:

Radioactive iodine uptake test is performed and reveals diffusely decreased uptake. Which of the following is most likely involved in the pathogenesis of this patient’s condition?

External References

Subacute granulomatous thyroiditis, also known as De Quervain’s thyroiditis, belongs to a group of disorders featuring inflammation “-itis” of the thyroid gland.

This inflammation is “granulomatous”, meaning there are aggregations of immune cells, mainly activated macrophages, that form tiny nodules within the thyroid gland.

Subacute implies that it’s somewhere between acute and chronic, typically developing after an acute event, like a viral infection.

Normally, the hypothalamus, which is located at the base of the brain, secretes thyrotropin-releasing hormone, known as ΤRH, into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary.

The anterior pituitary then releases a hormone of its own, called thyroid-stimulating hormone, thyrotropin or simply TSH.

TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”.

If we zoom into the thyroid gland, we’ll find thousands of follicles, which are small hollow spheres whose walls are lined with follicular cells, and are separated by a small amount of connective tissue.

Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.

Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins.

Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body.

Once inside the cell T4 is mostly converted into T3, and it can exert its effect. T3 speeds up the basal metabolic rate.

So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats. It’s as if the cells are in a bit of frenzy.

T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response.

Thyroid hormone is important - and the occasional increase can be really useful when you need a boost to get through the final rounds of a sporting competition or to stay warm during a snowstorm!

Meanwhile, thyroid hormones are involved in a number of other things, such as normal function of sebaceous and sweat glands, growth of hair follicles and regulation of the synthesis of proteins and mucopolysaccharides by skin fibroblasts.

Now, subacute granulomatous thyroiditis is typically triggered by a viral infection of the upper respiratory system, for example, adenovirus, mumps, measles or coxsackievirus.

Sometimes, these viruses spread to the thyroid gland and target the thyroid cells. And when they get in and infect these cells, they can cause the thyroid cells to present weird and abnormal proteins on their MHC class 1 molecules.

Soon, immune cells, particularly CD8 positive T cells and antigen- presenting cells, like macrophages, rush into the thyroid tissue.

When the CD8 positive T cells identify the abnormal proteins on the MHC class 1 molecules, they typically destroy the thyroid cells.

As these thyroid cells die, they spill out viral antigens, as well as some of their own cellular antigens, like thyroid peroxidase, thyroglobulin, or TSH receptors.

And while macrophages try to clean away those viral remnants, they sometimes pick up the thyroid antigens as well.

Next, these macrophages carry both viral and thyroid self- antigens to a nearby lymph node to activate CD4+ T-helper cells.

T-helper cells secrete inflammatory cytokines, like interferon- (gamma) γ, which help activate more macrophages.


Subacute granulomatous thyroiditis is a self-limited inflammatory condition of the thyroid gland that commonly occurs after an upper respiratory tract infection. It presents as a transient, painful enlargement of the thyroid gland, which can sometimes press on the esophagus, causing dysphagia. There can also be hyperthyroidism signs, like feeling hot and sweating excessively, diarrhea, and rapidly losing weight even without any change in diet or exercise. In rare cases, there may be progression to a hypothyroid state, with symptoms of a decreased metabolic rate like feeling cold and weak, developing dry and rough skin, having constipation, and rapidly gaining weight without any change in diet or exercise. Subacute granulomatous thyroiditis generally resolves on its own, and treatment is supportive care with pain medications, such as nonsteroidal anti-inflammatory drugs.