How the disease develops
It is believed that the virus or the immune response to it damages thyroid cells. Granulomatous inflammation develops, the tissue is destroyed, and the supply of hormones stored in the follicles immediately enters the blood. That is why in the first phase there are signs of thyrotoxicosis, although the gland does not produce excess hormones, but only loses what it has accumulated. When the supply is depleted, hormone levels drop below normal and a phase of hypothyroidism occurs, usually temporary. As the tissue heals, it is restored and function returns to its original state.
- Thyrotoxicosis phase - first weeks
- Euthyroid phase - transition period
- Hypothyroidism phase - several weeks or months
- Function recovery phase
- In some people, hypothyroidism remains persistent
Causes and risk factors
The direct causative agent has not been identified, but the connection with a previous viral infection is clearly visible: the disease often begins a few weeks after a runny nose, sore throat or flu-like condition. Hereditary predisposition associated with the characteristics of the tissue compatibility system plays a role. Women aged approximately thirty to fifty years are most often affected. The incidence increases during the season of respiratory infections. Unlike suppurative thyroiditis, there is no bacterial infection of the gland itself, so antibiotics do not help.
- Past viral respiratory tract infection
- Hereditary predisposition
- Female gender
- Age 30–50 years
- Seasonality during respiratory infections
Symptoms
The main symptom is pain in the front of the neck, which radiates to the ear, lower jaw or back of the head and increases with swallowing, coughing and turning the head. The gland is enlarged, dense, sharply painful at the slightest touch; pain can move from one lobe to another. The temperature is usually low-grade, but can also be high, with chills and severe weakness. In the first weeks, palpitations, trembling hands, sweating, irritability, and poor heat tolerance occur. After a few weeks, these complaints are replaced by drowsiness, chilliness and swelling.
- Pain in the front of the neck radiating to the ear and jaw
- Sharp pain in the gland when touched
- Fever, weakness, body aches
- Palpitations, sweating, trembling hands
- Losing weight while maintaining appetite
- Later - drowsiness, chilliness, swelling
Diagnostics
Diagnosis usually consists of characteristic pain, recent viral infection, and laboratory findings. A typical sign is a sharply accelerated ESR and elevated C-reactive protein with a normal or slightly altered general blood test. In the first phase, TSH is reduced and free T4 is increased. Ultrasound shows unclear hypoechoic zones in painful areas with poor blood flow, which distinguishes the disease from diffuse toxic goiter. Antibodies to TSH receptors are not elevated. A biopsy is usually not required and is performed only in unclear cases.
- ESR and C-reactive protein
- General blood test
- TSH and free T4 in dynamics
- Ultrasound of the thyroid gland with blood flow assessment
- Antibodies to TSH receptors when in doubt
- Repeat hormone tests every 4–6 weeks
Treatment and observation
For moderate pain, non-steroidal anti-inflammatory drugs are prescribed for one to two weeks. If the pain is severe or there is no improvement, the doctor starts a short course of glucocorticoids with a reduced dose; This treatment usually relieves pain quickly. Thyrostatics are not needed because the gland does not produce excess hormones, and beta-blockers are used to reduce heart rate. During the hypothyroidism phase, if there are complaints and a noticeable increase in TSH, replacement therapy is temporarily prescribed. All medications are selected by the doctor; It is important to repeat tests until gland function returns to normal.
- Nonsteroidal anti-inflammatory drugs
- Short course glucocorticoids for severe pain
- Beta blockers for heart rate control
- Replacement therapy during the hypothyroidism phase if necessary
- Antibiotics are not indicated
- Monitor TSH every 4–6 weeks until normalization
- Ultrasound and examination by an endocrinologist over time