Subacute thyroiditis is an infectious granulomatous thyroid disease with destruction of thyrocytes. It is manifested by pain in the front of the neck, localized in a limited area or radiating into the ears, lower jaw, nape. The infectious process leads to the development of fever with moderate hyperthermia. When the follicles rupture, iodine-containing hormones enter the bloodstream, hyperthyroidism occurs, accompanied by irritability, anxiety, tremor, a feeling of heat and weight loss, followed by euthyroidism and transient hypothyroidism. Specific diagnostic methods – blood and thyroid hormone tests, thyroid sonography. Medical treatment includes taking NSAIDs, corticosteroids, beta-blockers.
ICD 10
E06.1 Subacute thyroiditis
Meaning
Subacute thyroiditis is an acute viral inflammatory lesion of the thyroid gland. Clinical manifestations persist longer than in acute thyroiditis, but are more pronounced than in chronic forms. Synonymous names are granulomatous thyroiditis, giant cell thyroiditis and de Quervain thyroiditis (after the name of the Swiss doctor who first described the disease in 1904). The prevalence among all thyroid pathologies ranges from 1 to 5%. Women are more susceptible to diseases, the gender ratio is 5:1. The vast majority of patients belong to the age category of 30-60 years. The peak incidence is recorded in the autumn-winter period, which is associated with the spread of ARI.
Causes
The factors provoking the development of granulomatous thyroiditis have not been precisely clarified. Currently, the theory of the viral origin of the disease has become the most widespread in endocrinology. The lesion of the gland tissues is probably caused by exposure to viruses, this fact is confirmed by the presence of clinical and laboratory signs of an infectious disease. According to statistics, thyroiditis is most often diagnosed after an upper respiratory tract infection. A genetic predisposition has also been determined – the carrier of the HLA-BW 35 gene, which causes high susceptibility to viral diseases.
Pathogenesis
The pathogenetic basis of subacute thyroiditis is the formation of granulomas of infectious origin in the glandular tissue. The disease occurs 2-6 weeks after a viral infection. Viruses penetrate into thyrocytes, where they activate the synthesis of atypical proteins. The immune system perceives them as foreign and responds with the development of inflammation. The production of monocytic phagocytes is stimulated, they accumulate in the inflammatory focus and turn into macrophages. Macrophage granulomas are formed. At the same time, some phagocytes and macrophages mature and transform into epithelioid cells. Epithelioid cellular and giant cell granulomas are created.
If phagocytosis is reduced in granulomas and the absorbed proteins do not completely disintegrate, a persistent delayed hypersensitivity reaction is observed. If phagocytosis in granulosa cells is sufficient, there is no immune response. The thyroid gland increases in size, is infiltrated by lymphocytes and giant cell granulomas. Due to follicle ruptures, a large amount of thyroxine and triiodothyronine enters the blood plasma, hyperthyroidism develops. After 4-8 weeks, hormone reserves are depleted, hyperthyroidism is replaced by euthyroidism, transient hypothyroidism. Upon recovery, granulomas are scarred, the functions of the gland are restored.
Classification
Taking into account the functionality of the gland, three phases are distinguished during the disease. The first (thyrotoxic) is characterized by the release of iodine-containing hormones into the bloodstream. The second (euthyroid) is accompanied by normalization of triiodothyronine and thyroxine levels. The third (hypothyroid) is observed during a period of hormone deficiency associated with depletion of tissue reserves and a decrease in the number of functional thyrocytes. According to the features of symptoms, the presence or absence of an autoimmune component, two types of disease are distinguished:
- Kerven’s thyroiditis. The most common variant of the disease, which is why the name is often used as a synonym for subacute thyroiditis in general. Symptoms are pronounced, differentiated by stages. There is a tendency to relapse.
- Subacute lymphocytic thyroiditis. It is rare. It can develop at any age (without increasing the frequency by middle and old age). It has an autoimmune component. Sometimes it debuts after childbirth, called subacute postpartum lymphocytic thyroiditis.
Symptoms
A wave-like flow is characteristic, due to changes in the activity of the infectious process and the secretion of thyroid hormones. The onset of the disease is manifested by an increase in general weakness, hyperthermia from 37.5 to 38.5-38.7 ° C. There are pains in the area of the thyroid gland, which increase when swallowing, chewing, turning the head or probing. Some patients note that the pain radiates to the ear, jaw, and back of the head. Within one or two months, symptoms of thyrotoxicosis are observed: irritability, tearfulness, fatigue, palpitations, hot flashes, sweating, trembling, tremor, weight loss. Patients become excitable, restless, absent-minded, do not tolerate stuffiness and noise.
The thyrotoxic stage is replaced by the euthyroid stage, the symptoms of hyperthyroidism are reduced. The pain of the gland persists, but the general well-being of patients improves. A few weeks later, transient hypothyroidism occurs. Its severity and duration vary, some patients have no symptoms, as the gland quickly compensates for hormone deficiency. With the expanded stage of hypothyroidism, chilliness and a decrease in body temperature are determined. There are swelling around the eyes, shortness of breath, increased drowsiness, slow down the processes of thinking.
Complications
Prolonged course of subacute thyroiditis without adequate medication depletes the thyroid gland. A decrease in the activity of her cells is manifested by persistent hypothyroidism. In patients, metabolism slows down, heart rate decreases, myxedema develops, hypotension, and jaundice of the skin appears. The risk of early atherosclerosis, heart failure, gallstone disease increases. To maintain the normal concentration of hormones, constant hormone replacement therapy is required. 2% of patients are diagnosed with relapses of the disease. The recurrence of symptoms may occur 10-20 years after recovery.
Diagnostics
The examination is carried out by an endocrinologist. The presumptive diagnosis is established on the basis of anamnesis and clinical picture: symptoms appear after an infectious disease, the temperature remains stably elevated, the gland is dense, enlarged and painful during palpation, the pain is local or diffuse, the skin above the gland is hyperemic, the nearby lymph nodes are not enlarged. At the second stage of diagnostics, instrumental and laboratory tests are performed. Their results allow us to confirm the diagnosis of subacute thyroiditis, differentiate it with diffuse toxic goiter, autoimmune thyroiditis, oncopathology, tuberculous inflammation of the gland, fungal infection, neck phlegmon, otitis media, acute pharyngitis. The following methods are used:
- Echography. Ultrasound of the thyroid gland is characterized by an increase in the size of the organ, a zone of reduced echogenicity in one or two lobes. Sometimes migrating zones or diffuse hypoechogenicity are determined.
- Thyrooscintigraphy. In the first phase of the disease, the results of thyroid scintigraphy indicate low absorption or complete absence of capture of radioactive iodine. The focus of inflammation is displayed as a “cold” area. In the phase of hypothyroidism, the absorption of iodine increases dramatically.
- Blood test. According to the test results, there is a sharp increase in ESR, an increased level of lymphocytes, a relatively low level of neutrophilic leukocytes, increased indicators of fibrinogen, liver enzymes, immunoglobulins. The concentration of C-reactive protein is consistently high at the initial stage.
- Analysis for thyroid hormones. In the thyrotoxic stage, the number of bound fractions of triiodothyronine (T3), thyroxine (T4) increased, the level of thyroid-stimulating hormone (TSH) in the blood decreased. With the development of transient hypothyroidism, T4 and T3 indicators are below normal.
- Antibody test. An increase in the titer of antibodies to thyroglobulin (ab-TG) and thyroperoxidase (ab-TPO) may be detected in the blood serum. The values peak in the first weeks of the disease, after a few months the antibodies disappear.
- Fine needle aspiration biopsy. According to histological examination, lymphocytic infiltration, giant cell infiltration, follicle ruptures are detected. Cytological analysis confirms the predominance of neutrophils and giant cells (polynuclear macrophages), the presence of epithelioid cells.
- A test with glucocorticoids. A characteristic feature of the granulomatous form of thyroiditis is the disappearance of pain syndrome 12-48 hours after the first intake of glucocorticoids. If the pain persists for more than 3 days, the diagnosis is questioned.
Treatment
Drug therapy is carried out aimed at eliminating the infectious and inflammatory process, restoring the normal level of thyroxine, triiodothyronine, relief of pain. Therapeutic measures are aimed at improving the current state of health and preventing relapses. Patients are prescribed drugs of the following groups:
- Glucocorticoids. Synthetic glucocorticosteroids have a pronounced anti-inflammatory effect, effectively eliminate pain and symptoms of intoxication, suppress the formation of antibodies. The dosage is selected individually, adjusted throughout the treatment, depending on the change in the patient’s well-being, ESR indicators. The average duration of the course is 1.5–2 months, with a tendency to relapse – 4-6 months.
- NSAIDs. Nonsteroidal anti-inflammatory drugs prevent the synthesis of pro-inflammatory prostaglandins, thereby reducing inflammation, have an analgesic effect and immunosuppressive effect. NSAIDs are often prescribed for mild forms of the disease, a moderate increase in ESR and focal lesions of the gland.
- Beta-blockers. Medications of this group are indicated at the first stage for the relief of thyrotoxicosis manifestations. Beta-blockers eliminate the symptoms of tachycardia, stimulate the transition of thyroxine to the inactive form of triiodothyronine.
- Thyroid medications. Treatment with synthetic thyroid hormones begins a month after the start of the use of glucocorticoids, when the manifestations of hyperthyroidism are reduced. The use of medications can reduce autoimmune lesions, normalize the consistency of the gland tissue, and reduce the severity of hypothyroidism.
- Local anti-inflammatory drugs. Local treatment includes application of gels and ointments to the thyroid gland area. Semi-alcoholic compresses, dry heat, electroregulation of a glucocorticoid drug are also used.
Prognosis and prevention
Subacute thyroiditis lasts 2-3 months, and then in most cases it is completely cured. Destructive changes and relapses are rare, so the prognosis is regarded as favorable. Prevention should be aimed at prevention, timely diagnosis and proper treatment of viral diseases. It is necessary to carry out measures that increase the body’s resistance to infections: hardening procedures, vitamin therapy, proper nutrition and optimal physical activity. If symptoms of infection are detected, you should immediately seek medical help, strictly adhere to the prescriptions of the attending physician.
Literature
- Thyroid diseases: A Practical guide/ Valdina E.A. – 2006.
- Clinical features of the course of subacute thyroiditis and modern methods of its treatment: Abstract of the dissertation/ Al-Jadri M. Ya. – 2008.