Silent thyroiditis is a thyroid disease characterized by lymphoid infiltration and an immunodestructive process in glandular tissues. It is manifested by symptoms of transient thyrotoxicosis in the absence of pain syndrome. Patients complain of irritability, fatigue, general weakness, weight loss, palpitations. Diagnostics includes ultrasound and thyroid scintigraphy, blood tests for T4, TSH, anti-TPO. Medical treatment is aimed at eliminating the symptoms of thyrotoxicosis, restoring the balance of hormones (glucocorticoids, NSAIDs, beta-blockers, thyroxine).
ICD 10
E06.1 Subacute thyroiditis
Mening
Silent thyroiditis was isolated in the 1970s and described as occult subacute thyroiditis, transient hyperthyroidism in patients with lymphatic thyroiditis. Currently, most researchers consider it a variant of subacute thyroiditis, less often a form of Hashimoto’s thyroiditis. Synonymous names are silent, mute, sporadic thyroiditis, hyperthyroiditis, transient thyroiditis with hyperthyroidism, silent lymphocytic thyroiditis. Sometimes this type of disease includes a more specific form – postpartum thyroiditis. Epidemiology among all forms of thyrotoxicosis reaches 1%. The prevalence is twice as high among women.
Causes
Etiological factors of silent thyroiditis have not been clarified. Possible causes and mechanisms of the development of this disease continue to be studied. The most common infectious theory of triggering autoimmune reactions affecting the thyroid gland. Viral infections of the upper respiratory tract are considered to be the key cause of the disease. The response of the immune system leads to lymphocytic infiltration of glandular tissues and active synthesis of autoantibodies, under the influence of which the production of thyroid hormones is suppressed.
Pathogenesis
The disease develops as a result of provocation of the activity of the immune system by infectious agents. In clinical endocrinology, this theory is considered as the most probable. Through the lymphatic and blood vessels, viruses enter the thyrocytes. Inside the cells, they produce atypical proteins that are recognized by the immune system as foreign. Inflammatory processes are triggered, the synthesis of autoantibodies to the receptor-TSH and AT-TPO is activated. There is a destruction of follicles and follicular cells of the thyroid gland.
The course of silent thyroiditis has a phase structure. The first phase is hyperthyroid. It is caused by the destruction of follicles, the release of hormones into the bloodstream. It lasts 3-4 months and is replaced by an euthyroid state that persists for 1-1.5 months. This period is characterized by an improvement in the patient’s well-being, reduction of symptoms of the disease. After it comes the phase of hypothyroidism: the functions of the gland decrease, the cellular reserves of hormones run out. Duration – up to 4 months. In the recovery phase, the activity of glandular cells normalizes.
Symptoms
The clinical picture changes according to the phases of the disease. At the initial stage, symptoms of mild and moderate thyrotoxicosis prevail. Patients are irritable and emotionally labile, sleep poorly at night, restless and anxious during the day, get tired and tired quickly. Patients often experience hot flashes, do not tolerate being in the sun or in stuffy rooms. Palpitations are rapid, blood pressure is elevated. Due to the short duration of hyperthyroidism, weight loss and myopathy are rarely observed.
The second phase is asymptomatic. The plasma level of iodine-containing hormones normalizes, patients feel better and at this stage often stop treatment on their own, believing that recovery has come. After 4-6 weeks, hypothyroidism unfolds. The first symptoms are chilliness, drowsiness, and a decrease in blood pressure. There is a slowness of movements, some inhibition of emotional reactions and thought processes. The skin is pale and dry, swelling appears on the face and limbs, headaches occur. During the recovery period, the symptoms are gradually reduced, but the transition of transient hypothyroidism to permanent is possible.
Complications
In the absence of adequate therapy, silent thyroiditis acquires a recurrent course. In many patients, after several episodes of alternating thyrotoxic, euthyroid and hypothyroid phases, permanent hypothyroidism is formed – a persistent decrease in the production of thyroid hormones, requiring constant replacement therapy. A possible complication of silent thyroiditis against the background of acute thyrotoxicosis is cardiovascular insufficiency. Cases are described when patients needed urgent hospitalization in the cardiology department.
Diagnostics
Examination of patients with suspected silent thyroiditis is carried out by an endocrinologist. The nature of complaints depends on the phase of the disease, most often patients seek medical help with the appearance of thyrotoxicosis. They report tachycardia, uncomfortable sensations in the heart, a feeling of heat in the body, irritability, restless sleep. During examination, the size of the thyroid gland is normal or slightly increased, during palpation, sensitivity is reduced. A complex of specific diagnostic procedures is carried out:
- Scintigraphy. Visual analysis of thyroid scintigraphy makes it possible to assess the shape and size of the organ, the intensity of drug accumulation and the features of its distribution. There is a reduced capture of the radiopharmaceutical, a relatively uniform distribution of cold zones.
- Sonography. According to the ultrasound of the thyroid gland, a uniform decrease in echogenicity is determined. When nodular formations are detected, dynamic ultrasound is performed, a fine needle aspiration biopsy followed by cytological examination.
- Blood test. According to the results of the general analysis, increased ESR is detected, sometimes – lymphocytosis, leukopenia, mild anemia. The TSH level is slightly reduced, the concentration of T4 is slightly higher than normal (in the first phase of thyroiditis), the titer of TPO-AT is one and a half times higher than the threshold value.
Differential diagnosis implies the distinction of silent thyroiditis with postpartum thyroiditis, Graves’ disease, Hashimoto’s thyroiditis. In postpartum thyroiditis, the pathogenetic mechanisms and clinical manifestations are similar, but pregnancy and childbirth are the starting point for the development of autoimmune processes. A distinctive feature of basedova disease is increased absorption of iodine radioisotopes by the gland, more persistent and pronounced signs of hyperthyroidism. With Hashimoto’s thyroiditis, there is a motley picture of the scan (uneven capture of the radiopreparation), persistent symptoms of hypothyroidism.
Treatment
Specific methods of therapy have not been developed. Patients are prescribed symptomatic treatment aimed at maintaining normal hormone levels, relieving cardiovascular disorders, reducing the severity of inflammatory processes, inhibiting the autoimmune component, correcting the activity of immune reactions. Drugs of the following groups are used:
- Glucocorticosteroids. Medications reduce the titer of antibodies, eliminate inflammation. The duration of the course of treatment and the dosage are determined individually, depending on the severity of the autoimmune process.
- Beta-blockers. They are used in patients with vivid cardiovascular symptoms. The drugs stop tachycardia, lower blood pressure, enhance the reaction of the transition of active thyroxine to inactive triiodothyronine.
- NSAIDs. Nonsteroidal anti-inflammatory drugs are effective in mild and moderate manifestations of thyroiditis. They suppress inflammation in the glandular tissue, inhibit the activity of the immune system, which slows down the production of autoantibodies.
- Thyroxine preparations. In order to prevent hypothyroidism at the euthyroid stage, a synthetic analogue of thyroxine (L-thyroxine) is administered. In the course of treatment, the serum TSH level is periodically monitored. With the development of persistent hypothyroidism, the timing of hormone replacement therapy increases.
Prognosis and prevention
In most patients, thyroiditis has a favorable outcome, the phases of thyrotoxicosis and hypothyroidism are transient, with proper treatment they do not resume. The incidence of permanent hypothyroidism is less than 2% of cases. Preventive measures have not been developed, since the causes of the disease have not been definitively established. To minimize the risk of the disease, it is necessary to treat infections in a timely manner, especially acute respiratory viral infections, if there is a predisposition to autoimmune pathology of the thyroid gland, regularly undergo preventive examinations.