De Quervain's thyroiditis

The Subacute thyroiditis de Quervain is named after the discoverer and describer Fritz de Quervain's disease of the thyroid gland, the cause of which is still largely unclear. Maybe preceding viral infections and genetic predisposition play a role in the development.

The disease starts subacute, that is, within a few days. It is an inflammation of the thyroid, thyroiditis, which is histologically characterized by typical giant cells. The disease is associated with a slightly enlarged thyroid gland usually (goiter ) and pronounced symptoms such as severe pain and difficulty swallowing. The ongoing for several months disease typically runs in phases. First, there is an overactive thyroid (hyperthyroidism ), followed by a short period with normal thyroid function, which is called euthyroid, and then into a period of low thyroid (hypothyroidism ) transitions. During a recovery phase, finally the thyroid function returns to normal and it usually comes to a complete healing.

The diagnosis is made clinically in the context of history, clinical examination and by laboratory parameters. When in doubt, can be secured with the help of a tissue sampling (biopsy) diagnosis. Subacute granulomatous thyroiditis is usually a self-limiting condition, ie it heals without therapeutic measures within one year from. By treatment with anti- inflammatory and pain-relieving drugs the disease and the symptoms can be alleviated.

Synonyms

The disease is also referred as de Quervain's thyroiditis, not to be confused with the named after Fritz de Quervain also Quervain 's disease ( tenosynovitis stenosing de Quervain ). In addition, there are more synonyms for the disease: Subacute non- suppurative thyroiditis, a term that is used to distinguish from the suppurative or acute thyroiditis, giant cell thyroiditis, since typical giant cells characterize the histological picture and subacute granulomatous thyroiditis. Since the cause of infection with viruses is thought designate some medical disease as viral thyroiditis. Very often used as a synonym the term subacute thyroiditis. Since a subacute course but also in other thyroid inflammation occurs, especially in the subacute lymphocytic thyroiditis ( thyroiditis Silent thyroiditis and postpartum ), there can be confusion here.

Epidemiology

The mean age of onset is between 30 and 50 years. Women are 3-5 times more frequently affected than men. Precise information on the epidemiology and in particular the frequency of the disease, there are few. After one of the largest cohort studies, the incidence in Olmsted County, Minnesota in the years 1960 to 1997 4.9 cases per 100,000 population per year. The disease occurs more frequently than at other seasons in the spring.

Causes

The cause of subacute thyroiditis de Quervain is not known. It is likely that inflammation is the result of a viral infection, as did elicit a recent previous infection of the upper respiratory tract in previous studies in most patients. However, a connection with the classical respiratory viral infections ( enterovirus, coxsackie viruses ) could not be shown.

Furthermore, known genetic predispositions for human leukocyte antigens HLA- carrier of B35 and HLA- B67. Individuals who have one of these haplotypes have a - in the case of HLA -B35 up to 50-fold - increased risk of suffering from subacute thyroiditis de Quervain. The HLA -B35 haplotype was detected in more than half of the patients suffering from subacute thyroiditis de Quervain patients in several studies. A familial occurrence has so far been detected only in a few cases. One common assumption is made, the context of the disease with the HLA -B35 haplotype for a contribution from both a viral infection and an autoimmune reaction, ie a reaction of the immune system against their own organism, in this case against the thyroid tissue. Be the underlying mechanism is thought the Molecular mimicry. However, the fact that the subacute thyroiditis de Quervain unlike other autoimmune diseases is self-limiting argues against this hypothesis.

Disease progression and disease

Inflammation leads to a destruction of the thyroid, which is accompanied by a reduction of the thyroglobulin stored therein. The thyroid hormones triiodothyronine (T3) and thyroxine ( T4) the uncontrolled release into the blood. Due to the increased blood concentration of thyroid hormones, the formation of thyrotropin (TSH ) in the pituitary gland (hypophysis ) is inhibited, so that the formation of thyroid hormones is reduced. It comes to the clinical picture of hyperthyroidism. This condition continues until stocks are exhausted of thyroid hormones and ultimately, after a short phase euthyroid with normal thyroid function, leads to an underactive thyroid. Depending on the severity and stage of the disease may thus lead to signs of hyperthyroidism or underactive thyroid, which is why the symptoms of this disease is highly variable.

Independently of the function of the thyroid gland subacute thyroiditis de Quervain is often characterized as a result of the inflammatory response by the presence of pain. These can radiate often be enhanced to the ear and to the lower jaw and pressure on the thyroid camp. Other possible symptoms include malaise, difficulty swallowing, muscle and joint pain and fever.

The disease can last several months. In general, it is also without the use of medication in a complete and spontaneous healing ( self- limiting ). In about five percent of these patients, it may cause permanent hypothyroidism.

Histology

The histological picture of subacute thyroiditis is characterized by a granulomatous inflammation with granuloma formation and the characteristic appearance of giant cells. The granulomas exist alongside the giant cells from cell necrosis and macrophages. As part of the inflammatory response leads to a destruction of the follicular epithelial cells of the thyroid gland and leakage of colloid phagocytosed by giant cells. The granulomas occur only in some places in the thyroid tissue. The remaining thyroid tissue appears intact.

Diagnosis

On clinical examination, a painful pressure thyroid is typical, which may be enlarged asymmetrical.

A suspected or existing enlargement of the thyroid can be confirmed by a thyroid sonography. This reveals a not occurring in inhomogeneous "healthy" thyroid tissue samples, in which hypoechoic and hyperechoic regions alternate. The hypoechoic regions is the inflammation of the disease. Imagine the monitor dark, since they reflect sound worse than normal thyroid tissue (see also examination of the thyroid gland ).

The diagnosis can be supported by the provision of various laboratory parameters in the blood. As a sign of the inflammatory response the inflammation parameters C -reactive protein ( CRP), erythrocyte sedimentation rate (ESR ) and interleukin- 6 (IL -6) is almost always significantly increased. The white blood cell count is normal or slightly elevated (leukocytosis ). The latter is also a sign of active inflammation. Depending on the stage of the disease, thyroid function parameters are changed. In the hyperthyroid phase TSH were decreased and increased thyroid hormones in euthyroid phase, the parameters are within the normal range and in the hypothyroid phase are increased TSH and thyroid hormones decreased. For the differential diagnostic determination of the thyroid specific antibody plays an important role.

If there is doubt about the diagnosis, differential diagnosis comes to the thyroid as well as the fine needle aspiration with subsequent histological examination question. Both methods do not belong in this disease for routine diagnostics and are only in individual cases, especially in atypical course, necessary. The Radioiodaufnahme, which can be measured quantitatively with the thyroid is usually greatly reduced by the inflammation-induced iodine transport disruption and decreased TSH levels. When fine-needle biopsy ( fine needle aspiration ) is sonographically controlled thyroid tissue is removed with a thin needle ( biopsy), which is then examined histologically in pathology.

For comparison, normal echogenicity of the thyroid

Subacute thyroiditis in thyroid scintigraphy: decreased uptake.

Normalization after therapy.

Differential diagnosis should primarily at an acute suppurative thyroiditis, which is usually caused by bacteria. The thyroid gland is also sensitive to pressure. The lymph nodes in the neck are enlarged and also painful. In the laboratory, usually show signs of severe bacterial infection or sepsis. In the thyroid sonography may abscesses can be detected. The skin over the thyroid gland may be flushed. Hashimoto's thyroiditis may also be accompanied by a slightly painful thyroid swelling. The erythrocyte sedimentation rate is not accelerated in this disease and in Schilddrüsensonogramm is usually a continuous hypoechoic thyroid.

Therapy

Treatment is usually symptomatic. We primarily use analgesic and anti-inflammatory substances from the group of non-steroidal anti-inflammatory drugs (NSAIDs ) such as acetylsalicylic acid (ASA ) and ibuprofen. If these drugs for symptomatic treatment is not sufficient, glucocorticoids, primarily used prednisolone for inflammation. Can either the NSAID or with the glucocorticoid therapy pain relief be brought about, the diagnosis must be questioned.

Significant symptoms of hyperthyroidism, such as acceleration of the heart rate ( tachycardia), occur only in a few cases. They can be treated symptomatically with beta-blockers. The antithyroid drugs used in many thyroid functions play no role in the treatment of subacute thyroiditis de Quervain. Even in the most mild hypothyroid phase specific treatment is necessary only in rare cases. An exception exists when the hypothyroid phase is significantly extended. In this case, the substitution of thyroid hormones is indicated. For this purpose, usually L -thyroxine preparations are used.