Also called chronic lymphocytic thyroiditis or autoimmune thyroiditis, Hashimoto’s thyroiditis is the most common chronic thyroid disease in the United States. The condition is inherited. It affects approximately 14 million Americans. The prevalence among women is about 7 times more than men. It is characterized by the production of immune cells, as well as autoantibodies by the immune system. These can damage the thyroid, compromising their ability to produce thyroid hormone. As a result, hypothyroidism occurs when the body is unable to produce enough thyroid hormones. Goiters may also form as a result of the thyroid’s enlargement.
Hashimoto first described the disorder in four patients. In these patients, the thyroid glands were characterized by diffuse lymphocytic infiltration, parenchymal atrophy, and fibrosis. Since Hashimoto’s original description, clinical and pathologic studies of the disease have since appeared in the literature. Classically, the disease appears as a diffuse and painless enlargement of the thyroid glands in middle-aged or young women. For many years, the disease was thought to be uncommon. However, it has become one of the most common thyroid disorders.
Although a person may already have Hashimoto’s thyroiditis, the disease may not manifest for many years. The diagnosis only becomes apparent once the thyroid gland enlarges prominently, causing the patient to seek consult. Sometimes, the disease is discovered during routine blood tests. However, when symptoms develop, they are usually experienced as localized pressure on the neck caused by the enlarged thyroid gland or by low levels of thyroid hormone. Thus, the first sign of the disease may be a painless swelling on the lower part of the neck. Over time, the enlargement may become visible, prompting consult. Once the thyroid gland enlarges enough, it causes pressure on surrounding structures, which may cause difficulties in swallowing.
Aside from this, patients with Hashimoto’s thyroiditis may also develop symptoms that are not specific to the disease but are related to hypothyroidism. These include fatigue, forgetfulness, drowsiness, difficulty learning, dry, brittle nails and hair, dry, itchy skin, puffy face, weight gain, sore muscles, increased probability of miscarriages, increased sensitivity to medications, and heavy menstrual flow.
Enlargement of the thyroid caused by Hashimoto’s thyroiditis, as well as hypothyroidism, tends to progress in many patients. This leads to worsening of symptoms over time. Patients with these findings should receive adequate treatment with thyroid hormone. Optimal treatment with thyroid hormone will be able to stop many of the symptoms associated with hypothyroidism. They may also cause shrinkage of the enlarged thyroid gland.
Hashimoto’s thyroiditis is primarily an attack on the immune system. The attacks are particularly aggressive and destructive. Grave’s disease, another autoimmune disease, is similar to Hashimoto’s thyroiditis. The difference is in the characteristics of the immune attack. There are two reported varieties of Hashimoto’s thyroiditis: atrophic and goitrous.
In a number of studies, associations between cytotoxic T cell antigen-4 (CTLA-4) and autoimmune diseases were found. CTLA-4 is a major negative regulator of immune functions associated with T-cells.
With regard to environmental factors, deficient in selenium have been implicated as causes for Hashimoto’s thyroiditis. High iodine intake and pollutants such as tobacco smoke are also causes. Chronic hepatitis C, as well as certain drugs, are implicated in the acquisition of the disease. Long-term exposure to high levels of iodine increases the level of iodination of thyroglobulin. This increases its antigenicity, which leads to autoimmune responses in individuals who are already susceptible to the disease. Selenium deficiency, on the other hand, causes the decreased activity of selenoproteins, raising the concentration of hydrogen peroxide. This promotes inflammation and leads to Hashimoto’s thyroiditis.
The process of autoimmunity and inflammation may be triggered by environmental pollutants such as tobacco smoke, as well as metals, solvents, and polychlorinated biphenyls.
It is clear that there is genetic susceptibility for Hashimoto’s thyroiditis. The disease tends to occur in families, and it sometimes occurs in conjunction with Grave’s disease. The risk for the disease recurring in siblings is greater than 20. In monozygotic twins, the risk of concordance is 30-60%, despite the fact that T cell receptors and antibody V genes may be randomly combined. The disease also occurs with increased frequency in individuals with Turner’s syndrome and Down’s syndrome. In addition, there is a weak association between the occurrence of Hashimoto’s thyroiditis and HLA alleles, such as DR3.
Stress has been identified as a precipitating factor in causing Hashimoto’s thyroiditis. The proposed mechanism for this phenomenon is immune suppression by non-antigen-specific mechanisms. It was proposed that this was due to the effects of cortisol, as a stress hormone, on immune cells.
The disease is more common in females and research suggests that this may be due to skewed X-chromosome inactivation. In addition, there is a marked increased in CD4+CD25+ regulatory T-cells during pregnancy. This leads to the decreased function of both T-cells and B cells. The rebound from this immunosuppression is the proposed mechanism that contributes to their development of postpartum thyroiditis.
Radiation exposure is also a risk factor. For instance, children exposed to the nuclear disaster at Chernobyl were found to have a disproportionately high incidence of thyroiditis. Exposure to ionizing radiation is a risk factor for Hashimoto’s thyroiditis, especially in females.
Patients with untreated hypothyroidism develop sensitivity to drugs. These drugs are common in the form of tranquilizers, barbiturates, and narcotics. Thus, these drugs must be used with caution in these patients. Smoking can also worsen the disease. Susceptibility to infection is another complication, which needs to be addressed by pharmacotherapy. Megacolon, or the abnormal enlargement of the large intestines, is another complication. Psychiatric problems may also occur in the form of psychosis with paranoia.
Infertility is common in patients with severe disease, usually accompanied by an increased risk for miscarriages. Myxedema, a heart disease, can also occur in patients with Hashimoto’s thyroiditis. In this condition, pericardial effusion and dilation cause cardiac enlargement. Although it should be noted, patients with myxedema are usually asymptomatic and the condition resolves after several months.
In untreated hypothyroidism, stressful situations such as surgical operations, cold, and infections may precipitate hypothyroid coma. In the majority of patients, bradycardia, myxedema, and severe hypotension are usually present. In severely hypothyroid elderly patients, myxedematous coma occurs, most often in the winter months. It has a high mortality rate. In addition, hypoglycemia and hyponatremia may also occur, necessitating treatment with saline or glucose.
Making an accurate diagnosis of Hashimoto’s thyroiditis necessitates assessing the metabolic status and identifying the type of lesion present. The thyroid hormone status should be assessed first because it reflects the patient’s glandular function. The presence of goiter is strongly suggestive of Hashimoto’s thyroiditis. Triiodothyronine (T3), thyroid stimulating hormone (TSH), and tetraiodothyronine (T4) levels are usually assessed using laboratory tests to assess the function of the thyroid gland. TSH is reported to be the most sensitive indicator of hypothyroidism. Even after the diagnosis has been made, periodic monitoring of TSH levels is required to assess the progression of the disease and response to treatment.
The presence of antithyroid antibodies is assessed next. The presence of antithyroid peroxidase (ATPO) and antithyroglobulin (TGAB) are correlated with a diagnosis of Hashimoto’s thyroiditis, although the correlation is higher for TGAB than ATPO.
Cytological findings may also be used as an adjunct to diagnostic tests. Lymphocytic infiltration and the presence of Hurtle cells are indicative of Hashimoto’s thyroiditis. In addition, the proportion of these cells is indicative of the severity of the disease. As the disease progresses, the spaces between follicular cells shrink due to the destruction of the colloid. This alters the appearance of the thyroid specimen under fine needle aspiration biopsy.
Radioactive iodine intake (RAIU) is another means of diagnosing the disease. This method is more obtrusive than an ultrasound, which is why the latter is recommended in most cases. Ultrasonography allows the physician to view the anatomic characteristics of the thyroid gland. An ultrasound reading will also reveal major anatomical changes of the thyroid.
The treatment of Hashimoto’s thyroiditis is commonly conducted through medication therapy or surgical resection of the thyroid gland. Any use of medicine must be with the advice of a doctor. The choice of whether to perform surgery or to administer medications depends on the severity of the disease and its presentation.
In patients with documented hypothyroidism, thyroid hormone replacement therapy is instituted. This treatment modality is also indicated in the presence of goiter, granted that the size of the goiter is small and causes minimal pressure on the surrounding structures. The initial dose of thyroid hormone is determined based on the patient’s cardiac function, body mass, co-morbid conditions, and pregnancy status. Thyroid hormone replacement therapy in the form of thyroxine is recommended for all patients with Hashimoto’s thyroiditis as it modifies the course of the disease.
Surgery is recommended if the goiter is unresponsive to thyroxine therapy, if it increases in mass, if malignancy is found or suspected, and if findings on cutting needle biopsy are indeterminate.