What is autoimmune thyroid disease

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Skip to main content. Hormonal system endocrine. Home Hormonal system endocrine. Thyroid - Hashimoto's disease. Actions for this page Listen Print. Summary Read the full fact sheet.

On this page. The symptoms and signs vary depending on individual factors including the severity of the condition, but may include: Unrelenting fatigue Feeling the cold Constipation Swollen face Dry, coarsened skin Dry hair that is prone to breakage, hair loss Voice changes, such as persistent hoarseness Fluid retention oedema Sudden weight gain that cannot be explained by dietary or lifestyle changes High blood cholesterol Stiff and tender joints, particularly in the hands, feet and knees Cognitive changes, such as depression or forgetfulness Enlargement of the thyroid gland goitre In women, heavy menstrual bleeding menorrhagia.

The steps in the process are: The chain of command begins at the hypothalamus, which prompts the pituitary gland to make a chemical called thyroid-stimulating hormone TSH.

The immune system creates antibodies that attack thyroid tissue. In response, the pituitary gland secretes more thyroid-secreting hormone TSH. The thyroid may enlarge goitre as it attempts to obey the pituitary gland.

Current theories include: Some type of microbe, such as a bacterium or virus, may prompt the immune system to attack the thyroid. A genetic defect may trigger the immune response. Genetic factors may play an important role, since women are more commonly affected. Patients with subacute granulomatous thyroiditis presumed to be a viral infection and congenital rubella may have thyroid antibodies for a few months after their illnesses, and the infections could initiate expression of MHC class II molecules in the thyroid gland.

However, neither disorder is known to be commonly followed by chronic thyroiditis although evidence of thyroid autoimmunity may persist [ 64 ]. The proposed mechanisms include induction of immune suppression by nonantigen-specific mechanisms, perhaps due to the effects of cortisol or corticotropin-releasing hormone on immune cells, followed by immune hyperactivity leading to autoimmune thyroid disease [ 58 ].

Another possible explanation for female predominance is skewed X-chromosome inactivation, which was found in 34 percent of female twins with autoimmune thyroid disease and only 11 percent of controls [ 45 , 66 ].

It is possible that the self-antigens on the inactivated X-chromosome might not be expressed sufficiently to allow tolerance. Pregnancy-associated immune suppression is associated with a shift to Th 2 T cells and a shift in cytokine profiles [ 65 ]. A variety of local factors at the immune cell-trophoblast interface are also known to be important modulators of immune function in pregnancy.

The trophoblast cells located in the placenta, and subject to maternal immune surveillance serve as physical barriers between mother and fetus and have been shown to express several immune modulating molecules, such as HLA-G, FasL, and indoleamine 2,3-dioxygenase as well as secreting a variety of cytokines [ 67 ].

HLA-G is one of the members of the MHC class I family and is known to inhibit natural killer cell function and dendritic cell maturation. Fas ligand interacts with Fas antigen and induces apoptotic cell death of fetal antigen-reactive maternal lymphocytes. Indoleamine 2,3-dioxygenase, which catalyzes tryptophane in lymphocytes, has proven to be critical in the maintenance of allogeneic pregnancy in mouse [ 68 ].

Other than these local modulators, progesterone produced by the placenta affects cytokine profiles across the whole maternal immune system. As an example, in China, autoimmune thyroiditis was found in 0.

Following the tragic Chernobyl nuclear accident, the exposed children developed a high frequency of thyroid autoantibodies [ 71 ]. All the evidence suggests that the presence of thyroid antibodies increases the risk of developing thyroid dysfunction [ 4 , 72 ]. Whether background radiation to which we are all exposed has any role in susceptibility to autoimmune thyroid disease is unknown.

In a population-based study of subjects, had an occupational exposure to ionizing radiation, nearly 60 percent of the subjects worked in a nuclear power plant, while the rest were either medical or laboratory workers. Subjects with greater than five years of exposure to ionizing radiation were particularly at high risk [ 73 ]. Fetal cells have been identified within maternal thyroid glands in patients with autoimmune thyroid disease.

To date, however, this remains hypothetical. All forms of thyroid autoimmunity are associated with a lymphocytic infiltrate in the thyroid. These lymphocytes are largely responsible for generating both T- and B-cell-mediated autoreactivity. Other sites such as thyroid draining lymph nodes and bone marrow may also contain thyroid autoreactive lymphocytes in AITD. This most likely triggers expansion of autoreactive T cells and gives rise to the characteristic inflammatory response, and as the disease progresses, thyrocytes are targeted for apoptosis resulting in hypothyroidism.

Thyroid peroxidase TPO antibodies are the key thyroid enzyme catalyzing both the iodination and coupling reaction for the synthesis of thyroid hormone. It is membrane bound and found in the cytoplasm and in high concentration on the apical microvillar surface of thyrocytes. It is of mol wt between to kDa and previously was known as thyroid microsomal antigen [ 75 ].

Multiple T- and B-cell epitopes exist within the molecule, and the antibody response to TPO is restricted at the level of the germ line heavy and light chain variable V region [ 76 ]. Together with thyroglobulin TG antibodies, these are the predominant antibodies in autoimmune hypothyroidism AH.

It is secreted by the thyroid follicular cells into the follicular lumen and stored as a colloid substance within the thyroid follicles. Each TG molecule has around tyrosine residues, a quarter of which are iodinated. These residues couple to for triiodothyronine T3 and thyroxine T4. The sequence of human TG has been determined [ 80 ]. The exact location of T- and B-cell epitopes within TG is uncertain [ 81 ].

They are polyclonal and mainly of IgG class with all four subclasses represented. TSH regulates the cell surface expressions of TPO and TG altering the transcription of these two proteins, possibly at the gene promoter level. It is located on the basal surface of thyroid follicular cells [ 83 ]. In patients with atrophic thyroiditis, the major antibody is the TSH to its receptor, thus preventing stimulation of thyroid cell.

This results in diminished thyroid hormone output, atrophy of thyroid gland, and the clinical state of hypothyroidism [ 83 , 84 ]. Several antibody and cell-mediated mechanisms contribute to thyroid injury in autoimmune thyroid disease. Also the expression of positive effectors of apoptosis and caspases 3 and 8 as well as Bax and Bak appear to be relatively high in thyroiditis samples as compared to controls.

This supports the role for apoptosis inhibitory mechanism. The role of cytokines in the development of autoimmune disorders has also been explained [ 85 ].

This proves the necessary modulatory roles played by the TH1 and TH2 cytokines in the development of autoimmune disorders [ 74 ]. Both of the antibodies show partial restriction to the IgG4 subclass [ 76 ]. TG antibodies usually mediate antibody-mediated cytotoxicity ADCC , whereas TPO antibodies form terminal complement complexes within the thyroid gland.

Cell-mediated injury may be necessary for TPO antibodies to gain access to their antigen and become pathogenic [ 87 ]. This response increases the ability of cytotoxic T cell to mediate lysis. Complement attack initiated via the classic or alternative pathway impairs the metabolic function of thyroid cells and induces them to secrete IL-1, IL-6, reactive oxygen metabolites, and prostaglandins. All of these enhance the autoimmune process [ 90 ].

Diagnosis of AITD is based upon clinical features and supported laboratory investigations. The patient may be euthyroid, hypothyroid, or hyperthyroid depending on the type of disease and the stage of the disease. They can be measured by thyroid receptor assays or bioassays. Thyroiditis and thyroid antibodies are found in a quarter to a third of the patients with thyroid cancer [ 91 ].

Studies have also shown that there is an increased frequency of autoimmune thyroiditis in women with breast cancer [ 93 ]. Endocrine abnormalities have been reported in patients with kidney diseases [ 94 ].

Thyroid dysfunction causes remarkable changes in glomerular and tubular functions, and in electrolyte and water homeostasis [ 95 ]. From a clinical practice viewpoint, it should be mentioned that both hypothyroidism and hyperthyroidism are accompanied by remarkable alterations in the metabolism of water and electrolyte, as well as in cardiovascular function [ 96 ].

Autoimmune thyroid disease occurs as a result of a complex interaction between genetic and environmental factors. The disease occurs due to autoreactive lymphocytes escaping tolerance. Both cell-mediated and humoral responses contribute to tissue injury in autoimmune thyroid disease.

AITD has been associated with neoplasm and kidney disorders. The authors would like to thank all the staff members of the Department of Pathology, Moi Teaching, and Referral Hospital for their assistance during the writing of this review.

Iddah and B. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Iddah 1,2 and B. Academic Editor: D. Received 09 May Accepted 04 Jun Published 26 Jun Abstract Purpose of Review.

Introduction The principal diseases of the human thyroid gland are goiter diffuse or nodular , hyperthyroidism, hypothyroidism, autoimmune thyroiditis, and neoplasm [ 1 ]. Molecular Mimicry Molecular mimicry implies structural similarity between some infectious or other exogenous agent and human proteins, such that antibodies and T cells activated in response to the exogenous agent react with the human protein, in this instance one or more thyroid proteins.

Bystander Activation In order for HLA class II antigen expression and presentation of antigens to be realized, there must be a local insult to initiate the responses.

Radiation Exposure Following the tragic Chernobyl nuclear accident, the exposed children developed a high frequency of thyroid autoantibodies [ 71 ]. Fetal Microchimerism Fetal cells have been identified within maternal thyroid glands in patients with autoimmune thyroid disease.

Autoimmune Features All forms of thyroid autoimmunity are associated with a lymphocytic infiltrate in the thyroid. Autoantibodies Thyroid Peroxidase TPO Antibodies Thyroid peroxidase TPO antibodies are the key thyroid enzyme catalyzing both the iodination and coupling reaction for the synthesis of thyroid hormone.

Mechanism of Thyroid Cell Injury Several antibody and cell-mediated mechanisms contribute to thyroid injury in autoimmune thyroid disease. Autoimmune Thyroid Disease and Neoplasms Thyroiditis and thyroid antibodies are found in a quarter to a third of the patients with thyroid cancer [ 91 ]. Autoimmune Thyroid Disease and Kidney Disorder Endocrine abnormalities have been reported in patients with kidney diseases [ 94 ].

Conclusion Autoimmune thyroid disease occurs as a result of a complex interaction between genetic and environmental factors.

Acknowledgments The authors would like to thank all the staff members of the Department of Pathology, Moi Teaching, and Referral Hospital for their assistance during the writing of this review. References V. View at: Google Scholar N.

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But it can cause these symptoms:. These symptoms may look like other health problems. Always see your healthcare provider for a diagnosis. Your healthcare provider will ask about your medical history and give you a physical exam. You will also have blood tests. These can measure your thyroid hormone levels and check for some antibodies to proteins in the thyroid.

You will not need treatment if your thyroid hormone levels are normal. But Hashimoto's thyroiditis often looks like an underactive thyroid gland. If so, it can be treated with medicine. The medicine replaces lost thyroid hormone. That should stop your symptoms. It can also ease a goiter if you have one. A goiter can cause problems like pain or trouble swallowing, breathing, or speaking.

If these symptoms don't get better, you may need surgery to remove the goiter. Join endocrinologist Paul Ladenson, M. Health Home Conditions and Diseases. Women are about 7 times more likely to have the disease. Hashimoto's thyroiditis sometimes begins during pregnancy. Middle age. Most cases happen between 40 to 60 years of age.

But it has been seen in younger people. The disease tends to run in families.