Hashimoto’s thyroiditis

“ Hashimoto ‘s disease ” redirects here. For the brain disorder, see Hashimoto ‘s brain disorder Autoimmune disease

medical condition

Hashimoto’s thyroiditis, besides known as chronic lymphocytic thyroiditis and Hashimoto’s disease, is an autoimmune disease in which the thyroid gland gland is gradually destroyed. [ 1 ] [ 6 ] early on on, symptoms may not be noticed. [ 1 ] Over time, the thyroid may enlarge, forming a painless goiter. [ 1 ] Some people finally develop hypothyroidism with accompanying system of weights amplification, fatigue, stultification, depression, hair loss, and cosmopolitan pains. [ 1 ] After many years the thyroid typically shrinks in size. [ 1 ] Potential complications include thyroid gland lymphoma. [ 2 ] furthermore, because it is coarse for untreated patients of Hashimoto ’ south to develop hypothyroidism, far complications can include, but are not limited to, high cholesterol, heart disease, heart failure, high blood atmospheric pressure, myxedema, and electric potential pregnancy problems. [ 7 ] Hashimoto ‘s thyroiditis is thought to be due to a combination of genic and environmental factors. [ 4 ] Risk factors include a family history of the discipline and having another autoimmune disease. [ 1 ] Diagnosis is confirmed with lineage tests for TSH, T4, and antithyroid autoantibodies. [ 1 ] other conditions that can produce similar symptoms include Graves ’ disease and nonpoisonous nodular goiter. [ 5 ] Hashimoto ‘s thyroiditis is typically treated with levothyroxine. [ 1 ] [ 8 ] If hypothyroidism is not present, some may recommend no treatment, while others may treat to try to reduce the size of the goiter. [ 1 ] [ 9 ] Those affected should avoid eating large amounts of tincture of iodine ; however, sufficient iodine is required particularly during pregnancy. [ 1 ] Surgery is rarely required to treat the goiter. [ 5 ] Hashimoto ‘s thyroiditis affects about 5 % of Caucasians at some point in their lives. [ 4 ] It typically begins between the ages of 30 and 50 and is much more coarse in women than men. [ 1 ] [ 3 ] Rates of the disease appear to be increasing. [ 5 ] It was first base described by the japanese doctor Hakaru Hashimoto in 1912. [ 10 ] In 1957, it was recognized as an autoimmune disorder. [ 11 ]

Signs and symptoms [edit ]

many symptoms are attributed to the development of Hashimoto ‘s thyroiditis. The most coarse symptoms include : fatigue, weight gain, pale or puffy face, feeling cold, joint and muscle pain, stultification, dry and thinning hair, heavy menstrual menstruate or irregular periods, depression, panic disorder, a decelerate heart rate, and problems getting fraught and conserve pregnancy. [ 12 ] Hashimoto ’ mho disease is about seven times more common in women than in men. It can occur in teens and young women, but more normally appears in in-between age, peculiarly for men. People who develop Hashimoto ’ second disease much have family members who have thyroid or other autoimmune diseases, and sometimes have other autoimmune diseases themselves. [ 13 ] The thyroid gland may become firm, large, and lobulated in Hashimoto ‘s thyroiditis, but changes in the thyroid can besides be nonpalpable. [ 14 ] Enlargement of the thyroid is due to lymphocytic percolation and fibrosis, rather than tissue hypertrophy. While their character in the initial destruction of the follicles is indecipherable, antibodies against thyroid peroxidase or thyroglobulin are relevant, as they serve as markers for detecting the disease and its badness. [ 15 ] They are thought to be the secondary coil products of the T cell -mediated destruction of the gland. [ 16 ] It is besides characterized by invasion of the thyroid gland tissue by leukocytes, chiefly T-lymphocytes. A rare but unplayful complicatedness is thyroid lymphoma, generally the B-cell character, non-Hodgkin lymphoma. [ 17 ]

hazard factors [edit ]

The strong familial component is borne out in studies on monozygotic twins, with a harmony of 38–55 %, with an even higher concordance of circulating thyroid gland antibodies not in relation to clinical presentation ( up to 80 % in monozygotic twins ). Neither result was seen to a alike degree in dizygotic twins, offering potent favor for high genetic etiology. [ 18 ]

Medications that influence thyroid serve [edit ]

Certain medications or drugs have been associated with interpolate and interfering with thyroid serve. Of these drugs, there are two independent mechanisms of hindrance that they can have. One of the mechanisms of noise is when a drug alters thyroid hormone serum transfer proteins. [ 19 ] Estrogen, estrogen antagonist, heroin, methadone, clofibrate, 5-flurouracile, mitotane, and perphenazine all increase thyroid binding globulin ( TBG ) assiduity. [ 19 ] Androgens, anabolic steroids such as danazol, glucocorticoids, and slow unblock nicotinic acid all decrease TBG concentrations. Furosemide, fenoflenac, mefenamic acid, salicylates, diphenylhydantoin, diazepam, sulphonylureas, barren fatty acids, and heparin all interfere with thyroid hormone dressing to TBG and/or transthyretin. The other mechanism that medications can utilize to interfere with thyroid function would be to alter extra-thryoidal metabolism of thyroid hormone. Propylthiouracil, glucocorticoids, propanolol, iondinated contrast agents, amiodarone, and clomipramine all inhibit conversion of T4 and T3. [ 19 ] Phenobarbital, rifampin, diphenylhydantoin and carbamazepine all increase hepatic metabolism. [ 19 ] Finally, cholestryamine, colestipol, aluminum hydroxide, ferric sulfate, and sucralfate are all drugs that decrease T4 concentration or enhance body waste. [ 19 ]

HLA genes [edit ]

The beginning gene locus associated with autoimmune thyroid disease was major histocompatibility complex ( MHC ) region on chromosome 6p21. It encodes HLAs. Specific HLA alleles have a higher affinity to autoantigenic thyroid peptides and can contribute to autoimmune thyroid disease development. specifically, in Hashimoto ’ randomness disease, aberrant construction of HLA II on thyrocytes has been demonstrated. They can present thyroid autoantigens and initiate autoimmune thyroid disease. [ 20 ] Susceptibility alleles are not consistent in Hashimoto ’ randomness disease. In Caucasians, versatile alleles are reported to be associated with the disease, including DR3, DR5 and DQ7. [ 21 ] [ 22 ]

CTLA-4 genes [edit ]

This gene is the second base major immune-regulatory gene related to autoimmune thyroid gland disease. CTLA-4 gene polymorphisms may contribute to the reduced inhibition of T-cell proliferation and increase susceptibility to autoimmune response. [ 23 ] CTLA-4 is a major thyroid autoantibody susceptibility gene. A linkage of the CTLA-4 region to the presence of thyroid autoantibodies was demonstrated by a whole-genome linkage analysis. [ 24 ] CTLA-4 was confirmed as the main locus for thyroid autoantibodies. [ 25 ]

Protein tyrosine phosphatase nonreceptor-type 22 gene [edit ]

PTPN22 is the most recently identified immune-regulatory gene associated with autoimmune thyroid disease. It is located on chromosome 1p13 and expressed in lymphocytes. It acts as a negative regulator of T-cell energizing. mutation in this gene is a gamble gene for many autoimmune diseases. Weaker T-cell signal may lead to impair thymic deletion of autoreactive T cells, and increased PTPN22 affair may result in inhibition of regulative T cells, which protect against autoimmunity. [ 26 ]

Immune-related genes [edit ]

IFN-γ promotes cell-mediated cytotoxicity against thyroid gland. Mutations causing increase product of IFN-γ were associated with the severity of hypothyroidism. [ 27 ] Severe hypothyroidism is associated with mutations leading to lower production of IL-4 ( Th2 cytokine suppressing cell-mediated autoimmunity ), [ 28 ] lower secretion of TGF-β ( inhibitor of cytokine production ), [ 29 ] and mutations of FoxP3, an necessity regulative component for the Tregs development. [ 30 ] Development of Hashimoto ’ s disease was associated with mutant of the gene for TNF-α ( stimulator of the IFN-γ production ), causing its higher concentration. [ 31 ] preventable environmental factors, including eminent iodine intake, selenium insufficiency, and infectious diseases and sealed drugs, have been implicated in the development of autoimmune thyroid gland disease in genetically predisposed individuals. [ 32 ]

tincture of iodine [edit ]

excessive tincture of iodine intake is a well-established environmental factor for triggering thyroid autoimmunity. A higher preponderance of thyroid autoantibodies is in the areas with higher iodine provision. several mechanisms by which tincture of iodine may promote thyroid autoimmunity have been proposed. Iodine vulnerability leads to higher iodination of thyroglobulin, increasing its immunogenicity by creating new iodine-containing epitopes or exposing cabalistic epitopes. It may facilitate presentation by APC, enhance the binding affinity of the T-cell receptor, and activating specific T-cells. [ 33 ] iodine exposure has been shown to increase the level of reactive oxygen species. They enhance the formulation of the intracellular adhesiveness molecule-1 on the thyroid follicular cells, which could attract the immunocompetent cells into the thyroid gland. [ 34 ] Iodine is toxic to thyrocytes since highly reactive oxygen species may bind to membrane lipids and proteins. It causes thyrocyte damage and the free of autoantigens. Iodine besides promotes follicular cellular telephone apoptosis and has an influence on immune cells ( augment maturation of dendritic cells, increased number of T cells, stimulated B-cell immunoglobulin production ). [ 35 ] [ 36 ] Data from The danish Investigation of Iodine Intake and Thyroid Disease shows that within two cohorts ( males, females ) with centrist and mild tincture of iodine insufficiency, the levels of both thyroid peroxidase and thyroglobulin antibodies are higher in females, and prevalence rates of both antibodies increase with age. [ 37 ]

sex [edit ]

Study of goodly Danish twins divided to three groups ( monozygotic and dizygotic lapp sex, and antonym sex twin pairs ) estimated that genetic contribution to thyroid peroxidase antibodies susceptibility was 61 % in males and 72 % in females, and contribution to thyroglobulin antibodies susceptibility was 39 % in males and 75 % in females. [ 38 ] The high female predominance in thyroid autoimmunity may be associated with the X chromosome. It contains sex and immune-related genes creditworthy for immune tolerance. [ 39 ] A higher incidence of thyroid gland autoimmunity was reported in patients with a higher rate of X chromosome monosomy in peripheral white blood cells. [ 40 ] Another potential mechanism might be skewed X-chromosome inactivation, leading to the escape of x-linked self-antigens from presentation in the thymus and loss of T-cell tolerance. [ citation needed ] Having other autoimmune diseases is a risk factor for developing Hashimoto ’ south thyroiditis, and the opposite is besides true. [ 1 ] Autoimmune diseases most normally associated to Hashimoto ’ s thyroiditis include celiac disease, type 1 diabetes, vitiligo, and alopecia. [ 41 ] The genes implicated change in different ethnic groups and the incidence is increased in people with chromosomal disorders, including Turner, Down, and Klinefelter syndromes normally associated with autoantibodies against thyroglobulin and thyroperoxidase. liberal depletion of these cells as the cytotoxic immune response leads to higher degrees of primary coil hypothyroidism, presenting with low T3/T4 levels, and compensatory elevations of TSH. [ citation needed ]

Pathophysiology [edit ]

multiple mechanisms by which the pathology of Hashimoto ‘s thyroiditis develops have been suggested. versatile autoantibodies may be present against thyroid gland peroxidase, thyroglobulin and TSH receptors, although a little share of people may have none of these antibodies present. As indicated in diverse counterpart studies, a percentage of the population may besides have these antibodies without developing Hashimoto ‘s thyroiditis. Nevertheless, antibody-dependent, cell-mediated cytotoxicity is a substantial factor behind the apoptotic fall-out of Hashimoto ‘s thyroiditis. activation of cytotoxic T-lymphocytes ( CD8 + T-cells ) in reception to cell-mediated immune response affected by helper T-lymphocytes ( CD4 + T-cells ) is central to thyrocyte destruction. As is characteristic of type IV hypersensitivities, recruitment of macrophages is another impression of the benefactor T-lymphocyte activation, with Th1 axis lymphocytes producing incendiary cytokines within thyroid tissue to far macrophage energizing and migration into the thyroid gland gland for direct consequence. [ citation needed ] Gross morphologic changes within the thyroid gland are seen in the general expansion, which is far more locally nodular and irregular than more soft patterns ( such as that of hyperthyroidism ). While the encapsulate is intact and the gland itself is still distinct from surrounding tissue, microscopic examination can provide a more unwrap indication of the degree of damage. [ 42 ] histologically, the hypersensitivity is seen as diffuse parenchymal percolation by lymphocytes, particularly plasma B-cells, which can often be seen as secondary lymphoid follicles ( germinal centers, not to be confused with the normally present colloid-filled follicles that constitute the thyroid ). atrophy of the colloid bodies is lined by Hürthle cells, cells with intensely eosinophilic, farinaceous cytoplasm, a metaplasia from the normal cubelike cells that constitute the lining of the thyroid follicles. Severe thyroid gland atrophy presents much with denser fibrotic bands of collagen that remains within the confines of the thyroid gland ejection seat. [ 42 ]

diagnosis [edit ]

Ultrasound image of the thyroid gland ( justly lobe longitudinal ) in a person with Hashimoto thyroiditis diagnosis is normally made by detecting elevated railway levels of antithyroid peroxidase antibodies in the serum, but seronegative ( without circulating autoantibodies ) thyroiditis is besides possible. [ 43 ] Given the relatively nonspecific symptoms of initial hypothyroidism, Hashimoto ‘s thyroiditis is often misdiagnosed as low, cyclothymia, premenstrual syndrome, chronic tire syndrome, fibromyalgia, and less frequently, as erectile dysfunction or an anxiety disorder. On crude interrogation, a hard goiter that is not painful to the touch much presents ; [ 42 ] other symptoms seen with hypothyroidism, such as periorbital myxedema, depend on the current department of state of progress of the answer, particularly given the normally gradual development of clinically relevant hypothyroidism. Testing for thyroid-stimulating hormone ( TSH ), release T3, free T4, and the antithyroglobulin antibodies ( anti-Tg ), antithyroid peroxidase antibodies ( anti-TPO, or TPOAb ) and antimicrosomal antibodies can help obtain an accurate diagnosis. [ 44 ] Earlier judgment of the person may present with lift levels of thyroglobulin owing to transient hyperthyroidism, as ignition within the thyroid gland causes damage to the integrity of thyroid gland follicle storage of thyroglobulin ; TSH secretion from the front tooth pituitary increases in reply to a decrease in negative feedback inhibition secondary to decreased serum thyroid hormones. typically, T4 is the prefer thyroid hormone examination for hypothyroidism. [ 45 ] This exposure of the body to significant amounts of previously isolated thyroid enzymes is thought to contribute to the exacerbation of allowance breakdown, giving raise to the more marked symptoms seen later in the disease. lymphocytic infiltration of the thyrocyte -associated tissues much leads to the histologically significant detect of germinal center development within the thyroid gland. [ citation needed ] Hashimoto ‘s when portray as mania is known as Prasad ‘s syndrome after Ashok Prasad, the psychiatrist who foremost described it. [ 46 ]

treatment [edit ]

Managing hormone levels [edit ]

hypothyroidism caused by Hashimoto ‘s thyroiditis is treated with thyroid hormone successor agents such as levothyroxine, triiodothyronine, or desiccated thyroid gland extract. A tablet taken once a day by and large keeps the thyroid gland hormone levels normal. In most cases, the discussion needs to be taken for the remainder of the person ‘s life. If hypothyroidism is caused by Hashimoto ‘s thyroiditis, the TSH levels may be recommended to be kept under 3.0 thousand IU /l. [ 47 ]

prognosis [edit ]

Overt, symptomatic thyroid gland dysfunction is the most common complication, with about 5 % of people with subclinical hypothyroidism and chronic autoimmune thyroiditis progressing to thyroid failure every year. Transient periods of hyperthyroidism ( over-activity of the thyroid ) sometimes occur, and rarely the illness may progress to broad hyperthyroid Graves ‘ disease with active orbitopathy ( bulging, inflame eyes ). rare cases of hempen autoimmune thyroiditis show with severe shortness of breath and difficulty immerse, resembling aggressive thyroid gland tumors, but such symptoms always improve with operation or corticosteroid therapy. Although basal thyroid B-cell lymphoma affects fewer than one in 1000 persons, it is more likely to affect those with long-standing autoimmune thyroiditis, [ 48 ] as there is a 67 to 80 fold increased risk of developing primary thyroid lymphoma in patients of Hashimoto ’ s thyroiditis. [ 49 ]

epidemiology [edit ]

Hashimoto ‘s thyroiditis disorder is thought to be the most common cause of primary hypothyroidism in North America. [ 42 ] Within person, set, and time descriptive trends of epidemiology, it becomes more well-defined on how Hashimoto ‘s thyroiditis develops in and impacts differing populations .

personal Characteristic Trends [edit ]

overall, Hashimoto ‘s thyroiditis affects up to 2 % of the general population. [ 50 ] About 5 % of Caucasians will develop Hashimoto ‘s at some item in their lives. [ 4 ] In the U.S., it affects fewer African-Americans, but is linked to greater mortality in the african-american population. [ 51 ] It is besides less patronize in asian populations. [ 52 ] About 1.0 to 1.5 in 1000 people have this disease at any time. [ 42 ] It occurs between 8 and 15 times more much in women than in men. Some research suggests a connection to the role of the placenta as an explanation for the sex deviation. [ 53 ] Though it may occur at any historic period, including in children, it is most much observed in women between 30 and 60 years of age. [ 48 ] The highest prevalence from one study was found in the aged members of the community. [ 54 ] Those that already have an autoimmune disease are at greater risk of developing Hashimoto ‘s as the diseases by and large coexist with each other. [ 50 ] Common diseases seen coexisting with Hashimoto ‘s include celiac disease, multiple sclerosis, type 1 diabetes, vitiligo, and arthritic arthritis. congenital hypothyroidism affects 1 in 3500-4000 newborns at parentage and is a version of mental retardant that can be treated if caught early, but can be hard to diagnose given that symptoms are minimal at a young age. [ 54 ] Congenital hypothyroidism is by and large caused by defects of the thyroid gland gland, but for most cases in Europe, Asia, and Africa, the iodine consumption can cause hypothyroidism in newborns .

geographic Influence of Dietary Trends [edit ]

Diets consisting of first gear or high iodine intake determine a population ‘s risk of developing thyroid-related disorders. [ 55 ] It is more coarse in regions of high tincture of iodine dietary intake, and among people who are genetically susceptible. [ 48 ] Geography plays a bombastic function in which regions have access to diets with low or high iodine. Iodine levels in both urine and salt should be heavy monitored in decree to protect at-risk populations from developing hypothyroidism. [ 56 ] Geographic trends of hypothyroidism deviate across the world as unlike places have different ways of defining disease and report cases. Populations that are spread out or defined ailing may skew data in unexpected ways. [ 50 ] Iodine Deficiency Disorder ( IDD ) is combated using an increase in tincture of iodine in a person ‘s diet. When a dramatic change occurs in a person ‘s diet, they become more at-risk of developing hypothyroidism and other thyroid gland disorders. Combatting IDD with gamey salt intakes should be done cautiously and cautiously as gamble for Hashimoto ‘s may increase. [ 55 ] If making modifications to one ‘s diet, it is authoritative to use a clinician ‘s discretion to ensure that the dietary changes are the best choice as recommendations can vary person to person .

layman Trends [edit ]

The secular trends of hypothyroidism reveal how the disease has changed over the course of time given changes in engineering and treatment options. even though ultrasound technology and treatment options have improved, the incidence of hypothyroidism has increased according to data focused on the US and Europe. Between 1993 and 2001, per 1000 women, the disease was found varying between 3.9 and 4.89. between 1994 and 2001, per 1000 men, the disease increased from 0.65 to 1.01. [ 54 ] Changes in the definition of hypothyroidism and discussion options modify the incidence and prevalence of the disease overall. discussion using levothyroxine is individualized, and therefore allows the disease to be more manageable with prison term but does not work as a remedy for the disease. [ 50 ]

history [edit ]

besides known as Hashimoto ‘s disease, Hashimoto ‘s thyroiditis is named after japanese doctor Hakaru Hashimoto ( 1881−1934 ) of the medical school at Kyushu University, [ 57 ] who inaugural described the symptoms of persons with struma lymphomatosa, an acute infiltration of lymphocytes within the thyroid, in 1912 in the german journal called Archiv für Klinische Chirurgie. [ 58 ] [ 59 ] This newspaper was made up of 30 pages and 5 illustrations all describing the histological changes in the thyroid tissue. Furthermore, all results in his first study were collected from four women. These results explained the pathological characteristics observed in these women particularly the infiltration of lymphoid and plasma cells angstrom well as the formation of lymphoid follicles with germinal centers, fibrosis, degenerated thyroid gland epithelial cells and leukocytes in the lumen. [ 58 ] He described these traits to be histologically similar to those of Mikulic ‘s disease. Like mentioned above, once he discovered these traits in this new disease, he names the disease struma lymphomatosa. This disease emphasized the lymphoid cellular telephone infiltration and formation of the lymphoid follicles with germinal centers, neither of which had always been previously reported. [ 58 ] Despite Dr.Hashimoto ‘s discovery and publication, the disease was unfortunately not recognized as distinct from Reidel ‘s Thyroiditis which was a coarse disease at that time in Europe. Although many other articles were reported and published by other researchers, Hashimoto ‘s goiter lymphomatosa was only recognized as an early phase of Reidel ‘s thyroiditis in the early 1900s. It was not until 1931 that the disease was recognized as a disease in its own good when researchers Allen Graham et alabama from Cleveland reported its symptoms and presentation in the lapp detail manner as Hakaru. [ 58 ] In 1956, Drs.Rose and Witebsky were able to demonstrate how immunization of certain rodents with extracts of early rodent ‘s thyroid resembled the disease Hakaru and early researchers were trying to describe. [ 58 ] These doctors were besides able to describe anti-thyroglobulin antibodies in blood serum samples from these same animals. later on in the same year, researches from the Middlesex Hospital in London were able to perform human experiments on patients who presented with similar symptoms. They purified anti-thyroglobulin antibody from their serum and were able to conclude that these ghastly patients have an immunological reaction to human thyroglobulin. [ 3 ] From this data, it was proposed that Hashimoto ‘s scrofula could be an autoimmune disease of the thyroid gland gland. In 1957, it was recognized as an autoimmune perturb and was the foremost organ-specific autoimmune disorder identified. [ 11 ] Following this recognition, the lapp researchers from Middlesex Hospital published an article in 1962 in Lancet which ended up including a portrait of Hakaru Hashimoto. [ 58 ] The disease was able to become thus much more well known from that here and now and Hashimoto ‘s disease became to appear more frequently in textbooks. [ citation needed ] Since those discoveries, a number of autoimmune diseases have been able to be discovered with several of them having to do with thyroid-specific antibodies. [ citation needed ]

pregnancy [edit ]

meaning women who are incontrovertible for Hashimoto ‘s thyroiditis may have decreased thyroid gland function or the gland may fail wholly. [ 60 ] If a woman is TPOAb-positive, clinicians can inform her of the risks for herself and her baby if the disease goes untreated. “ thyroid peroxidase antibodies ( TPOAb ) are detected in 10 % of meaning women, ” which presents risks to those pregnancies. [ 60 ] Women who have first gear thyroid function that has not been stabilized are at greater risk of having an baby with : low give birth weight, neonatal respiratory distress, hydrocephalus, hypospadias, miscarriage, and preterm delivery. [ 60 ] [ 61 ] The embryo transplantion rate and successful pregnancy outcomes are improved when Hashimoto ‘s is treated. [ 61 ] Recommendations are to treat fraught women only if they are TPOAb-positive throughout the entirety of their pregnancies and to screen all fraught women for thyroid levels. [ 60 ] Close cooperation between the endocrinologist and obstetrician benefits the woman and the baby. [ 60 ] [ 62 ] [ 63 ] The Endocrine Society recommends screening in fraught women who are considered bad for thyroid autoimmune disease. [ 64 ] Thyroid peroxides antibodies testing is recommended for women who have ever been fraught careless of pregnancy consequence. “ … [ P ] revious pregnancy plays a major role in development of autoimmune overt hypothyroidism in premenopausal women, and the numeral of previous pregnancies should be taken into account when evaluating the risk of hypothyroidism in a new women [ sic ]. ” [ 65 ] hormonal changes and trophoblast expression of key immunomodulatory molecules lead to immunosuppression and fetal allowance. independent players in regulation of the immune reply are Tregs. Both cell-mediated and humoral immune responses are attenuated, resulting in immune allowance and suppression of autoimmunity. It has been reported that during pregnancy, levels of thyroid peroxidase and thyroglobulin antibodies decrease. After giving birth, Tregs quickly decrease and immune responses are re-establish. It may lead to the happening or aggravation of the autoimmune thyroid gland disease. [ 66 ] In up to 50 % of females with thyroid peroxidase antibodies in the early pregnancy, thyroid gland autoimmunity in the postnatal period exacerbates in the phase of postnatal thyroiditis. [ 67 ] Higher secretion of IFN-γ and IL-4, and lower plasma hydrocortisone concentration during pregnancy has been reported in females with postnatal thyroiditis than in healthy females. It indicates that weaker immunosuppression during pregnancy could contribute to the postnatal thyroid gland dysfunction. [ 68 ]

fetal microchimerism [edit ]

several years after the pitch, the chimeric male cells can be detected in the maternal peripheral lineage, thyroid, lung, skin, or lymph nodes. The fetal immune cells in the enate thyroid gland may become activate and act as a trigger that may initiate or exaggerate the autoimmune thyroid disease. In Hashimoto ’ sulfur disease patients, fetal microchimeric cells were detected in thyroid in importantly higher numbers than in healthy females. [ 69 ]

See besides [edit ]

References [edit ]

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