Hashimoto Thyroiditis

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Chronic lymphocytic thyroiditis (Hashimoto) is an autoimmune disease closely related to Graves disease [49]. It was first described by Hashimoto [50]

in 1912. Although lymphocyte and cytokine-mediated thyroid destruction predominates in Hashimoto thyroiditis (HT), antibody-mediated thyroid stimulation occurs in Graves disease and overlap may occur in some patients. HT arises from a combination of genetic traits that heighten susceptibility in conjunction with some environmental trigger.

HT occurs in 1% of children and adolescents and is the most common cause of acquired hypothyroidism in the pediatric population [51]. The disease has a predilection for females 4 to 7 times and a family history is present in 30-40% of patients. The prevalence increases with age with the common age of adolescence [52]. HT accounts for many of the enlarged thyroids formerly designated as adolescent or simple goiter [53]. Goiter is present in two thirds of children, resulting from lymphocytic infiltration and from the stimulatory effect of TSH. The remaining one third of children have no goiter [54]. The patients could be euthyroid, hypothyroid or hyperthyroid. Opthalmopathy may occur in HT in the absence of Graves disease [55]. The course is variable. The goiter may become smaller or may disappear spontaneously or it may persist unchanged for years while the patients remain euthyroid. Some euthyroid children acquire hypothyroidism gradually within months or years, and some adolescent patients achieve spontaneous remission. Thyroid function tests are often normal in HT, although the level of TSH may be slightly or moderately elevated in some individuals. Thyroid scintigraphy can be entirely normal, but in most instances the radioiodine uptake is decreased. Early in the course of the disease, increase uptake could be noted. Thyroid ultrasonography shows scattered hypoechogenicity in most patients [56].

Genetic susceptibility is present in HT. Associations have been observed between HT and HLA-DR3, DR4 or DR5 [57, 58]. Familial clusters of HT are common. The incidence in siblings or parents of affected children may be as high as 25% [57]. TPOAbs are demonstrable in the sera of 90% of children with HT. TGAbs occur in a smaller percentage of affected children but much more common in adults. Thyrotropin receptor-blocking antibodies are frequently present especially in hypothyroid HT patients and believed to be the cause of hypothyroidism [51].

HT, a typical organ-specific autoimmune disease, is characterized histologically by lymphocytic infiltration of the thyroid. There is infiltration of lymphocytes and plasma cells between follicles and atrophy and fibrosis of the follicles are present. HT is seen more frequently with type 1 DM, celiac disease, Addison, autoimmune atrophic gastritis, chronic candidiasis and hypoparathyroidism, and juvenile chronic arthritis [59-61]. HT is also associated with certain chromosomal aberrations, in particular Turner, Down and Klinefelter syndromes [51, 53]. Progressive dementia and Hashimoto-related encephalopathy has been reported in some HT patients [62, 63].

Because the disease may be self-limited in some instances, there should be periodic checks in treatment. Untreated patients should also be checked periodically. A TSH level greater than 10 |xU/ml warrants treatment with Na L-T4. The initial dose should be arranged according to the age of the patient (25 |xg/day to 100-150 |xg/day). The goiter may decrease in size as may persist for years. Antibody titers fluctuate in both treated and untreated patients and persist for years.

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