I haven't dealt with Hashimoto's in my practice as it is pretty rare in children. I looked it up in uptodate.com as I could use a refresher anyway. From current data and guidelines there is no way to stop or reverse the process of thyroid damage. The only long term treatment plan is to monitor TSH/Free T4 over time and once/if you become hypothyroid you then take thyroxine to replace the thyroid hormone your body can no longer make.
Here is the summary from the text:
SUMMARYHashimoto's thyroiditis is characterized clinically by gradual thyroid failure, with or without goiter formation, due primarily to autoimmune-mediated destruction of the thyroid gland involving apoptosis of thyroid epithelial cells. (See
'Introduction' above.)
The two major forms of Hashimoto's thyroiditis are goitrous autoimmune thyroiditis and atrophic autoimmune thyroiditis (often called primary myxedema), with the common pathologic feature being lymphocytic infiltration and follicular destruction (
picture 1) and the common serological feature being the presence of high serum concentrations of antibodies to thyroid peroxidase (TPO) and thyroglobulin (Tg) (
table 1). (See
'Clinical characteristics' above.)
The usual course of Hashimoto's thyroiditis is gradual loss of thyroid function. Among patients with this disorder who have mild (subclinical) hypothyroidism, exhibited as slight increases in thyroid-stimulating hormone (TSH) and the presence of thyroid antibodies, overt hypothyroidism occurs at a rate of approximately 5 percent per year. Overt hypothyroidism, once present, is permanent in nearly all cases, except in some children and postpartum women in whom it is often transient. (See
'Clinical characteristics' above.)
B cells from thyroid tissue of patients with Hashimoto's thyroiditis are activated, as indicated by their ability to secrete thyroid antibodies spontaneously in vitro. T cells in patients with Hashimoto's thyroiditis react with processed thyroid antigens and peptides derived from these antigens. These activated T cells secrete cytokines which themselves activate a variety of other immune cells. T cells have three major roles in this disease: a role in antibody production (a Th2 type of function), a role in the apoptotic destruction of thyroid cells by activating cytotoxic T cells (a Th1 function), and a role in immunoregulation (Treg cells) (
table 2). (See
'Role of B cells'above and
'The role of T cells' above.)
Several mechanisms have been proposed for the pathogenesis of Hashimoto's thyroiditis. These include molecular mimicry and bystander activation including the involvement of thyroid cell expression of human leukocyte antigens (HLAs) and activation of thyroid cell apoptosis by a Fas ligand-Fas interaction (
table 3). (See
'Potential mechanisms of thyroid injury' above.)
The cause of Hashimoto's thyroiditis is thought to be a combination of genetic susceptibility and environmental factors (
table 3). (See
'Genetic susceptibility' above and
'Precipitating factors' above.)
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