Related Experiment Video
Updated: May 29, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
Published on: March 17, 2023
[A possible effect of the immunomodulating therapy with beta-interferons and glatimer acetate on the development of
Abstract:
Autoimmune thyroiditis and subclinical hypothyreosis occurred in 20-25% of patients with multiple sclerosis (MS) before the beginning of immunomodulating therapy. No correlation was found between thyroid disease and demographical characteristics (age, sex), type of MS course, rate of disease progression and disability scores on the EDSS. Thyroid disease in patients with MS may be provoked or enhanced by disease-modifying drugs (DMD). Female sex and a history of autoimmune thyroid disease were predict the thyroid gland dysfunction during the therapy with beta-interferons. Clinical thyreotoxicosis is the most dangerous and the therapy should be discontinued. We present the own data on thyroid function in 191 patients managed in the Central administrative okrug of Moscow and in the Moscow Center for Multiple Sclerosis. Thyroid disease was found in 34.6% of patients (the formation of nodes and subclinical hypothyreosis). Changes in the thyroid function were seen in patients treated with beta-interferon and the development of node goiter was found in patients treated with glatimer acetate (copaxon). The dynamics of thyroid gland structure during the treatment with DMD was followed during one year. Beta-interferons provoked the development of hypothyreosis. The study of thyroid gland in MS patients, in particular, those treated with DMD is needed.
Related Concept Videos
Inhibitors of Viral Protein Synthesis
Graves' Disease I: Introduction
Graves Disease II: Pathophysiology
Myasthenia Gravis: Overview and Treatment
These antibodies interfere with the function of the nicotinic receptors in three ways: by binding to the receptor and disrupting acetylcholine binding; by causing cross-linking of receptors which leads...
Hypothyroidism II: Pathophysiology
Hyperthyroidism II: Pathophysiology