For long Hashimoto’s thyroiditis has been characterized as a well-defined clinicopathologic entity. Though nowadays it is considered a heterogeneous disease (has several etiologies). There are different variants of Hashimoto thyroiditis:
– fibrous, fibrous atrophic (Ord’s disease), or goitrous forms
– IgG4 thyroiditis
Thyroid autoantibody levels differ between goitrous and atrophic thyroiditis in that inhibitory TSH receptor antibodies are higher in Ord’s thyroiditis. These antibodies block cAMP (a messenger, used for intracellular signal transduction) production as well as TSH-induced DNA synthesis and iodide uptake. Antibody production leads to hypothyroidism because higher levels of antibodies against Tg and TPO accompany deterioration of the thyroid. Destruction of the thyroid gland >90% leads to hypothyroidism.
IgG4-related thyroiditis is more prevalent in males, associated with more frequent subclinical hypothyroidism and higher levels of thyroid autoantibodies. IgG4-thyroiditis should be considered in all patients with an aggressive form of Hashimoto’s thyroiditis. Patients with assumed IgG4-thyroiditis should get blood test for IgG4/IgG ratio. The identification of IgG4-related thyroiditis provides for patient’s treatment with Hashimoto’s and for the development of new therapeutic approaches for this rapidly progressive destructive subtype of Hashimoto thyroiditis.