- Also known as chronic lymphocytic/autoimmune thyroiditis
- M/C cause of hypothyroidism in developed countries (inadequate dietary intake of iodine M/C cause worldwide)
- Associated with gastric disorders (10-40% cases): Thyrogastric syndrome: Polyglandular autoimmune syndrome (PAS)
- Thyroid gland develops from the primitive gut, and therefore the thyroid follicular cells share similar characteristics with parietal cells of the same endodermal origin.
Autoimmune thyroid disease (AITD):Prototypical organ-specific autoimmune disease
- Hyperthyroid Graves disease
- Hypothyroid autoimmune thyroiditis
- Subtle subclinical thyroid dysfunctions
In 1912, Dr Hakaru Hashimoto described 4 patients with a chronic disorder of the thyroid, which he termed struma lymphomatosa. The thyroid glands of these patients were characterized by diffuse lymphocytic infiltration, fibrosis, parenchymal atrophy, and an eosinophilic change in some of the acinar cells. Clinical and pathologic studies of this disease have appeared frequently since Hashimoto’s original description. The disease has been called Hashimoto’s thyroiditis, chronic thyroiditis, lymphocytic thyroiditis, lymphadenoid goiter, and recently autoimmune thyroiditis.
- Human Leukocyte Antigen (HLA) Genes
- Cytotoxic T Lymphocyte Antigen-4 (CTLA-4) Gene
- Protein Tyrosine Phosphatase Nonreceptor-Type 22 (PTPN22) Gene
- Thyroglobulin Gene
- Vitamin D Receptor (VDR) Gene
- Cytokine Genes and other Immune-Related Genes
- Female sex: ♀:♂::10:1
- Pregnancy and Postpartum period: Tolerance of the fetal semi-allograft during pregnancy is enabled by the state of immunosuppression which is a result of hormonal changes and trophoblast expression of key immunomodulatory molecules. The pivotal players in regulation of the immune response are Tregs, which rapidly increase during pregnancy. Postpartum rapid decrease of Tregs and re-establishment of the immune response to the pre-pregnancy state may lead to the occurrence or aggravation of the autoimmune thyroid disease.
- Fetal Microchimerism (28-83% cases): Presence of fetal cells in maternal tissues which are transferred in the maternal circulation during pregnancy. The fetal immune cells, settled in the maternal thyroid gland, may become activated in the postpartum period when the immunotolerance ceases, representing a possible trigger that may initiate or exaggerate the autoimmune thyroid disease.
- Excessive iodine intake
- Drugs: Interferon α (IFN-α), lithium, amiodarone
- Infection: Hepatitis C, parvovirus, rubella, herpes simplex virus, Epstein Barr virus, and HTLV type 1
- Chemicals: Polyaromatic hydrocarbons or polyhalogenated biphenyls
PathophysiologyIntrathyroidal lymphocytic (T-cell) infiltration followed by a gradual destruction and fibrous replacement of the thyroid parenchymal tissue which may lead to subclinical or overt hypothyroidism.
- Thyroid peroxidase (TPO): TPO antigen, located at the apical membrane of the thyrocyte, is essential for thyroid hormone synthesis, catalysis of iodine oxidation, iodination of tyrosine residues in Tg, and coupling of the iodothyronine into thyroxine (T4) and triiodothyronine (T3).
Classically, the disease occurs as painless, diffuse enlargement of the thyroid gland in a young or middle-aged woman. It is often associated with hypothyroidism.
- Thyroid MALToma
- Diffuse large B-cell lymphoma (DLBCL)
Diagnosis is made by the finding of a diffuse, smooth, firm goiter in a young woman, with strongly positive titers of TG Ab and/or TPO Ab and a euthyroid or hypothyroid metabolic status.
Serology:Low total T4 or free T4 level in the presence of an elevated TSH level confirms the diagnosis of primary hypothyroidism.
- ↑ Thyroid-stimulating hormone (TSH) (best initial test)
- ↓ Thyroxine (T4) levels (T3 levels have no place in the diagnosis of hypothyroidism)
- ↑ Anti-thyroid peroxidase (anti-TPO) antibodies (90%)
- ↑ Antithyroglobulin (anti-Tg) (80%) and TSH receptor-blocking antibodies (TBII)
Needle biopsy (M/accurate test) & ultrasound (USG):
Fluorescent thyroid scan:
- Graves’ disease
- Nontoxic nodular goiter
Life-long disorder with no cure.
Thyroid hormone replacement agents:
- Levothyroxine (DOC)
- Desiccated thyroid extract