Postpartum thyroiditis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
The exact pathogenesis of postpartum thyroiditis is not fully understood. However, studies have shown that it is an autoimmune disorder in which thyroid tissue antigens are recognized as non-self-antigens and our immune cells mediate inflammatory response to thyroid gland and destroy it, then lead to sudden release of stored thyroid hormone in blood and appearance of clinical and laboratory hyperthyroid picture transiently followed by recovery to euthyroid state or hypothroid state depending on level of destruction of thyroid gland, persistence of inflammatory state, and recovery strength of gland. Studies have also shown that pregnancy is stage of reduced immunity to protect fetus from unwanted exposure of immunity which at the end of pregnancy escalate sudden immunity, leading to beginning of slowly evolving autoimmune response to thyroid auto-antigens, in apid sequences and appearance of thyroiditis. Studies are going on in search of exact autoantibody and autoantigens triggering an autoimmune response, which correlates with a clinical and pathological picture of postpartum thyroiditis. TPO autoantibody is significantly linked to occurrence of postpartum thyroiditis.
Pathophysiology
Pathogenesis
Physiology:
- Thyroid is endocrine gland which synthase and secretes thyroid hormones in bloodstream directly. It is regulated by hypothalamus and pituitary gland. Thyroid hormones are of two biochemical structures. , triiodothyronine (T3), which is true and potent form and its prohormone, thyroxine (T4) majorly is secretory form later converted to T3 in peripheral tissues by deiodinase enzyme. Thyroid hormones has negative feedback on thyroid receptors located on hypothalamus and pituitary gland. Thyroid hormones majorly effects every part of body and maintains metabolic rate by acting on thyroid receptors which are nuclear receptors mediating gene expression. Functional unit of thyroid gland is thyroid follicles, which are aliened in continuous circular form forming hallow cavity between them called thyroid cavity. On basal side of thyroid follicle is connective tissue containing blood vessels for transport of thyroid hormone and blood cells and iodine. Apical side of thyroid follicle faces toward thyroid cavity where it has TPO enzymes located, which help in conversion of iodide to iodine. Iodine is organified to tyrosine residue of thyroglobin, which is synthesized and stored in thyroid follicle cavity. It forms mono-idodo or di-iodo thyroglobin and then they combine to form tri-iodo or trata-iodo thyroglobin. On demand of body thyroglobin goes in proteolysis and release T3,T4 in blood stream across thyroid follicle.
Pathogensis:
- Pregnancy is challenging for body immune system to accept alloantigen of paternal origin. It is overcome by dormant set of regulatory T cells PMID: 24996040 cd25 cd 4 positive, a subset of T helper cell, which withholds T cell sensitization to fetal antigens PMID: 28618983 PMID: 21314851. However it does not suppress immunity but modulates towards fetal alloantigen. In fact, successful implantation of fetus in uterine cavity requires adequate NK cell, dendritic cell, macrophages, T cell, and B cells. PMC3025805. Subsequently after delivery on first day there is significant decline in T reg cells and this elevates CD4 T cells and so forth immune and autoimmune responses to foreign and self-antigens. PMID: 28618983.
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis it hs rer sermblance to Hishimoto thyriodtis but less degree of fibrosis and atrophy , [feature1], [feature2], and [feature3] are characteristic findings of [disease name].