Postpartum thyroiditis overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
Historical Perspective
Thyroid dysfunction was first associated to pregnancy by Dr. W.E.H. Robertson, Newzeland physician, latter awarded the Sir Charles Hastings Prize for his essay in 1946. He diagnosed postpartum patients with symptoms of Hypothyroidism after pregnancy and their improvement on treatment with thyroid extracts in 1946.
Classification
There is no established system for the classification of PPT but it may be classified according to clinical course into three groups: Transient hyperthyroidism, Classic Triphasic, and Transient/ Permanent hypothyroidism.
Pathophysiology
The exact pathogenesis of pppostpartum thyroiditis "PPT" 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 hypothyroid 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 rapid sequences and appearance of thyroiditis. Studies are going on in search of exact auto-antibody and auto-antigens triggering an autoimmune response, which correlates with a clinical and pathological picture of postpartum thyroiditis. TPO auto-antibody is significantly linked to occurrence of postpartum thyroiditis.
Causes
PPT is considered to be sub-acute lymphocytic thyroiditis that occurs due autoimmune response towards thyroid gland in postpartum period, miscarriage or abortion. The cause of PPT is autoimmune disorder. To review risk factors for the development of PPT, click here. PPT is caused by a mutation in the G-allele mutation of CD60 CTLA-4 gene and mutation of HLA DR-3. HLA DR-4, and HLA DR-5 gene.
Differentiating Postpartum thyroiditis from Other Diseases
Postpartum thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain's thyroiditis, Hashimoto's thyroiditis, Riedel's thyroiditis, and suppurative thyroiditis. Postpartum thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain's thyroiditis, Riedel's thyroiditis, and suppurative thyroiditis. Postpartum thyroiditis must also be differentiated from other diseases which cause hypothyroidism. As Postpartum thyroiditis may cause transient thyrotoxic symptoms, the diseases causing thyrotoxicosis must also be considered in the differential diagnosis.
Epidemiology and Demographics
In 2012, the incidence of PPT was estimated to be 1600 to 18200 cases per 100,000 women. Incidence of PPT increase with patients having type 1 DM up to 25000 per 100,000 women. In 2012, the prevalence of PPT was estimated to be from 1000 to 20000, with a mean prevalence of 5000 cases per 100,000 women. PPT occurs in women in child bearing age. PPT usually affects individuals of the Mediterranean and Caucasians population race. Mongolian race is usually less affected. The majority of PPT cases are reported Europe and Japan.
Risk Factors
The most potent risk factor in the development of PPT are genetic and subsequent pregnancies. Other risk factors include smoking, increase or decreased intake of Iodine, hepatitis C, radiations and medications.