Thyroid dysfunction was first associated with pregnancy by Dr. W.E.H. Robertson a Newzeland physician who was later awarded the Sir Charles Hastings Prize for his essay in 1946. He diagnosed<unk>  patients with symptoms of Hypothyroidism after pregnancy and their improvement on treatment with thyroid extracts in 1946.There is no established system for the classification of<unk>  but it may be classified according to clinical course into three groups: Transient hyperthyroidism, classic triphasic, and transient/ permanent hypothyroidism. The exact parthenogenesis of<unk>  "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.<unk>  is considered to be sub-acute lymphocytic thyroiditis that occurs due autoimmune response towards thyroid gland in<unk>  period, miscarriage or abortion. The cause of<unk>  is autoimmune disorder. To review risk factors for the development of<unk> , click here.<unk>  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.<unk>  must be differentiated from other causes of thyroiditis, such as De Quervain's thyroiditis, Hashimoto's thyroiditis, Riedel's thyroiditis, and suppurative thyroiditis<unk>  must also be differentiated from other diseases which cause hypothyroidism. As<unk>  may cause transient thyrotoxic symptoms, the diseases causing thyrotoxicosis must also be considered in the differential diagnosis. In 2012, the incidence of<unk>  was estimated to be 1600 to 18200 cases per 100,000 women. Incidence of<unk>  increase with patients having type 1 DM up to 25000 per 100,000 women. In 2012, the prevalence of<unk>  was estimated to be from 1000 to 20000, with a mean prevalence of 5000 cases per 100,000 women. The most potent risk factor in the development of<unk>  are genetic and subsequent pregnancies. Other risk factors include smoking, increase or decreased intake of Iodine, hepatitis C, radiations and medications.
Postpartum thyroiditis
Silent thyroiditis
Toxic multinodular goiter
De Quervain's thyroiditis
Riedel's thyroiditis
Hashimoto's thyroiditis
Thyroid adenoma
Graves' disease