Women in this phase experience low energy, poor memory, impaired concentration, carelessness, dry skin, cold intolerance, and general aches and pains. After one year postpartum, euthyroid function resumes. Any case with hypothyroid symptoms extending beyond one year postpartum is not considered postpartum thyroiditis.Women who test positive for thyroid antibodies may be at increased risk of developing symptoms associated with postpartum depression than women without thyroid antibodies. Cause
During pregnancy, immunologic suppression occurs which induces tolerance to the presence of the fetus. Without this suppression, the fetus would be rejected causing miscarriage. As a result, following delivery, the immune system rebounds causing levels of thyroids antibodies to rise in susceptible women.Specifically, the immunohistological features of susceptible women are indicated by:
antibodies to thyroglobulin (TgAb)
antibodies to thyroid peroxidase (TPOAb)
increase in TPOAb subclasses IgG1-IgG3
lymphocyte infiltration and follicle formation within thyroid gland (Hashimotos thyroiditis)
T-cell changes (increased CD4:CD8 ratio)
TSH-receptor antibodies (TSH-R Abs)

Diagnosis
This condition is commonly undiagnosed by physicians due to either unfamiliarity with the disease, the subtlety of symptoms, or the attribution of the symptoms to the stresses of having a newborn. Usual screening begins with assessing the thyroid stimulating hormone (TSH) level. A suppressed TSH could represent the hyperthyroid phase, but warrants further testing to investigate for possible Graves disease. A normal TSH with persistent symptoms could represent the shift between phases and requires repeat testing 4–6 weeks later; an elevated TSH at this time could indicate the hypothyroid phase. Treatment
For most women, the hyperthyroid phase presents with very mild symptoms or is asymptomatic; intervention is usually not required.
Causes
DEB is caused by genetic defects (or mutations) within the human COL7A1 gene encoding the protein type VII collagen (collagen VII). DEB-causing mutations can be either dominant or recessive. Most families with family members with this condition have distinct mutations.Collagen VII is a very large molecule (300 kDa) that dimerizes to form a semicircular looping structure: the anchoring fibril. Anchoring fibrils are thought to form a structural link between the epidermal basement membrane and the fibrillar collagens in the upper dermis. Pathophysiology
In the absence of mutations of the COL7A1 gene, an autoimmune response against type VII collagen can result in an acquired form of epidermolysis bullosa called epidermolysis bullosa acquisita.There exist other types of inherited epidermolysis bullosa, junctional epidermolysis bullosa and epidermolysis bullosa simplex, which are not related to type VII collagen deficiency. These arise from mutations in the genes encoding other proteins of the epidermis or the basement membrane at the junction between the epidermis and the dermis. Diagnosis
Classification
See also
Epidermolysis bullosa

References
Sources
Freedberg, Irwin M.; Eisen, Arthur Z.; Wolff, Klauss; Austen, K. Frank; Goldsmith, Lowell A.; Katz, Stephen I., eds. (2003). Fitzpatricks Dermatology in General Medicine (6th ed.). McGraw-Hill. ISBN 978-0-07-138076-8. James, William; Berger, Timothy; Elston, Dirk (2005). Andrews Diseases of the Skin: Clinical Dermatology (10th ed.). Saunders. ISBN 978-0-7216-2921-6. Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 978-1-4160-2999-1. External links

ebd at NIH/UW GeneTests