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Herpes gestationis is a bullous disease that can develop in association with pregnancy, choriocarcinoma, or other similar tumors. Subsequent pregnancies are likely to produce an earlier onset than the preceding pregnancy. Lesions consist of urticarial plaques and annular wheals, often surmounted by multiple small tense vesicles. Use of images for any purpose including but not limited to research, commercial, personal, or non-commercial use is prohibited without prior written consent.
Diagnosis of PG becomes clear when skin lesions progress to tense blisters during the second or third trimester. PG often is confused with pruritic urticarial papules and plaques of pregnancy (PUPPP), especially if it occurs in a first pregnancy. Pregnant women with PG should be monitored for conditions that may affect the fetus, including, but not limited to, low or decreasing volume of amniotic fluid, preterm labor, and intrauterine growth retardation.
Based on work by Lakshmi Gopalakrishnan, Alara Eren, Jacki Buros (bot) and Alexandra Almonacid and wikidoc anonymous user Beland.


Please consult your physician or other medical care provider regarding any medical questions you may have. PG typically starts as a blistering rash in the navel area and then spreads over the entire body.
The primary site of autoimmunity seems not to be the skin, but the placenta, as antibodies bind not only to the BMZTemplate:Explain of the epidermis, but also to that of chorionic and amniotic epitheli. When a pregnant mother develops PG, the risk for the development of other autoimmune diseases increases, specifically Grave’s disease.
Aberrant expression of MHC class II molecules on the chorionic villi suggests an allogenic immune reaction to a placental matrix antigen, thought to be of paternal origin .Recently, both IgA22 and IgE24 antibodies to either BP180 or BP230 have also been detected in pemphigoid gestationis. PG usually occurs in subsequent pregnancies; however, it often seems more manageable because it is anticipated. Prognosis of the fetus is usually good, but the rate of premature births and small-for-date babies rises. After one to two weeks, large, tense blisters typically develop on the red plaques, containing clear or blood-stained fluid.[4] PG creates a histamine response that causes extreme relentless itching (pruritus).


Recent studies have shown the risks are related to the severity of the disease and are not caused by the treatment with corticosteroids.[8] PG usually reoccurs with following pregnancies, and symptoms appear earlier and more severely. PG is characterized by flaring and remission during the gestational and sometimes post partum period. Usually after delivery, lesions will heal within months, but may reoccur during menstruation. Passive transfer of the mother’s antibodies to the fetus causes some (about 10%) newborns to develop mild skin lesions, but these typically will resolve within weeks of parturition.
In the post partum period, if necessary, the full range of immunosuppressive treatment may be administered for cases unresponsive to corticosteroid treatments, such as tetracyclines, nicotinamide, cyclophosphamide, ciclosporin, goserelin, azathioprine, dapsone, rituximumab, or plasmaphoresis, or intravenous immunoglobulin may sometimes be considered when the symptoms are severe.



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