[2] It presents with tense blisters, small bumps, hives and intense itching, usually starting around the navel before spreading to limbs in mid-pregnancy or shortly after delivery.

[4] It can resemble pruritic urticarial papules and plaques of pregnancy, erythema multiforme, drug reactions and blistering scabies.

After one to two weeks, large, tense blisters typically develop on the red plaques, containing clear or blood-stained fluid.

[citation needed] Pathogenically, it is a type II hypersensitivity reaction where circulating complement-fixing IgG antibodies bind to an antigen (a 180-kDa protein, BP-180) in the hemidesmosomes (attach basal cells of epidermis to the basal lamina and hence to dermis) of the dermoepidermal junction[further explanation needed], leading to blister formation as loss of hemidesmosomes causes the epidermis to separate from dermis.

The primary site of autoimmunity seems not to be the skin, but the placenta, as antibodies bind not only to the basement membrane zone of the epidermis, but also to that of chorionic and amniotic epithelia.

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.

[citation needed] Pregnant women with GP 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.

Systemic corticosteroid treatment, in contrast, does not substantially affect pregnancy outcomes, and its use for GP in pregnant women is justified.

[7] 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.