妊娠期皮肤病__培训课件.pptVIP

Herpes gestationis 妊娠疱疹 Autoimmune bullous disorder, closely related to bullous pemphigoid (BP) Rare with incidence of approximately 1 in 60,000 Onset usually in second and third trimester or postpartum period Recurrence common in subsequent pregnancy at earlier gestation and with increased severity (apart from skip pregnancies, which occur when a woman with known PG has a subsequent unaffected pregnancy) Pruritic erythematous plaques, which become annular or polycyclic, developing into vesicles or bullae Periumbilical involvement in 87% of cases Transplacental transfer of antibodies can result in neonatal involvement Associated with low birth weight and premature birth caused by placental insufficiency Histopathologic features: Similar to PEP in early phases; subepidermal separation with basal cell necrosis; eosinophilic spongiosis Immunofluorescence diagnostic test: Positive direct immunofluorescence with IgG and complement 3 staining at the basement membrane zone and staining to the roof on indirect immunofluorescence using salt-split skin Pathophysiology: HLA-DR3, DR4 subtypes associated; close relationship to BP, sharing same target antigen BP-180 kd (BP-AG2), a component of hemidesmosomes; anti-HLA antibodies found in serum of patients with PG Treatment: Mild cases will respond to potent topical steroids; most cases require systemic corticosteroids with gradual dose reduction as disease remits; postpartum flare often occurs; oral contraceptive therapy also leads to disease flare; Goserelin (LHRH analogue)(chemical oophorectomy) used in severe cases in postpartum phase Pruritic folliculitis of pregnancy妊娠瘙痒性毛囊炎 Pruritic erythematous follicular papules and urticarial lesions on limbs and abdomen in most cases Onset in second and third trimester with resolution within 2 to 3 weeks postpartum Histopathologic features: Acute folliculitis with mixed inflammatory cells, upper dermal edema and spongiosis; negative Gram’s stain Pathophysiology: Unknown; maternal a