Herpes gestationis — Bullae from hormones that cause increased extracellular matrix (autoantibodies to epidermal basement membrane as a secondary phenomenon)

Mechanisms of epithelial damage: are there parallels between bullous skin diseases and asthma?

“…The presence of BMZ autoantibodies in blistering disorders may be responsible for disease symptoms, however, this need not necessarily be the case. Herpes Gestationis (HG) is characterized by a high incidence (30-40%) of epidermal BM autoantibodies of the IgG class [15]. Stone [15] proposed that the appearance of autoantibody is a secondary event in HG, a condition associated with the last 4 months of pregnancy (and postpartum) and producing bullous type symptoms.…”

“…there appears to be an association with an inflammatory cell infiltrate predominantly made up of eosinophils, which may be the cause of BM disruption [5,15,17]. The release of major basic protein (MBP) from eosinophils and its subsequent association with antigens present in damaged tissue was proposed [15] to present the immune system with a novel antigenic complex, leading to autoantibody synthesis and possibly providing an inflammatory cell chemotactic stimulus. Interestingly, it has been shown that a constituent of blister fluid converted normodense guinea-pig eosinophils to a hypodense, activated state [18].…”

“…Hooks et al (1993) discussed a number of possible reasons for post-infection autoantibody synthesis including the introduction of foreign material into the host that resembles native molecules, possible changes in the hosts own antigen or disruption of the immune system [22]. The second considers the normal production of autoantibodies to enhance the debridement of damaged (injured or infected) tissues [15], indicating that the inappropriate expression of a normal biological function may lead to the lesions described above. Were it to be shown that the incidence of autoantibodies in conditions such as BP was central to the aetiology of the disease, treatment may hinge on systemic removal of the autoantibodies.…”

“…Herpes Gestationis (HG) is characterized by a high incidence (30-40%) of epidermal BM autoantibodies of the IgG class [15]. Stone [15] proposed that the appearance of autoantibody is a secondary event in HG, a condition associated with the last 4 months of pregnancy (and postpartum) and producing bullous type symptoms. Increased oestrogen and progesterone levels were postulated to increase tissue viscosity, hindering the dispersal of tissue fluid and leading to blister formation.…”