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Pemphigoid gestationis (PG) is the least common, yet best-characterized, dermatitis specific to pregnancy.
PG appears to be caused by an anti-BMZ antibody that induces C3 deposition along the dermal-epidermal junction. Nearly all patients with PG [and most patients with bullous pemphigoid (BP)] have demonstrable antibodies to BP180 (type XVII collagen), a 180-kd transmembrane protein with its N-terminal end embedded within the intracellular component of the hemidesmosome and its C-terminal end located extracellularly (see Chap. Immunogenetic studies reveal an increase in HLA antigens DR3 or DR4, and curiously, nearly 50 percent of patients have the simultaneous presence of both.21 The extended haplotype HLA-A1, B8, DR3 is known to be in linkage disequilibrium with a deletion of C4A (the C4 null allele or C4QO). It is worth noting that patients with neither DR3 nor DR4 may have clinically indistinguishable disease; the presence of the characteristic HLA antigens alone is not sufficient to produce disease.
Essentially, 100 percent of women with a history of PG have demonstrable anti-HLA antibodies. The autoantibody of gestational pemphigoid binds to amniotic basement membrane, a structure derived from fetal ectoderm and antigenically similar to skin.25,26 Women with PG also show an increased expression of major histocompatibility complex class II antigens (DR, DP, DQ) within the villous stroma of chorionic villi but not skin.
On the other hand, PG has also been reported in association with hydatidiform moles30 and choriocarcinomas.31 This is an intriguing clinical observation, because most hydatidiform moles are produced by a diploid contribution of paternal chromosomes and contain neither fetal tissue nor amnion. Newborns may be affected up to 10 percent of the time, but the disease is typically mild and self-limited. The typical lesions of PG are urticarial or arcuate plaques that rapidly progress toward a mixed dermatitis, including tense, pemphigoid-like blisters . PG is seen exclusively in women and only in the presence of pregnancy (or trophoblastic tissue).
The sine qua non for a diagnosis of PG is the finding of C3, with or without IgG, in a linear band along the BMZ of perilesional skin . Since early lesions of PG can be urticarial, the most frequent frustration is differentiating PG from pruritic urticarial papules and plaques of pregnancy, otherwise known as polymorphous eruption of pregnancy . No increase in maternal morbidity or mortality has been documented, although the impression of such an increase remains from a review of individual case reports. Women with a history of PG appear to be at increased risk for the subsequent development of Graves disease.
Most disease spontaneously remits over weeks to months following delivery, although there are isolated reports of protracted postpartum involvement. In individual cases, alternatives to corticosteroids (dapsone, pyridoxine, cyclosporine) or adjuvants (gold, methotrexate, cyclophosphamide, plasmapheresis) have been tried. Only a small percentage of women who express DR3, DR4, or the combination of DR3 and DR4 ever develop PG, and the role of the paternal tissue in the development of disease (if any) is far from clear. Those with a history of PG face the likelihood (but not the assurance) of recurrent involvement during subsequent gestations and are likely to develop symptoms during the use of oral contraceptives. Peut affecter aussi les femmes non-enceintes par des tissus d'origine placentaire comme le choriocarcinome ou le MOLE HYDATIFORME.
It classically presents as an intensely itchy, urticarial rash during the later part of pregnancy or the immediate postpartum period, then rapidly progresses to a pemphigoid-like, vesiculo-bullous eruption.
It is associated with HLA-DR3 and DR4, and it appears likely that the incidence in various ethnic groups parallels the frequency of these genes in different populations.


The PG autoantibody is an IgG that is infrequently found by direct immunofluorescence (IF), although indirect, complement-added IF reveals the circulating IgG in the majority of patients. Because the only source of disparate HLA antigens is typically the placenta (which is primarily of paternal origin), the universal finding of anti-HLA antibodies implies a high frequency of immunologic insult during gestation. It has therefore been proposed that PG is a disease initiated by the aberrant expression of major histocompatibility complex class II antigens (of paternal haplotype) within the placenta that serves to initiate an allogeneic response to placental BMZ, which then cross-reacts with skin. It typically presents during late pregnancy with the abrupt onset of intensely pruritic urticarial lesions. Histopathology classically reveals a sub-epidermal vesicle with a perivascular infiltrate of lymphocytes and eosinophils .
In salt-split skin specimens, antibody deposition is found along the bottom of the epidermal fragment, a finding similar to that seen in BP. Cutaneous disease in the newborn is typically self-limited and rarely requires intervention. Many patients experience spontaneous resolution during the later part of gestation only to experience a flare, sometimes dramatically, at the time of delivery. It has often been said that once gestational pemphigoid develops, it tends to occur earlier and with greater severity during subsequent gestations, but there are no data to support this contention.
First onset during both primiparous and multiparous pregnancies has been reported, with and without a change in partners. Nonetheless, there is general consensus that treatment with topical corticosteroids and antihistamines is ineffective. None, with the possible exception of cyclosporine, is useful prior to term, and the experience with each has been variable at best. The extracellular section contains a series of 15 collagenous components alternating with 16 short, non-collagenous domains. Indeed, a slight increase in HLA-DR2 in the husbands of women with PG has been reported.23 It has been suggested that immunologically primed women may simply react more strongly to tissue with disparate HLA antigens. Fifty percent of patients experience first onset on the abdomen, often within or immediately adjacent to the umbilicus. Pruritic urticarial papules and plaques of pregnancy  can show microvesiculation but not the tense, sub-epidermal blisters of PG. Eosinophils may be lined up along the dermal-epidermal junction and typically fill the vesicular space. Although there is an increased risk of premature and small-for-gestational-age births, there are no data to suggest that treatment with systemic corticosteroids alters the risk of premature delivery. Others develop relatively trivial urticarial lesions during one pregnancy, only to suffer characteristic blistering during a subsequent gestation. PG appears to be mediated by a specific immunoglobulin G (IgG) directed against the cutaneous basement membrane zone (BMZ). An enzyme-linked immunosorbent assay (ELISA) for the PG antibody is now commercially available, and when this highly sensitive test is used, antibody titers appear to correlate with disease activity. The sixteenth non-collagenous segment closest to the plasma membrane of the basal keratinocyte is designated NC16A and contains the immunoreactive site.


Whether anti-HLA antibodies represent phenomenon or epiphenomenon, remains to be clarified. Because choriocarcinoma in women is entirely derived from placental tissue (which is largely of paternal derivation), the suggestion is that the development of PG is somehow dependent on the state of partial allograph, not necessarily on the presence of amnion. The other half present with typical lesions, but in an atypical distribution (extremities, palms, or soles). However, complement-added indirect IF reveals the circulating anti-BMZ IgG in nearly all patients.
Where doubt exists, IF (or ELISA) is the key to differentiation and is particularly relevant in helping patients plan for future pregnancies . That being the case, it is imperative that the risks of therapy be balanced against the severity of the symptoms. Still others develop classic disease during one pregnancy, then no disease during the next.
The PG autoantibody belongs to the IgG1 subclass and fixes complement via the classical complement pathway. The PG autoantibody is assumed to be pathogenic for several reasons: (1) It is found in essentially all patients. Rapid progression to a generalized, pemphigoid-like eruption, sparing only the face, mucous membranes, palms, and soles is the rule (although any site may be involved). Maintenance therapy, generally at a lower dosage, may or may not be required throughout gestation. T cells also show selective NC16A reactivity in PG, although their role in disease development remains to be elucidated.
The titer of anti-BMZ antibody in PG is usually so low that antibody cannot be detected without the use of complement-added or ELISA techniques.
Recurrences associated with menstruation are common, and flares during the subsequent use of oral contraceptives occur in at least 25 percent of patients.
As noted earlier, many patients experience spontaneous disease regression during the third trimester, only to experience flare during parturition. The explosive onset of blistering may occur within hours of delivery, either as a flare of pre-existing disease or as presentation de novo. Sera from most PG patients react to a 180-kd transmembrane protein with a collagenous domain coded for on a different chromosome. Until such time as nosology is driven by pathologic mechanism instead of clinical observation, naming is likely to remain fungible.



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