Neonatal pemphigus vulgaris

Storer, James S.; Galen, Wesley K.; Nesbitt, Lee T.; DeLeo, Vincent A.

doi:10.1016/s0190-9622(82)80127-8

Cited by 64 publications

(40 citation statements)

References 8 publications

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“…4 Finally, although it is tempting to speculate about the role of the mother's exposure to nitrofurantoin during the pregnancy, we believe it to be coincidental because we were unable to find any reported cases of pemphigus vulgaris induced by nitrofurantoin. The differential diagnosis of neonatal pemphigus vulgaris includes neonatal herpesvirus infection, bullous impetigo, epidermolysis bullosa, and other acquired blistering diseases, such as bullous pemphigoid or linear IgA bullous dermatosis.…”

Section: Discussionmentioning

confidence: 75%

“…Cases of neonatal pemphigus occurring while the mother is in clinical remission or is asymptomatic, such as the florid presentation of our patient in spite of the subtle maternal disease, suggest that neonatal skin is more sensitive to circulating anti-Dsg3 antibodies than maternal skin. 1,3,4 However, there is no clear correlation between the severity and pattern of maternal involvement, level of antibody titers or prematurity, and the neonatal clinical presentation. 5 Of note, in some cases of neonatal pemphigus, 3,4 including our case, DIF is positive for IgG and C3.…”

Section: Discussionmentioning

confidence: 99%

“…In previously reported cases, the infants' skin lesions completely healed within a few weeks of delivery. [4][5][6] However, if a pregnant woman is known to have pemphigus vulgaris, therapy during pregnancy should be aimed at reducing the antibody titer to lower the risk of transmission to the neonate. The most commonly used therapy is oral prednisone, but a recent report 7 showed that intravenous immunoglobulin administered at 4-week intervals throughout the pregnancy may be safe and effective.…”

Section: Discussionmentioning

confidence: 99%

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Blisters and Erosions in a Neonate

2014

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A newborn male infant was transferred to the neonatal intensive care unit for widespread vesicles and erosions evident at birth, following a spontaneous vaginal delivery complicated by fetal meconium exposure. The mother, initially unavailable for examination because she remained at the facility where she had given birth, reported via telephone that she was healthy except for a urinary tract infection for which she had taken a 7-day course of nitrofurantoin monohydrate approximately 3 to 4 weeks before delivery. She denied a history of herpesvirus infection, blistering disorder, or autoimmune disease. On physical examination, the neonate exhibited extensive erosions rimmed by purulent vesicles involving the groin, neck, scalp, fingers, and left side of the upper chest ( Figure, A and B). Mucous membranes were spared. Biopsy specimens were obtained, with results as shown in the Figure,

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Blisters and Erosions in a Neonate

2014

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“…Pemphigus foliaceus yes [9][10][11][12][13] yes [14,15] yes [16,17] yes [18] yes [19] IvIg [20] BP180/ collagen XVII…”

Section: Evidence For Pathogenicitymentioning

confidence: 99%

The Role of Pathogenic Autoantibodies in Autoimmunity

Rowley

Whittingham

2015

Antibodies

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Abstract:The serological presence of autoantibodies is diagnostic of autoimmunity, and these autoantibodies may be present for many years before the presentation of autoimmune disease (AID). Although a pathogenic role has been demonstrated for various autoantibodies reactive with cell surface and extracellular autoantigens, studies using monoclonal antibodies (mAb) show not all antibodies in the polyclonal response are pathogenic. Differences depend on Fab-mediated diversity in epitope specificity, Fc-mediated effects based on immunoglobulin (Ig) class and subclass, activation of complement, and the milieu in which the reaction occurs. These autoantibodies often occur in organ-specific AID and this review illustrates their pathogenic and highly specific effects. The role of autoantibodies associated with intracellular antigens is less clear. In vitro they may inhibit or adversely affect well-defined intracellular biochemical pathways, yet, in vivo they are separated from their autoantigens by multiple cellular barriers. Recent evidence that Ig can traverse cell membranes, interact with intracellular proteins, and induce apoptosis has provided new evidence for a pathogenic role for such autoantibodies. An understanding of how autoantibodies behave in the polyclonal response and their role in pathogenesis of AID may help identify populations of culprit B-cells and selection of treatments that suppress or eliminate them.

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“…Existen reportes previos de pénfigo vulgar neonatal (PVN) en hijos de pacientes con pénfigo vulgar (PV) en fase activa 7 y en remisión [8][9][10] . La enfermedad se desencadenaría por el pasaje transplacentario de autoanticuerpos dirigidos contra la epidermis.…”

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