A 33-year old woman delivered a boy at 38 weeks via cesarean delivery. The neonate had diffuse erosions present at birth. Further evaluation revealed superficial annular erosions with central granulation tissue and desquamating borders on the occipital scalp, postauricular region, nape, and right calf (Figure 1). The mother had a 5-year history of pemphigus vulgaris and originally presented with erosions of the buccal mucosa, palate, nare, and conjunctival injection (Figure 2). Indirect immunofluorescence was positive for IgG cell surface antibodies (1:1260) and anti-desmoglein-3 antibodies on enzyme-linked immunosorbent assay (196 units). At the time of delivery, the mother exhibited erosions at the proximal nail folds of the feet. Neonatal pemphigus vulgaris was suspected. Serum testing of the neonate supported the diagnosis with positive IgG cell surface antibodies (1:320) and anti-desmoglein-3 antibodies (146 units).Pemphigus vulgaris is a blistering disease of the mucous membranes and skin secondary to autoantibodies directed towards desmoglein-1anddesmoglein-3. 1 Desmogleinsaretransmembraneproteins that function as a structural component of the desmosome and facilitate cell-to-cell adhesion. 1,2 Neonatal pemphigus vulgaris is a transient blistering disorder caused by passive transfer of maternal IgG autoantibodies across the placenta during pregnancy. 1 The risk of an infant developing neonatal pemphigus exists independently of levels of maternal antibody titers and/or mucocutaneous presentation at time ofgestation. [2][3][4] Thedistributionofulcerativelesionsintheneonatefailed to reflect the pattern visible in the mother. [1][2][3][4] Widespread disease in the neonate was a result of desmoglein-3 expression in the neonatal mucosal and cutaneous surfaces. Despite the severity of symptoms, the prognosis was favorable.Immunoglobulin levels transferred from mother to fetus are reduced by age 3 to 6 months. 2 Often, undetectable levels of antibody titers are seen in the infant shortly postdelivery; resolution of symptoms can be seen by age 3 weeks. 3 Therapy aims to support reepithelization of the skin and mucous membranes and prevent concomitant infection. 2,4 Treatment comprises emollients, topical corticosteroids, and anitbiotics. 4 Follow-up with monitoring of symptoms and levels of antibodies is recommended until age 1 year. 1 Although the literature fails to associate the degree of disease in the mother with that of the infant, efforts to reduce antibody levels in pregnant women is recommended. 3,4 This can be achieved with oral prednisone, intravenous immunoglobulin, or plasmapheresis. 1,4

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Cardiovascular disease is the leading cause of death in pregnant and postpartum women. During pregnancy, the maternal heart rapidly adapts to the increasing physiological and metabolic demands of the growing fetus. This adaptation often takes the form of a physiological hypertrophy in which the maternal heart grows to increase cardiac output; however, the molecular processes underlying pregnancy-induced hypertrophy (PIH) are poorly understood. The goal of this study was to examine the transcriptomic and metabolic signatures associated with the structural and functional adaptations of the heart to pregnancy. Therefore, we performed timed pregnancy studies in 12-week-old female FVB/NJ mice, which were distributed into the following groups: non-pregnant control (NP; n = 14), mid-pregnancy (MP, 6d pregnant; n = 11), late-pregnancy (LP, 16d pregnant; n = 13), and 1-wk post birth (PB; n = 8). Heart weight to tibia length were higher in MP (7.77±1.02 mg/mm; p <0.05), LP (7.84±0.87 mg/mm; p <0.05), and PB mice (9.86±1.14 mg/mm; p <0.05) compared with NP mice (6.54±0.74 mg/mm). The sustained increase in PB heart weight was associated with increased myocyte cross sectional area, consistent with cardiomyocyte hypertrophy. Compared with NP hearts, echocardiographic measurements suggest significant increases in both end diastolic (36.0±5.1 vs 61.2±5.9 μl; p <0.05) and systolic LV volume (9.4±3.8 vs 21.0±1.4 μl; p <0.05) in PB hearts. These changes in PB hearts were associated with a significant increase in LV mass and a decline in ejection fraction. In LP and PB hearts, we also found higher expression of markers of hypertrophy ( Nppa, Nppb, Myh7 ). Subsequent RNA-seq analyses revealed enrichment in genes involved in cell proliferation, cytokinesis, and transcription in MP hearts; in metabolism genes in LP hearts; and in fibrotic and extracellular matrix genes in PB hearts. Together, these findings reveal the key molecular signature underlying the structural and functional adaptation of the heart during pregnancy and parturition, and may shed light on the molecular processes underlying PIH.