The Fc part of the antibody that represents the binding site for the neonatal Fc receptor (FcRn) is formed by the lower hinge region and the CH2/CH3 domains

The Fc part of the antibody that represents the binding site for the neonatal Fc receptor (FcRn) is formed by the lower hinge region and the CH2/CH3 domains. diagnosis, transplacental passage, immunoglobulins, dermatology, neonatology == 1. Introduction == Gestational pemphigoid is a rare autoimmune skin disorder arising in pregnancy and causing subepidermal blistering [1]. With an incidence of 1 1 in 50,000 pregnancies, primarily manifesting in the second and third trimesters, it poses unique challenges in diagnosis and management [2]. Multigravidae women are prone to an earlier onset and a longer time to remission [2]. The course is usually self-limiting within 6 months after delivery but can relapse with subsequent pregnancies, menstruation, or Isorhamnetin 3-O-beta-D-Glucoside oral contraceptives [3]. The pathogenesis resembles the one of bullous pemphigoid, with the presence of IgG autoantibodies against BP180 * and, in part, against BP230 *, constituents of the hemidesmosome, leading to the detachment of the dermis and epidermis and the emergence of blisters, inflammation and erosions [1]. The diagnosis is suggested by Isorhamnetin 3-O-beta-D-Glucoside the clinical findings such as pruritic erythema and urticarial papules and plaques BMP2B progressing into papulovesicles and tense bullae, mostly in the periumbilical area, abdomen, trunk, legs, and arms, usually sparing the mucosae [2]. Histopathological findings consist of subepidermal vesicles, with perivascular eosinophils and lymphocytes [4], and direct immunofluorescence reveals C3 complement and, more rarely, IgG deposition in a linear pattern along the basement membrane [1,4]. The therapeutic management is mainly based on the severity of the disease, with first-line treatment consisting of topical or systemic corticosteroids combined with second-generation antihistamines and second-line treatment with alternative or adjuvant therapies such as anti-inflammatory antibiotics, dapsone, and topic immunomodulators [5,6]. The newborns are usually unaffected, but 10% of them will present cutaneous lesions in the form of neonatal pemphigoid, caused by the transplacental passage of maternal antibodies into the fetal bloodstream [1,7,8]. The approach should be multidisciplinary and include a dermatologist, obstetrician, neonatologist, pediatrician, and endocrinologist. == 2. Clinical Case == We report the case of a 42-year-old woman with 31 weeks of gestation, previously diagnosed with polycystic ovary syndrome, showing intense pruritus and urticarial papules and plaques, Isorhamnetin 3-O-beta-D-Glucoside tense intact bullae localized around the periumbilical area, trunk, and the extremities, with a duration of three weeks and rapidly progressive onset (Physique 1). Previous to the presentation in our clinic, the patient accessed a few medical care models, including obstetrics-gynecology and internal medicine. The first diagnosis was intrahepatic cholestasis of pregnancy because the rash was absent at the moment, and the patient received treatment with ursodeoxycholic acid. The evolution was unfavorable with the formation of skin sores, and the patient was then referred to the dermato-venereology department with the following potential differential diagnosis: polymorphic eruption of pregnancy, atopic eruption of pregnancy, or gestational pemphigoid. == Physique 1. == Clinical aspects postpartum:(a) urticarial plaques and tense Isorhamnetin 3-O-beta-D-Glucoside bullae, with classic involvement of the umbilical area; (b) tense bullae on erythematous plaques affecting the thighs. Upon admission, laboratory tests showed slight increases in leukocytes (11.36 103/L, Isorhamnetin 3-O-beta-D-Glucoside normal: 4.610.2 103/L) and eosinophils (1.77 103/L, normal: 0.00.7 103/L; 15.6%, normal: 0.07.0%), increased C-reactive protein (14.3 mg/dL, normal: <10 mg/dL) and mixed dyslipidemia. Even though there was a high suspicion of gestational pemphigoid, there was no histopathological or direct immunofluorescence confirmation because the patient did not consent to a skin biopsy..