Perineal pyoderma gangrenosum in pregnancy: A case report

Pyoderma gangrenosum is a rare ulcerating neutrophilic dermatosis. We describe the case of a 28-year-old woman with pyoderma gangrenosum in the perineal region during pregnancy. Cytological analysis of a skin biopsy specimen showed neutrophilic infiltrates across all the layers of the dermis, confirming the diagnosis of pyoderma gangrenosum. Determining a management plan, including the mode of delivery, was difficult. Oral prednisolone was started and her ulcer started to improve, but she still had the ulcer when she reached full term. Because there was a concern that the ulcer would be worsened by vaginal delivery, cesarean section was performed. After her delivery, pyoderma gangrenosum had not appeared at the cesarean incision and the ulcer in the perineal region had improved. Obstetricians should be aware of pyoderma gangrenosum as a differential diagnosis when vulvar ulceration develops during pregnancy. Keywords: Pyoderma gangrenous, Pregnancy, Perineal regio

Alpha-1 Antitrypsin-Induced Endoplasmic Reticulum Stress Promotes Invasion by Extravillous Trophoblasts

Alpha-1 antitrypsin (A1AT) is a glycoprotein that has been shown to protect tissues from proteolytic damage under various inflammatory conditions. Several studies show that A1AT may be associated with pre-eclampsia. However, the role of A1AT expression in placental physiology is not fully understood. In the present study, we aim to characterize the expression and function of placental A1AT. A1AT knockdown is found to reduce the expression of the serine protease HTRA1 in a trophoblast cell line. In addition, A1AT overexpression (A1AT-OE) increases the expression of HTRA1, IL6, CXCL8, and several markers of endoplasmic reticulum (ER) stress. Treatment with tunicamycin or thapsigargin, which induces ER stress, increases HTRA1 expression. Furthermore, immunohistochemistry reveals that HTRA1 is expressed in trophoblasts and the endometrial decidual cells of human placentas. An invasion assay shows that A1AT and HTRA1 stimulate cell invasion, but treatment with the ER stress inhibitors reduces the expression of HTRA1 and ER stress markers and prevents cell invasion in A1AT-OE trophoblasts. These results suggest that endogenous A1AT regulates inflammatory cytokine expression and HTRA1-induced trophoblast invasion via the induction of ER stress. It is concluded that an imbalance in the functional link between A1AT and ER stress at the maternal–fetal interface might cause abnormal placental development