INTRODUCTION
Pyoderma gangrenosum (PG) is a rare neutrophilic dermatosis characterized by the sudden onset of painful, necrotic ulcers, most commonly affecting the lower extremities. PG is driven by abnormal accumulation and hyperactivation of neutrophils, leading to excessive infiltration that culminates in tissue destruction and ulceration.1 Although clinical manifestations of PG are well recognized, its etiology remains largely elusive, with research implicating autoinflammatory mechanisms as a driving force.
A distinctive feature of PG is pathergy, seen in about one-third of patients, where minor skin trauma triggers an exaggerated inflammatory response and ulcerative lesions. PG is also commonly associated with systemic conditions, with about 50% of patients having diseases such as inflammatory bowel disease (IBD), rheumatoid arthritis, or hematological malignancies, suggesting PG may reflect broader systemic inflammation.2 Pregnancy introduces additional complexity to the pathophysiology of PG due to the significant immunological and hormonal changes that occur during gestation and persist postpartum. While these changes are essential for fetal development, they also impact immune regulation and may exacerbate inflammatory conditions. Given the rarity of PG during pregnancy and the lack of consensus on optimal management, addressing gaps in the existing literature is critical. Current data on pregnant or postpartum patients with PG primarily stem from case reports and small-scale reviews. For example, Steele et al analyzed 26 cases and suggested that immune changes during pregnancy may play a role in the onset of PG.3 More recently, Wanberg et al reviewed 18 cases and proposed a treatment algorithm tailored to this population.4
Building on previous work, our review aims to broaden the scope with 3 key objectives: (1) analyzing the demographic and clinical features of PG in pregnant or postpartum patients,
A distinctive feature of PG is pathergy, seen in about one-third of patients, where minor skin trauma triggers an exaggerated inflammatory response and ulcerative lesions. PG is also commonly associated with systemic conditions, with about 50% of patients having diseases such as inflammatory bowel disease (IBD), rheumatoid arthritis, or hematological malignancies, suggesting PG may reflect broader systemic inflammation.2 Pregnancy introduces additional complexity to the pathophysiology of PG due to the significant immunological and hormonal changes that occur during gestation and persist postpartum. While these changes are essential for fetal development, they also impact immune regulation and may exacerbate inflammatory conditions. Given the rarity of PG during pregnancy and the lack of consensus on optimal management, addressing gaps in the existing literature is critical. Current data on pregnant or postpartum patients with PG primarily stem from case reports and small-scale reviews. For example, Steele et al analyzed 26 cases and suggested that immune changes during pregnancy may play a role in the onset of PG.3 More recently, Wanberg et al reviewed 18 cases and proposed a treatment algorithm tailored to this population.4
Building on previous work, our review aims to broaden the scope with 3 key objectives: (1) analyzing the demographic and clinical features of PG in pregnant or postpartum patients,
