We report a case of aggressive bullous pemphigoid (BP) concurrent with plaque psoriasis successfully treated with Janus kinase inhibitor Baricitinib. The 83-year-old Chinese man suffered 10 years of psoriasis and developed BP with typical intense blisters and significantly elevated serum anti-BP180 autoantibodies. Due to concerns

PASS syndrome is a rare inflammatory disease characterized by a chronic‐relapsing course of pyoderma gangrenosum, acne vulgaris, hidradenitis suppurativa, and spondyloarthritis, which is lack of any biological or genetic marker. Moreover, the optimal therapeutic management remains unclear. We herein describe a Yi Chinese man with PASS syndrome who was treated with secukinumab and showed a remarkable response with almost complete clinical improvement at the 2‐year follow‐up.

Lichen amyloidosis (LA) is the most common subtype of primary localized cutaneous amyloidosis (PLCA), usually manifested as hyperpigmented papules or plaques with intractable pruritus. 1 There is no

Mutations in ITGB4 are known to cause autosomal recessive junctional epidermolysis bullosa (JEB), which is manifested by severe blistering and granulation tissue, usually complicating pyloric atresia and even leading to death. ITGB4-associated autosomal dominant epidermolysis bullosa has rarely been documented. Herein, we identified a heterozygous pathogenic variant (c.433G>T; p.Asp145Tyr) in ITGB4 causing a mild phenotype of JEB in a Chinese family.

Enterokinase deficiency (EKD) is a rare autosomal recessive inherited disorder caused by loss‐of‐function mutations of the transmembrane protease serine 15 (TMPRSS15) gene. To date, only 12 cases of EKD have been described in the literature and skin involvement has seldom been described. We identified a novel homozygous nonsense mutation in the TMPRSS15 gene (c.1216C>T, p.R406*) in a female infant, who manifested with acrodermatitis enteropathica (AE)‐like lesions that were dramatically relieved within 11 days after initiation of a protein‐rich hydrolyzed formula. Our case shows that AE‐like rashes can be a manifestation of EKD and expands the spectrum of causative mutations in the TMPRSS15 gene.