The complement system is a fundamental part of the innate immune system, playing a crucial role in host defense against various pathogens, such as bacteria, viruses, and fungi. Activation of complement results in production of several molecules mediating chemotaxis, opsonization, and mast cell degranulation, which can contribute to the elimination of pathogenic organisms and inflammation. Furthermore, the complement system also has regulating properties in inflammatory and immune responses. Complement activity in diseases is rather complex and may involve both aberrant expression of complement and genetic deficiencies of complement components or regulators. The skin represents an active immune organ with complex interactions between cellular components and various mediators. Complement involvement has been associated with several skin diseases, such as psoriasis, lupus erythematosus, cutaneous vasculitis, urticaria, and bullous dermatoses. Several triggers including auto-antibodies and micro-organisms can activate complement, while on the other hand complement deficiencies can contribute to impaired immune complex clearance, leading to disease. This review provides an overview of the role of complement in inflammatory skin diseases and discusses complement factors as potential new targets for therapeutic intervention.

EVLA and HL+S show higher success rates than UGFS 5 years after GSV treatment. Recurrent reflux rates at the SFJ were significantly lower in HL+S than UGFS and EVLA. VCSS scores were similar between EVLA and HL+S.

NCT01637181 (http://www.clinicaltrials.gov).

We present a case of trichoblastic carcinosarcoma with panfollicular differentiation. An 80‐year‐old man presented with a lesion on the left ear, which had been present for several months. Histopathology revealed a well‐demarcated neoplasm in the dermis composed of intimately intermingled malignant epithelial and mesenchymal cells. The epithelial component showed multilineage follicular differentiation toward all of the elements of a normal hair follicle. Molecular analysis revealed identical molecular aberrations in both epithelial and mesenchymal components including CTNNB1 and SUFU mutations. To the best of our knowledge, this is the first report of panfollicular carcinosarcoma and of the presence of a CTNNB1 mutation in trichoblastic carcinosarcoma.