Epidermolysis bullosa acquisita is a chronic subepidermal blistering disease associated with humoral autoimmunity to type VII collagen, an integral part of anchoring fibrils that are important components of the dermoepidermal junction. The pathogenic relevance of collagen VII–specific autoantibodies in EBA has been recently shown in an animal model.52 Epidermolysis bullosa acquisita is refractory to many immunosuppressive treatments. At present, no controlled clinical therapeutic studies exist for this disease, to our knowledge. In a recent systematic review of the literature, it was stated that definitive conclusions for the treatment of EBA53 cannot be drawn. The bullous pemphigoid–like inflammatory presentation of EBA seems to be more responsive to immunosuppression than the classic mechanobullous form,1 which has been reported to be refractory to systemic corticosteroids, oral azathioprine, methotrexate, and cyclophosphamide.9,54 Immunoadsorption has increasingly been used to decrease autoantibody levels in autoimmune disorders refractory to established immunosuppressive agents. Reports on the successful use of IA in systemic lupus erythematosus,14 Sjögren syndrome,13 severe bullous pemphigoid,16 and diseases of the pemphigus group15,55 have been published. For patients with severe pemphigus, a treatment protocol was recently published that induced prolonged clinical improvement of mucosal and cutaneous lesions and was accompanied by a dramatic reduction in serum IgG autoantibodies.51 Therefore, IA may be an efficient technique to rapidly remove circulating autoantibodies as the pathogenic agent in EBA. In the previous study,51 the use of an adsorber system (Globaffin) as an adjuvant treatment in 4 patients with pemphigus vulgaris and in 2 patients with pemphigus foliaceus was investigated. The peptide matrix of the adsorber binds to IgG and circulating immune complexes with high affinity and with lower affinity to IgA and IgM. Its binding characteristics are similar to those of protein A Sepharose.56 In the IA study,51 all 6 treated patients tolerated IA well and showed no symptoms of allergic reactions or cardiovascular dysfunction; the adsorber system effectively reduced anti–desmoglein 1 and desmoglein 3–reactive IgG by a mean of 50% to 70% per IA cycle consisting of 4 consecutive IA treatments. In an earlier study by Schmidt et al,55 5 patients with severe pemphigus were treated with IA using Staphylococcus aureus protein A columns. The treatment schedule consisted of IA treatment on 3 consecutive days; a fourth IA treatment was given on day 8, followed by up to 19 IA treatments during intervals of 1 to 4 weeks. Protein A IA effectively reduced anti–desmoglein 1 and desmoglein 3 IgG by a mean of 76%, correlating with a good clinical response in all patients.55 In a study by Lüftl et al,15 a tryptophan-linked polyvinylalcohol adsorber system was applied. Three patients with acute onset and 6 patients with recalcitrant pemphigus received 2 IA treatments each during 3 days, followed by an intravenous prednisolone pulse. The tryptophan-linked polyvinylalcohol adsorber led to a 30% decrease in desmoglein-reactive autoantibodies, which was accompanied by significant clinical improvement. Findings from these studies, as well as other case reports,57,58 suggest that IA is an efficacious and safe treatment for severe and therapy-resistant bullous autoimmune disorders.