Inviting Innovations in autoantibody titers, antikeratinocyte cell surface antibodies, and anti-desmoglein-3 correlated with clinical response in a number of patients [2,[6][7][8][9]. The antiepidermal antibodies, which usually belong to the IgG category, can be easily eliminated with TPE [6,7].Bullous pemphigoid (BP) is another form of subepidermal blistering pemphigus; BP is rare. BP frequently involves a premonitory stage with pruritic urticarial erythema and eczematous lesions followed by the classical bullous stage with tense blisters, erosions, and crusts [8]. BP is a chronic dermatosis often associated with acute exacerbations, with the formation of bullae blisters usually on the inflamed skin, subepidermal blister formation, and antibodies against the epidermal basal membrane. Thus, BP can also occur in combination with other autoimmune disorders.The course of this pemphigus disorder is not as dramatic as other forms of the disease, with good response to high-potency corticosteroids, which are usually combined with dapsone, doxycycline, methotrexate, or azathioprine in usually dosages [3]. BP has an annual incidence of about 13-42 new cases per 1 million in central Europe and the United Kingdom [9,10]. Only a few cases have been treated with TPE up to noe [11]. After 3 to 5 treatments in one week, we could see if TPE or IA can decrease the antibody titer. In very low antibody titers, the frequency of the treatments can decrease, too. Because the pathogenic relevance of autoantibodies was clearly demonstrated in the majority of autoimmune bullous diseases, removal of autoantibodies, therefore, TPE is indicated. IA and rituximab have been establisheds additional therapeutic options [12]. D-Penicillamine induced pemphigus, steroid-resistant pemphigus, is a foliaceustype disease with high lethality and mortality rate, which can occur as a side effect in long-term penicillamine therapy, which is a particular indication for TPE [13]. Only case reports of D-penicillamine"-induced pemphigus" treated successfully with TA were reported in combination with immunosuppresion. IA is the most specific therapeutic option, in which only the pathogenic IgG is depleted in the patient's plasma. Three to 5 treatments of TPE or IA and immunosuppressive drugs in one or two weeks are necessary to an improvement of the disease. A combination of IA and rituximab showed rapid and long-lasting response of concomitant im-