Bullous pemphigoid (BP) is an acquired autoimmune bullous disease characterized by autoantibodies against the hemidesmosomal proteins found in the basal keratinocytes of the basement membrane zone (BMZ): a 180 kDa protein (type XVII collagen) mainly and the 230 kDa antigen. There is such evidence that the antibodies against the BMZ components are not only of IgG type, but also this bullous disease may have IgE antibodies directed to the BMZ that contribute to the pathogenesis of the disorder. IgE is not only thought to contribute to the pathogenesis of BP, it has also been suggested that eosinophils play a role in the development of the first signs associated with BP. A humanized monoclonal antibody directed to IgE, omalizumab, is approved for the treatment of severe asthma and chronic spontaneous urticaria, and it may be useful in the treatment of BP in the first stages of the disease.

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logic features. In 2002, Weenig et al 1 described 95 patients with skin ulcers resembling those found in PG. They described 6 disease categories that can mimic PG: vascular disorders, vasculitis, malignant diseases, primary infections, drug-induced or exogenous tissue injury, and other inflammatory disorders. 1 Cutaneous diphtheria is caused by C diphtheriae and usually affects inhabitants or travelers from endemic developing countries. Coinfection with other pathogens such as Streptococcus pyogenes or A hemolyticum is frequent. 2,3 Cutaneous diphtheria presents as painful nodules or nonhealing ulcers, and it can be highly contagious. 4 Recently, an outbreak among refugees from Africa and Syria was reported in Germany and Switzerland. 5 Early diagnosis is essential for preventing outbreaks of this disease.Treatment of CD differs from systemic diphtheria. It is based on systemic antibiotics like penicillin and erythromycin and isolation precautions. The lack of response to amoxicillin/clavulanate in our patient could be explained by the occasional resistance to penicillin that has been reported. 6 We describe a patient with CD resembling PG clinically and histologically. Strikingly, the patient also presented with a monoclonal IgG band, making the PG diagnosis even more plausible. However, the presence of conditions associated with PG such as inflammatory bowel disease, myeloproliferative disorders, or paraproteinemia has been described in almost 40% of patients misdiagnosed as having PG. 1 Clinicians must remember that PG is a diagnosis of exclusion, and it is mandatory to perform biopsies, cultures, and blood analysis to rule out neoplasms, infections, vascular, or autoimmune disorders.

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