Background: Bullous pemphigoid (BP) is an acquired subepidermal autoimmune blistering disease in which there are humoral and cellular responses against the BP180 and BP230 antigens. Dipeptidyl peptidase (DPP)-4 inhibitors enhance endogenous glucagon peptide-1 and glucose-dependent insulinotropic polypeptide secretion with food intake, which leads to insulin secretion, as well as to the reduction of glucagon secretion. Recently, several cases of DPP-4 inhibitor-associated BP have been reported. Objectives: To report 3 cases of DPP-4 inhibitor-associated BP, one of which is due to linagliptin use, as well as to review all currently published cases of DPP-4 inhibitor-associated BP. Case Reports: Three patients diagnosed with BP at our department showed a clear temporal relationship between the introduction of DPP-4 for the treatment of diabetes and the onset of BP. One case was due to linagliptin use, while the other 2 cases were due to an association with vildagliptin-metformin use. Conclusions: This is the first report of linagliptin-associated BP. Furthermore, 2 other cases of vildagliptin-associated BP are reported.

We report the case of a patient with a 13-year history of pemphigus vulgaris (PV) treated with immunosuppressive agents, prednisone and mycophenolate mofetil who had developed lesions of Kaposi's sarcoma (KS) on a sole plaque of PV that had been previously treated with intralesional injections of steroids. The lesions were surgically removed and polymerase chain reaction (PCR) demonstrated human herpesvirus-8 (HHV-8) DNA. There were neither recurrences nor later dissemination of KS following gradual decrease of the immunosuppressive therapy. We suggest that the treatment with intralesional steroids may have influenced the local reactivation of a latent infection of the virus, determining the appearance of this localized KS.

The era of targeted therapy has introduced a new therapeutic perspective for melanoma patients. Treatment with BRAFV600 inhibitors has improved overall and disease-free survival in metastatic melanoma patients whose tumors harbor BRAFV600 mutations. Although the BRAFV600E mutation appears to have a critical role in tumor initiation, its expression during tumor progression remains controversial. In fact, various authors claim that BRAFV600E heterogeneity is evident in melanoma tumors. Herein, we investigated the pattern of BRAFV600E expression in matched primary and metastatic samples from 140 patients. Using a combination of real-time PCR and immunohistochemical analyses, we demonstrated that BRAFV600E expression is homogeneous in melanoma tumors and hypothesized that the heterogeneity described by others might be attributable to technical issues when molecular methods are used. We also demonstrated the high efficiency of the anti-BRAFV600E VE1 antibody for the detection of BRAFV600E mutations in melanoma tumors.

After ruling out systemic involvement, the patient was followed up for 2 years with no evidence of recurrence. We report this case to the best of our knowledge and discuss the literature about atypical clinical and histological presentations of MC.

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