Background Bullous pemphigoid (BP) is a chronic immune-mediated vesiculobullous disorder. Recently, several reports have described dipeptidyl peptidase-4 inhibitors, also known as gliptins, as causative agents for drug-induced BP. Objective To report and describe clinical and histologic characteristics of 10 cases of gliptin-induced BP. Results We identified 10 patients with gliptin-induced BP. Nine were secondary to linagliptin, and 1 case was attributed to sitagliptin. All patients showed significant improvement after withdrawal of gliptin medications and proper medical treatment. There has been no evidence of relapse after 4 months of follow-up. Conclusion This report supports the proposed association between gliptins and BP. Physicians should be aware of this potential adverse effect, as gliptin-induced BP can be reversible once identified and the responsible medication is stopped. Early withdrawal of the offending drug and proper treatment can lead to rapid improvement and reduced morbidity.

Biologic drugs are increasingly being prescribed for the treatment of psoriasis. Very little information is available in the literature regarding potential drug interactions with these medications. This paper serves as a guide for prescribers to be aware of possible interactions between biologic drugs approved for the treatment of psoriasis in North America and concomitant therapies. Objective To provide an overview of reported drug interactions between biologic drugs and concomitant therapies. Methods Reports of potential drug interactions were compiled through a search of Micromedex, drug monographs (Canadian, American, and European), as well as a PubMed search of each biologic drug with the term “drug interaction.” Conclusion Generally, caution should be exercised when multiple immunosuppressive therapies are prescribed due to increased risk of infection. However, this is more the result of a synergistic effect as opposed to a true drug interaction. There have been cases where multiple biologic therapies have been concomitantly used without adverse events, as their mechanisms involved different pathways. The sources used to compile this guide were often comprised of low levels of evidence, reinforcing the idea that further studies are required to better direct prescribers.