Background Bullous pemphigoid (BP) is the most frequent autoimmune blistering dermatosis. Recently, the development of BP in patients treated with gliptins, also known as DPP-4 inhibitors, alone or in association with metformin has been outlined in case reports. A possible mechanistic explanation that links gliptins with BP comes from the findings that DPP-4 inhibition enhances the activity of proinflammatory eotaxin chemokine and promotes eosinophil activation in the skin, which is known to contribute to blister formation in BP.
Objective To investigate a potential role of the gliptins in the development of BP in patients at the department of Dermatology of the University Hospital in Lausanne.
Methods We reviewed all patients with BP diagnosed at the University Hospital of Lausanne (CHUV) between January 2007 and July 2013 (n= 93). We assessed the causal relationship between BP development and the intake of gliptins for each patient according to the World Health Organization and Uppsala Monitoring Centre (WHO-UMC) scale, a standardised causality assessment scale of adverse drug reactions. We compared our results with the existing literature.
Results The yearly number of BP cases increased between 2007 and 2013. 23/93 BP patients had type 2 diabetes. The proportion of diabetic patients treated with gliptins in our study was 9/23 (39%) which is higher than the estimated proportion of patients treated with gliptins among the diabetic population (10-20%). In all nine cases, the causal relationship between drug intake and BP onset was classified as "possible", according to the WHO-UMC scale, which represents a probability less than 50% for BP to cause the disease.
Conclusion Our study shows a weak but possible correlation between gliptins intake and BP development. Thus gliptins may entertain the disease or unmask a subclinical disease in predisposed individuals. We must be aware of this potential dermatological side effect and have to evaluate diabetic patients to benefit from this drug with very good tolerability and few side effects. Studies on a larger scale are needed to further elucidate the mechanisms that would confirm the role of gliptins in the pathogenesis of bullous pemphigoid.