Propylthiouracil‐induced antineutrophil cytoplasmic antibody positive vasculitis clinically mimicking pyoderma gangrenosum

work-up in our case excluded possible causes of LCV such as autoimmune disease, infection and malignancy. Furthermore, our patient made a remarkable clinical improvement after cessation of famciclovir which suggested that the cause of vasculitis was more likely to be drug-related rather than VZV-induced, as cessation of famciclovir would have probably exacerbated the latter. Thus, we believe that famciclovir was the causative drug in our case. Famciclovir is the prodrug of penciclovir, a guanosine analog that is indicated for herpes simplex virus and VZV infections. It is generally well tolerated and only few adverse reactions have been reported, with the most common being headache, nausea and diarrhea. Only two cases of famciclovir-induced LCV have been reported in the published work. There has been no report of acyclovir-induced vasculitis; however, famciclovir is both chemically and structurally different to acyclovir. The differences in molecular structures may explain why our patient tolerated acyclovir rather than famciclovir. Treatment of drug-induced LCV includes discontinuation of offending agents, anti-inflammatory medications and supportive care. Avoidance of rechallenge of offending drugs should be recommended to prevent subsequent complications. Anti-inflammatory medications such as corticosteroids, colchicine, antihistamines, dapsone and topical antibiotics can be used in cases with persistent disease activity. In conclusion, famciclovir-induced LCV is an exceedingly rare event and clinicians should be aware of famciclovir as a potential cause of LCV because it is widely used in the treatment of herpes simplex virus and VZV infections.