Integrated positron-emission tomography and computed tomography manifestations of cutaneous T-cell lymphoma.

Abstract

is highly suggestive of a UV-A–induced mechanism. Photosensitization is an adverse effect of many kinase inhibitors such as imatinib, sorafenib, and vemurafenib. Imatinib inhibits the adenosine triphosphate–dependent transporter ABCG2 resulting in intracellular porphyrin accumulation and phototoxic effects in vitro. Since vandetanib also inhibits the transporter activity of ABCG2, a similar porphyrin-induced mechanism might explain the similar effect. In a report of 2 cases, vandetanib-associated cutaneous pigmentation was preceded by photosensitization. In our more extensive experience, only half of the patients with cutaneous pigmentation had prior or concomitant skin photosensitization, making the hypothesis of post-photosensitization pigmentation less likely. In 3 patients, a multinucleated giant-cell granuloma was found in the dermis, which could result from a direct deposit of the drug in the skin. Vandetanib is being tested in the treatment of several types of cancers. In patients with medullary thyroid cancers, it has already demonstrated a significant efficacy, which led the US Food and Drug Administration and European Medicines Agency to label the drug for patients with advanced disease in 2011. Dermatologists should be aware of the spectrum of vandetanib toxic effects, and careful photoprotection should be used to facilitate compliance with treatment.