Diagnostic and therapeutic techniques in lentigo maligna: an update.

Please cite this article as: Collgros H, Lamas-Doménech N. FR-Lentigo maligno, actualización en técnicas diagnósticas y terapéuticas. Actas Dermosifiliogr. 2015;106:135--136. ∗ Corresponding author. E-mail address: [email protected] (H. Collgros). Differential diagnosis includes seborrheic keratosis, solar lentigo, lichenoid keratosis, actinic keratosis, and pigmented actinic keratosis. Dermoscopic criteria may assist in the diagnosis of LM and LMM, but lack full sensitivity and specificity. While histologic diagnosis is the gold standard, atypical melanocytes are rare and sparsely distributed in these two conditions. LM is thus difficult to distinguish from melanocytic hyperplasia in photodamaged skin, and lesion margins are hard to define. Some authors have recently highlighted the importance of questioning any histopathological diagnosis of junctional nevus, dysplastic nevus, or atypical lentiginous nevus for lesions occurring in photodamaged skin on the face and neck. Nevi in this area are typically papuletype lesions of the same color as adjoining skin, but are clinically different from LM. Any of the above nevus diagnoses may underestimate an LM lesion as a benign junctional melanocytic proliferation. Immunohistochemistry can be of use in these equivocal cases. Typical markers include S100, human melanoma black-45 antigen (HMB-45), melan-A (MART-1), and microphthalmia-associated transcription factor (MITF), all of which are highly sensitive to melanocytes. However, these markers fail to differentiate melanocytic nevi from melanoma lesions; P16 protein expression and proliferation markers Ki-67 and pHH-3 help with this. Identification of specific mutations in the BRAF, NRAS and KIT genes may be of use, especially given the recent availability of targeted drugs. Reflectance confocal microscopy (RCM) was introduced to improve diagnostic accuracy, define the extent of a lesion,