Ephelides in Adult
The pigment in ephelides occurs due to an increased number of melanized melanosomes and increased transportation of these melanosomes from melanocytes to keratinocytes. The gene encoding for melanocortin-1 receptor plays a role in the development of ephelides. Individuals with light skin phototypes and blond or red hair, and those with a family history of ephelides, are at a higher risk of developing these lesions.
Ephelides are benign and do not undergo malignant transformation. However, they are markers of ultraviolet (UV) damage and therefore may signal an increased risk of UV-induced skin malignancies including melanoma.
Multiple simple lentigines can be seen in genetic conditions such as Carney complex (LAMB / NAME syndromes), LEOPARD syndrome, Laugier-Hunziker syndrome, Bandler syndrome, and Peutz-Jeghers syndrome.
L81.2 – Freckles
403536009 – Ephelis
Differential Diagnosis & Pitfalls
- Simple lentigo
- Solar lentigo – Solar lentigines are often present at later ages, persist for life, do not change with sun exposure, and are generally larger than 5 mm. Dermoscopy demonstrates diffuse light brown, structureless areas and a reticular pattern with thin lines. Borders can be sharp or moth-eaten.
- Café-au-lait macules – Usually solitary, and larger than ephelides.
- Junctional nevi are typically darker.
- Amalgam tattoo
- Pigmented actinic keratoses appear later in life and feel rough or gritty on palpation.
- Seborrheic keratoses appear later in life and are raised.
- Atypical nevus
- Melanoma / melanoma in situ (see lentigo maligna)