Background
A lentigo is a small, sharply circumscribed, pigmented macule surrounded by normal-appearing skin. Histologic findings may include hyperplasia of the epidermis and increased pigmentation of the basal layer. A variable number of melanocytes are present; these melanocytes may be increased in number, but they do not form nests. Lentigines may evolve slowly over years, or they may be eruptive and appear rather suddenly. Pigmentation may be homogeneous or variegated, with a color ranging from brown to black.
Multiple clinical and etiologic varieties exist. The distinction of a lentigo from other melanocytic lesions (eg, melanocytic nevi, melanoma) and its role as a marker for ultraviolet damage and systemic syndromes is of major significance.
A case-controlled study in France comparing 145 adults with multiple solar lentigines on the upper back and 145 matched control subjects found that multiple solar lentigines on the upper back and shoulders of adults may serve as clinical markers of past severe sunburn and may be used to identify a population at higher risk of developing cutaneous melanoma.[1]
Note the images below.
Woman with solar lentigo.
Close-up view of a woman with solar lentigo. Pathophysiology
Depending on the type of lentigo present, a solitary lesion or multiple lesions that can occur anywhere on the body. Some lentigines have associated systemic manifestations that accompany the skin lesions, such as the LEOPARD syndrome.
A Japanese microarray analysis evaluation of solar lentigo in 16 adults demonstrated up-regulation of genes related to inflammation, fatty-acid metabolism, and melanocytes and down-regulation of cornified envelope-related genes.[2] The researchers suggested solar lentigo may be induced by the mutagenic effect of repeated past UV light exposures, leading to characteristic enhancement of melanin production.
Little is known about the genetic basis of human solar lentigines, which were analyzed for potential FGFR3 and PIK3CA mutations. FGFR3 mutations were detected in 5 (17%) of 30 solar lentigines, and PIK3CA mutations were detected in 2 (7%) of 28 solar lentigines, suggesting that FGFR3 and PIK3CA mutations are involved in their pathogenesis and further substantiating previous speculations that UV exposure may be a causative factor for FGFR3 and PIK3CA mutations in human skin.[3]
The LEOPARD syndrome may be associated with a mutation in the PTPN11 gene at Thr468Met.[4]
Epidemiology
Frequency
United States
In America, solar lentigines are observed in as many as 90% of whites older than 60 years and in 20% of whites younger than 35 years. Psoralen plus UVA (PUVA) lentigines are noted in almost one half of individuals with psoriasis who receive PUVA therapy for at least 5 years.
Lentigo simplex is the most common form of lentigo, but its frequency has yet to be determined. Alper and Holmes[5] noted multiple lentigines in 91 (18.5%) of 492 black newborns and 1 (0.04%) of 2682 white newborns; however, histologic confirmation of these lesions was lacking.
International
Lentigines are observed worldwide. The incidence depends on the type of lesion.
Seborrheic keratosis and lentigo solaris were found to be increased on the driver side of the face in an evaluation of truck drivers in Turkey assessing the effects of UV light.[6]
Mortality/Morbidity
Lentigines are benign by nature. However, some lentigines are associated with systemic abnormalities, in addition to the dermatologic manifestations.
Race
Solar lentigines are more abundant in fair-skinned whites than in dark-skinned individuals, in whom the disease is distinctly uncommon because they have a greater amount of natural pigment that provides some degree of photoprotection.
Inherited patterned lentiginosis can occur in blacks, particularly those with mixed American Indian heritage and those with relatives with red hair.[7]
Ephelides, PUVA lentigines, tanning-bed lentigines, vulvar lentigines, ink-spot lentigines,[8] oral and labial melanotic macules, and Laugier-Hunziker syndrome are also more common in people with light skin than in those with dark skin. Ink-spot lentigo occurs in patients of Celtic ancestry.
Acral lentigines are more common in dark-skinned individuals, but they may also be present in light-skinned individuals.
Sex
PUVA lentigines are more common in men than in women. Tanning-bed lentigines and oral and labial melanotic macules are more common in women than in men.
Age
Lentigines can appear in both children and adults; however, children are more likely to have genetically associated lesions such as those of Peutz-Jeghers syndrome.
Adults are more likely to acquire lesions due to chronic exposures, which cause solar lentigo for example.
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