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Multiple facial lentigines can be disfiguring and can have a big impact on quality of life. In patients with dark skin, treatment options are especially limited.
A 35-year-old Afro-Caribbean woman sought advice about the multiple small hyperpigmented macules on her face, limbs and trunk. She was distressed by her facial appearance and was reluctant to leave her house without heavy camouflage make-up. The dark brown macules had started to appear on her face at the age of 11 and had gradually involved her lips and ears, sparing the mucous membranes. There was a strong family history of this pigment abnormality, with her father, brother and one half-sister similarly affected and her other half-brother and half-sister having only facial lentigines (Figure 1). On examination she had numerous darkly pigmented macules on the face, lips, ears, neck, chest, shoulders, hands, buttocks and thighs. There was no mucous membrane involvement. Her electrocardiogram and echocardiogram were normal. A skin biopsy showed prominent basal hyperpigmentation but no increase in the number of melanocytes. These are characteristics of an ephelid (freckle) rather then a lentigo; however, the symmetrical distribution of the lesions on both sun-exposed and non-sun-exposed areas, and their lack of seasonal variability, was more in favour of lentigines. Satisfactory results were obtained with a test treatment with the Q-switched ruby laser (QSRL) to the lentigines on a small area of her left cheek. Subsequently her facial lesions were treated with QSRL at an energy of 5 J. After four treatment sessions at intervals of six weeks, the appearance of the face was much improved (Figure 2). Over the past seven months there has been no recurrence of the treated lesions and in particular there is no epidermal atrophy, hypopigmentation or reactive hyperpigmentation in the treated areas.
The term lentiginosis is applied to conditions in which lentigines are present in exceptionally large numbers or in a distinctive distribution. There are several pigmentary patterns of lentiginosis and some may be associated with internal abnormalities. The best known of these is the Peutz—Jeghers syndrome, an autosomal dominant condition in which hyperpigmented macules involving the perioral area of the face, mucous membranes, hands and feet are associated with polyps of the gastrointestinal tract and an increased risk of malignancies. The differential diagnosis also includes leopard syndrome, centrofacial lentiginosis and Carney's syndrome, all of which have associated internal abnormalities such as obstructive cardiomyopathy, cardiac myxomas, deafness, mental retardation and bone defects. These abnormalities need to be excluded by clinical examination and non-invasive tests such as electrocardiography and echocardiography. In 1989 O'Neill and James reported ten patients of black colour with autosomal dominant transmission of hyperpigmented macules on the face, hands, feet and buttocks but sparing mucous membranes with no associated internal abnormalities1. Our patient has all the features of the described inherited patterned lentiginosis in blacks.
The QSRL emits light with a wavelength of 694 nm, which is strongly absorbed by melanin and can destroy benign pigmented lesions by selective photothermolysis2. However, pigmented lesions in patients with dark skin are particularly difficult to treat because of the risk of producing hypopigmentation or reactive hyperpigmentation, which may be more prominent than the original lesion. Our patient had a good response to a test treatment at energies of 5.5 J and 7.5 J and further successful treatment with 5 J to the symmetrical parts of the face. We suggest that patients with coloured skin should not be discouraged from having laser treatment, though a test treatment should be done first.