Partial Unilateral Lentiginosis Successfully Treated with the Combination of 511 nm and 578 nm Copper Bromide Laser in an Indonesian Woman

Introduction

Lentigines are discrete, irregular, and hyperpigmented macules mainly caused by chronic ultraviolet (UV) light exposure.¹ Lentigines with a segmental pattern that do not cross the body midline are referred to as partial unilateral lentiginosis (PUL). The main histopathological feature of PUL is an increase in melanin pigmentation in the epidermal basal layer,^2,3 similar to lentigines.³

Patients with PUL often have a psychological burden due to aesthetically-unpleasing skin appearance.⁴ The treatment of PUL aims to improve the aesthetic aspect of the skin.⁵ One of the therapeutic options is laser therapy with melanin as its main target, including the 511 nm copper bromide (CuBr) laser, also known as a green laser. The CuBr laser also emits light with a wavelength of 578 nm, known as yellow laser, which is commonly used for vascular lesions.^6,7

Laser treatment using vascular targets is becoming increasingly popular. Vascular endothelial growth factor (VEGF) receptors that respond to angiogenic factors have been found in melanocytes.^6,7 Lee et al⁷ reported increased VEGF expression in patients with melasma who were subsequently treated with a 578 nm CuBr laser at two-week intervals. A decrease in VEGF expression was reported one month after the final laser treatment session. The 578 nm CuBr laser may have an effect on melanogenesis through VEGF on keratinocytes, dermal angiogenesis, and inflammatory mediators.⁷ This case report aims to report a case of improved PUL after treatment with a combination of 511 nm and 578 nm CuBr laser.

Case

A 35-year-old Indonesian woman of Sundanese ethnicity presented with brownish hyperpigmented macules at the level of the V1 and V2 nerves on the forehead and right cheek (Figure 1). Eleven years before admission, the patient worked as a tour guide and was often exposed to sunlight. The patient had Fitzpatrick-type IV skin. The lightness (L*) values of spectrophotometry were 56.16, 58.12, and 59.77 on the right forehead, upper right cheek, and lower right cheek, respectively. Histopathological examination showed increased melanin pigmentation in the basal layer of the epidermis and inflammatory cell lymphocytes in the papillary dermis fibrocollagenous connective tissue (Figure 2), which confirmed the diagnosis of PUL in the forehead and right cheek.

Figure 1 (A) Hyperpigmented macules at the level of the V1 and V2 nerves on the forehead and right cheek. (B) Hyperpigmented macules on the forehead. (C) Hyperpigmented macules on the right cheek.

Figure 2 Histopathological features of a punch biopsy of the hyperpigmented macule on the right cheek showed an increase in melanin pigmentation in the basal layer of the epidermis (red circle).

Topical treatment given included sun protection factor (SPF) 50 cream and the priming agent, a mixture of 0.01% tretinoin cream and 4% hydroquinone cream in a 1:1 ratio. The priming agent was applied to the entire face at night because the patient would undergo laser treatment in “shining bright” mode, which targeted the entire face. The patient also underwent a two-step CuBr laser treatment at different wavelengths. The first step involved the 511 nm, 30 J/cm² fluence, and 125 ms with a 0.6 mm handpiece until a grayish lesion is observed, which serves as the endpoint. The second step continued immediately after the first step, using the 578 nm laser in “shining bright” mode at 3.2 kW peak power for 100 cm² with a 1 mm handpiece until the skin became brighter. Informed consent related to the treatment has been obtained from the patient.

The hyperpigmented macules reduced and faded after one session of treatment (Figures 3A and B), and the spectrophotometry L* values became 57.04, 59.38, and 60.1 on the right forehead, upper right cheek, and lower right cheek, respectively (Figure 4). Significant improvement was observed after the two treatment sessions (Figure 3C). Spectrophotometry L* values were increased to 57.77, 59.56, and 61.45 on the right forehead, upper right cheek, and lower right cheek, respectively (Figure 4). The patient felt that she had brighter facial skin. We also observed that a favorable and sustainable result persisted after six months of laser treatment.

Figure 3 Comparison of hyperpigmented macules on the forehead and right cheek. (A) Before treatment. (B) After one session of treatment. (C) After two sessions of treatment.

Figure 4 The L* values of spectrophotometry.

Discussion

Partial unilateral lentiginosis is a skin pigmentation disorder in the form of asymptomatic lentigines⁷ that appear as brownish macules⁸ scattered on normal skin^2,3 in a segmental pattern with the involvement of one or more dermatomes^3,6 with well-defined midlines.² Park et al⁹ reported that the onset of PUL occurs at a mean age of 14 years (range = 6–26 years) and is mainly diagnosed between 7–41 years, with a mean age of 27 years. The prevalence is similar in males and females.¹⁰ PUL can occur anywhere on the body, including the face, neck, trunk, and extremities,² in one or more dermatomes.^2,3 The patient in this case report is a 35-year-old woman complaining of brown patches on her forehead and right cheek, which first appeared at age 15.

The pathogenesis of PUL is not fully understood but is thought to be related to somatic mosaicism during embryonic development due to mutations confined to melanoblasts from the neural crest.² Both melanocytes and nerve cells have an ectodermal origin.³ Mosaicism occurs in somatic cells, meaning that it is not inherited by subsequent generations. Several pigmentary genes in germ cells, such as SNAI2, KITLG, EDNRB, EFNB1, and EFNB2, are associated with pigmentary mosaicism, which plays a role in neural crest differentiation and melanoblast migration.²

The histopathological appearance of PUL is similar to that of lentigines,³ including increased melanin pigmentation in the basal layer of the epidermis^2,3 and elongation of rete ridges.¹⁰ Histopathological examination of the lesion on the current patient’s right cheek showed increased melanin pigmentation in the basal layer and elongation of the rete ridges, suggestive of lentigines, supporting the diagnosis of PUL.

The main etiology of lentigines is chronic exposure to UV light,¹ so counseling on photoprotection measures such as shelter or avoiding sun exposure, use of photoprotective clothing, hats, glasses, and sunscreen with an SPF of 30 or more is necessary.¹¹ Avoiding sun exposure and applying sunscreen regularly can also prevent post-inflammatory hyperpigmentation, which occurs 7–14 days after laser treatment.¹¹ Decreasing the melanin content in the skin before the laser treatment can decrease the rate of post-inflammatory hyperpigmentation.¹² Tretinoin works by motivating epidermal and dermal turn-over, which may cause rapid loss of cell pigment.¹³ Hydroquinone is considered the primary and most effective topical agent for blocking melanin production through inhibition of the tyrosinase enzyme in melanocytes.^12,13 The patient in this case report was counseled on photoprotection and given SPF 50 sunscreen cream on the first day of treatment. A mixture of 0.01% tretinoin and 4% hydroquinone cream at a ratio of 1:1 was applied nightly to the whole face to prime it for laser treatment. Complication in the form of post-inflammatory hyperpigmentation after laser treatment have not been reported.

The CuBr laser can emit two wavelengths, 511 nm and 578 nm.⁷ The 511 nm wavelength is often used for pigmented lesions and tends to be absorbed to a greater degree by melanin, resulting in a more selective damage.¹⁴ Dinehart et al¹⁴ reported the success of lentigine treatment after the administration of a CuBr 511 nm laser. The 578 nm CuBr laser is primarily used for vascular lesions; however, its targets consist not only of hemoglobin but also melanin. Melanocytes have VEGF receptors, which can respond to angiogenic factors.⁶ The interaction between skin vasculature and melanocytes is also associated with the development of pigmented lesions. Therefore, the CuBr 578 nm laser has direct and indirect effects on skin vasculatures and pigmented lesions, such as melasma.^6,7 Cho et al⁶ reported improvements of lentigines after two months of two-stage CuBr 578 nm laser at a one-month interval. The first stage was given in the fast edge micropulse (FEM) mode setting, 3 kW peak power, 100 cm² area, 2–3 passes with continuous movement using a 1 mm handpiece in contact with the gel. In the second stage, the gel was cleaned, then given an energy of 30 J/cm², off time of 250 ms, and 1 pass, using a 0.6 mm handpiece.⁶ In the first treatment session, a two-wavelength combination treatment of the CuBr laser was performed in two stages. The first stage was administered with a wavelength setting of 511 nm, 30 J/cm², and an off time of 125 ms using a 0.6 mm handpiece. In the current patient, the endpoint appeared grey. The second stage was set at a wavelength of 578 nm, Shining Bright mode, 3 kW peak power, 25 cm² area, and continuous movement using a 1 mm handpiece in contact with the gel. The endpoint of immediate whitening was observed in the patient. In the second treatment session, there was a clinically significant improvement as the brown spots on the forehead and right cheek faded. In addition, the skin appeared brighter. A significant improvement was also observed in the spectrophotometry of hyperpigmented macules on the forehead, upper right cheek, and lower right cheek as there was an increase in L* values from 56.16, 58.12; and 59.77, to 57.77, 59.56; and 61.45, respectively.

Conclusion

The favorable response in this case report were achieved by addressing interaction of cutaneous vasculature and melanocyte which detained the development of pigmented lesions. Although this is only one case report presented successful outcome, the use of the combination of 511 nm and 578 nm CuBr laser can be considered as an alternative and effective therapeutic option particularly in PUL.