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The treatment of postburn hypopigmentation was primarily surgical before the advent of new technologies. Medical devices and therapies are emerging to manage scar sequelae that can be disfiguring and associated with severe psychosocial impact. These innovations have been poorly investigated for hypopigmentation, but they represent a real hope. We reviewed all articles published on Pubmed up to June 2022. Included studies had to specifically focus on treating postburn hypopigmented scars. All articles evaluating transient solutions such as make-up, and articles describing inflammation-linked hypopigmentation with no etiological details or no burn injury history were excluded. Through this review, we have highlighted 6 different types of nonsurgical treatments reported in postburn leukoderma potentially allowing definitive results. Electrophoto-biomodulation or E light (combining intensive pulsed light, radiofrequency, and cooling), topical daylight psoralen UVA therapy, and lasers (fractional lasers using pulse energies or CO2FL devices, lasers-assisted drug delivery as local bimatoprost and tretinoin or pimecrolimus) have been explored with encouraging results in hypopigmented burns. Finally, other promising medical strategies include using FK506, a nonsteroidal anti-inflammatory drug, to induce melanogenesis or using melanocyte-stimulating hormones with fractional laser-assisted drug deliveries, which are expected to emerge soon.

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Vitiligo patients may desire laser hair removal, skin rejuvenation, vascular treatments, and other laser or intense pulsed light (IPL) assisted treatments. However, there is a risk of inducing new depigmented patches (Koebner phenomenon). In absence of guidelines on the safe use of laser or IPL in vitiligo patients, dermatologists tend to be reluctant to administer these treatments. The aim of this survey study was to provide an estimation of the occurrence and related risk factors of laser/IPL-induced leukoderma or vitiligo. A cross-sectional survey study was performed among 15 vitiligo experts from 11 countries, with 14 questions about affected patients, involved laser/IPL treatments and the physicians' approach. In a total of 11,300 vitiligo patients, laser/IPL-induced leukoderma or vitiligo was reported in 30 patients (0.27%). Of these, 12 (40%) patients had a medical history of vitiligo and seven (58%) of these patients had stable (> 12 months) vitiligo before the treatment. Most frequently reported were hair removal procedures and localization of the face and legs. Side effects like blistering, crusting, and erosions occurred in 56.7% of the cases. These vitiligo experts based their advice on the risk of the laser treatment on stability of the vitiligo (43%) and activity signs (50%), and 50% discuss the risks before starting a laser treatment. Relevant activity signs are the Koebner phenomenon (57.1%), confetti-like lesions (57.1%) and hypochromic borders (50%). Laser-induced leukoderma or vitiligo is an uncommon phenomenon. Remarkably, a minority had a medical history of vitiligo of which 58% were stable. Consequently, most cases could not have been prevented by not treating vitiligo patients. However, a majority had laser/IPL-induced skin damage. Therefore, caution is advised with aggressive settings and test-spots prior to the treatment are recommended. This study showed significant variation in the current recommendations and approach of vitiligo experts regarding laser/IPL-induced leukoderma or vitiligo.

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OBJECTIVES: Nevus of Ota is a benign melanocytic lesion that presents as a unilateral blue gray to brown facial patch favoring the distribution of the first two branches of the trigeminal nerve. Incidence is highest in Asian and Black populations, however, the overwhelming majority of studies are limited to diagnosis and treatment in Asian patients. We herein present 10 Black patients with Fitzpatrick skin types (FST) V and VI who underwent laser treatment for Nevus of Ota. METHODS: We performed a retrospective review of Black patients presenting with Nevus of Ota. Race was self-designated by all patients and documented in the medical record at the time of initial consultation. Primary outcomes were based on improvement using before and after photographs which were graded by three independent board-certified dermatologists using a 5-point visual analog scale. RESULTS: Ten FST V or VI patients with an age range of 9 months to 45 years were treated for Nevus of Ota. All patients were treated with the 1064 nm Q-switched neodymium doped yttrium aluminum garnet (QS Nd:YAG) and on average received 4.7 treatments at 2-10 month intervals. Fluence ranged from 1.8 to 2.3 J/cm2 , and total pulse count ranged from 510.9 to 776.6. 2/10 patients were additionally treated with 1550 nm nonablative fractional resurfacing (NAFR), and 1/10 patients underwent combination therapy with both NAFR and 1064 nm picosecond laser therapy. Overall, patients saw a mean improvement of 51%-75% at follow-up 5-254 weeks (mean 51.5 weeks) after treatment. Three patients experienced mild guttate hypopigmentation in treated areas. No other long-term adverse events were encountered. CONCLUSION: 1064 nm QS Nd:YAG laser therapy is a safe and efficacious treatment for Nevus of Ota in patients with FST V and VI. When patient improvement plateaus, combining therapy with 1550 nm NAFR or transitioning to 1064 nm picosecond laser may be of benefit. Patients should be counseled on the risk of guttate hypopigmentation. This is the largest case series to date of Black patients with Nevus of Ota, highlighting the need for further investigation to determine optimal device settings and treatment parameters for this population.

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Postinflammatory hypopigmentation is an acquired form of hypopigmentation that occurs secondary to an exogenous or endogenous insult to the skin. It can occur in all skin phototypes but is more visually apparent in skin of color. Due in part to greater attention given to its counterpart, postinflammatory hyperpigmentation, there is a dearth of literature describing this entity and treatment options remain limited. This review provides a comprehensive update on the pathogenesis, diagnostic evaluation and treatment of postinflammatory hypopigmentation, with a focus on newly reported treatment modalities.

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BACKGROUND: Despite history of multiple treatment modalities, repigmentation of hypopigmented scars remains a difficult clinical problem. OBJECTIVE: The purpose of this review is to evaluate the literature on laser and combination laser plus adjunct topical therapy for hypopigmented burn and traumatic scars. MATERIALS AND METHODS: A search on PubMed and on Oxford Academic was conducted with additional relevant literature obtained from reference lists. RESULTS: Treatment regimens that address hypopigmentation within scars were reviewed. A combination of nonablative fractional or ablative fractional laser treatment with topical prostaglandin analogue with or without topical retinoid were found to result in superior repigmentation. CONCLUSION: Reliable improvement of hypopigmentation in scars after laser treatment is challenging. Laser can achieve success in some cases. Ultraviolet laser can achieve modest repigmentation; however, results are short-lived and require continued re-treatment. Modest improvement in pigmentation is seen with nonablative fractional laser or ablative fractional laser alone and enhanced repigmentation is demonstrated when combining fractional laser resurfacing with topical application of synthetic prostaglandin analogues and other known modulators of melanogenesis.

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La hipomelanosis macular progresiva es un trastorno adquirido de la pigmentación que aparece con más frecuencia en mujeres, adolescentes y adultas jóvenes. Se caracteriza por máculas hipopigmentadas asintomáticas, mal delimitadas, no descamativas, simétricas y de predominio en región lumbar. El estudio histopatológico evidencia disminución del contenido de melanina en la epidermis afectada, con número y distribución de los melanocitos conservados. En su etiopatogenia interviene el Cutibacterium acnes tipo III, bacteria responsable de la característica fluorescencia rojiza de distribución folicular que se observa con la lámpara de Wood. Por este motivo, los tratamientos propuestos incluyen el uso de tetraciclinas por vía oral y tratamientos tópicos como el peróxido de benzoílo, asociados a fototerapia UVA o UVB de banda angosta. Se presenta una paciente con hipomelanosis macular progresiva del tronco que respondió satisfactoriamente al tratamiento con doxiciclina vía oral

Progressive macular hypomelanosis is an acquired pigmentation disorder that occurs mostly in adolescent and young women. It is characterized by asymptomatic, poorly defined, non-scaly, symmetrical hypopigmented macules localized predominantly in the lumbar area. Histopathology shows a decrease in melanin content with preserved number and distribution of melanocytes in the affected epidermis. Cutibacterium acnes type III appears to be the responsible for the dermatosis and for the characteristic reddish fluorescence of follicular distribution observed with Wood´s lamp. Treatment include oral tetracyclines and topical benzoyl peroxide associated with UVA or narrow band UVB phototherapy. We present a patient with progressive macular hypomelanosis of the trunk with excellent response to treatment with oral doxycycline

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Idiopathic guttate hypomelanosis (IGH) is a benign, typically asymptomatic, acquired leukoderma characteristically affecting mature individuals. Although the etiopathogenesis is unclear, chronic sun exposure and senile degeneration are important triggers. Researchers have been engaged in a continuous effort to unveil the gray areas encompassing different aspects of IGH pathogenesis. IGH is a clinical diagnosis; however, histopathology and dermoscopy may aid in quetionable cases. Patients often seek cosmetic treatment. There has been no standard therapy for this condition. Newer treatment modalities range from topical agents to procedure-based therapies and have enhanced the therapeutic armamentarium. Here we discuss the pathogenesis, presentation, and management of IGH.

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Primary immunodeficiency diseases (PIDs) are a group of more than 400 disorders representing aberrant functioning or development of immune system. Hypopigmentation syndromes also characterize a distinguished cluster of diseases. However, hypopigmentation may also signify a feature of genetic diseases associated with immunodeficiency, such as Chediak–Higashi syndrome, Griscelli syndrome type 2, Hermansky–Pudlak syndrome type 2 and type 10, Vici syndrome, and P14/LAMTOR2 deficiency, all of which are linked with dysfunction in vesicular/endosomal trafficking. Regarding the highly overlapping features, these disorders need a comprehensive examination for prompt diagnosis and effective management. As an aid to clinician, distinguishing the pathophysiology, clinical phenotype, and diagnosis as well as treatment options of the six mentioned PID disorders associated with hypopigmentation are described and discussed in this review (AU)

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Primary immunodeficiency diseases (PIDs) are a group of more than 400 disorders representing aberrant functioning or development of immune system. Hypopigmentation syndromes also characterize a distinguished cluster of diseases. However, hypopigmentation may also signify a feature of genetic diseases associated with immunodeficiency, such as Chediak-Higashi syndrome, Griscelli syndrome type 2, Hermansky-Pudlak syndrome type 2 and type 10, Vici syndrome, and P14/LAMTOR2 deficiency, all of which are linked with dysfunction in vesicular/endosomal trafficking. Regarding the highly overlapping features, these disorders need a comprehensive examination for prompt diagnosis and effective management. As an aid to clinician, distinguishing the pathophysiology, clinical phenotype, and diagnosis as well as treatment options of the six mentioned PID disorders associated with hypopigmentation are described and discussed in this review.

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Pigmentation disorders are a frequent skin problem and incorporate a broad spectrum of diseases, caused by an abnormal melanin pigmentation or also non-melanin pigmentation of the skin. Both hypermelanosis and hypomelanosis can be hereditary or acquired. This article summarizes the treatment approaches that are used in the majority of acquired pigmentation disorders of the skin. The following forms of hypermelanosis are addressed: lentiginosis, hyperpigmentation due to endocrine disorders or other systemic diseases, drug-induced hyperpigmentation. Acquired hypomelanoses include postinflammatory hypomelanosis, chemical depigmentation, idiopathic guttate hypomelanosis and punctate leucoderma. With reference to non-melanin pigmentation, the exogenous pigmentation due to chemicals, metals and drug exposure are discussed. The treatment is primarily based on finding the cause of the alterations to the pigment. The affected area, age and ethnic origin are also important factors. The spectrum of therapeutic options is broad: topical agents, chemical peeling, systemic agents, laser and light-based treatment. As some of these treatment procedures can have side effects, the availability of a protocol that contains information on the drug concentration, dose, parameters for laser treatment and the number of sessions is important. For every disorder the specific dermatological treatment is presented even when some pigmentation alterations that occur in association with systemic diseases, are cured by the treatment of the primary disease. Most diseases are exacerbated by exposure to UV light. Therefore, sun protection is recommended and a cosmetic coverage is indicated.

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Skin resurfacing techniques allow improvement of skin texture and color. This includes the effacement of wrinkles, signs of photoaging, and the softening of scars. Laser resurfacing, chemical peels, and dermabrasion are associated with overlapping risks of complications. The most common of these include infection, hypopigmentation, hyperpigmentation, and scarring. Patient evaluation helps provide treatment that gives the maximal benefit with a minimization of risks. This includes understanding the extent of each patient's issues (Glogau scale) and Fitzpatrick type. A thorough knowledge of potential risks will reduce their incidence and optimize early recognition and treatment of these complications when they do occur.

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Nevus depigmentosus, a disorder of hypopigmentation, occurs in both sexes and all races. It most commonly presents in early infancy and childhood as a nonprogressive hypomelanotic macule. It is considered a form of cutaneous mosaicism due to somatic mutation in pigmentary genes, which results in functional impairment of melanocytes. Clinical forms include localized, segmental, and systemized. Rare cases of nevus depigmentosus may be associated with systemic features. Treatment is usually not required, although certain techniques such as suction-blister grafting, excimer laser, and cosmetic camouflage have been tried with variable results. Counseling of parents plays a significant role to allay apprehension and anxiety.

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Depigmented lesions may occur as postinflammatory sequelae of subacute cutaneous lupus erythematosus (SCLE), leading to great psychosocial impact. A 53-year-old male patient presented with post-SCLE depigmented facial lesions after five years of disease stability. We proposed surgical treatment with melanocyte-keratinocyte transplantation procedure (MKTP), and after five months the patient achieved 90% repigmentation, without Koebner phenomenon (KP). In theory, KP is a possible complication of MKTP procedure since the preparation of the receptor area involves the use of dermabrasion. In an attempt to avoid it, we suggest to maintain the treatment of the underlying disease and wait for a minimum period of disease stability before the procedure.

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Nevus depigmentosus (ND), also known as nevus achromicus or achromic nevus, is an uncommon congenital hypomelanosis of the skin that is often characterized as being nonprogressive and having serrated borders. It needs to be distinguished from other hypopigmented skin conditions such as nevus anemicus, hypomelanosis of Ito, Fitzpatrick patches (ash leaf spots) of tuberous sclerosis, vitiligo, indeterminate leprosy, and pigment demarcation lines. Treatment may be desired for aesthetic and possible psychosocial considerations. We review and update knowledge about ND and its simulants.

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Aging skin is subject to morphological change due to both intrinsic (skin tone, genetics, endogenous hormones) and extrinsic (chronic sun exposure, medications, exogenous pigments) factors. The broad spectrum of transformation includes both hypo- and hyperpigmentation. Although cutaneous pigmentary disorders are common in younger individuals, certain disorders are more prevalent in the geriatric population. This article reviews the epidemiology, pathophysiology, clinical appearance, treatment, and prognosis of pigmentary lesions that are predominant in the elderly.

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