Melasma is a notoriously recidivist condition with yet unclear etiopathogenesis. It seems to have a multifactorial origin with both genetics and environment playing an important role. A genetic predisposition is suggested by a high reported incidence in family members in certain racial groups. Among the environmental factors, exposure to ultraviolet and visible light constitutes the biggest risk factor. Onset or worsening of melasma during pregnancy and during or following intake of hormonal oral contraceptive pills suggest the involvement of hormonal factors. The role of cutaneous vasculature in its pathogenesis is suggested by presence of clinically appreciable telangiectatic erythema confined to the melasma lesional skin in many patients, a finding reinforced by dermatoscopic evaluation and detection of upregulated expression of vascular endothelial growth factor, in the lesional skin. Various other factors such as thyroid disorder, drugs, cosmetics, stress may exacerbate existing melasma in a subset of patients. Although the precise molecular pathogenesis of melasma remains mysterious, up regulation of inducible nitric oxide synthase and many melanogenesis-related genes and melanocyte markers such as TYR, MITF, SILV, and TYRP1, Wnt pathway modulator genes, genes of prostaglandin metabolic processes, and those regulating lipid metabolism seem to be operative. In summary, though the exact etiopathogenesis of melasma remain appalling, newer studies have provided corporeal evidence in favor of certain previously suspected and some novel factors. Further research in this area will not only provide more evidence for their involvement in the pathophysiology of melasma, but also offer attractive targets for development of newer treatment modalities. This article exhaustively reviews the validity of the previously postulated etiological factors based on hitherto-accrued evidence, and explores the newer suggested pathogenetic mechanisms, which may pave way for development of novel therapeutic strategies.

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Tranexamic acid (TXA), an antifibrinolytic drug, is now gaining popularity as a depigmenting agent. It is a synthetic lysine amino acid derivative which mainly blocks the conversion of plasminogen to plasmin by inhibiting plasminogen activator. This results in less free arachidonic acid production, and hence a reduction in the prostaglandin (PG) levels as well. Thus, by reducing PG production, TXA reduces the melanocyte tyrosinase activity and plays an important role in the treatment of melasma, ultraviolet-induced hyperpigmentation, and other postinflammatory hyperpigmentation. It has been tried topically, orally, and intradermally in the management of melasma with minimal adverse effects. However, more randomized trials are needed to fully elucidate the exact mechanism of action, ideal route, frequency, and duration of administration of the drug, along with its potential to treat other pigmentary disorders.

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Lichen planus pigmentosus (LPP) is a condition characterized by persistent and asymptomatic slaty-gray pigmentation, predominantly in the face. Classically, the pattern is “actinic” with symmetric and diffuse pigmentation in sun-exposed areas, commonly in dark-skinned individuals. It can also rarely present as macular pigmentation of the flexures in the lighter-skinned. LPP is a disease of the middle-aged, with onset in the third to fourth decades of life and few studies show as slightly greater incidence in females. The photo-distributed or actinic pattern, which is more common, is a disease of tropics and Type IV–Type V skin types. Reports are mainly from India, the Middle East, and South America. The inversus type is relatively rare, predominantly occurring in Caucasians. LPP is thought to be a type hypersensitivity IV reaction to unknown antigen with lichenoid inflammation, leading to melanin incontinence and superficial dermal pigmentation. The natural course of the disease is not clear with some cases showing spontaneous resolution, and some cases with persistence of pigmentation for years. In addition, LPP may have marked overlap clinically and histologically with conditions such as pigmented contact dermatitis, differentiation of which may not be possible in routine practice. Because of these issues, as well as the relative rarity of the condition, there is not much evidence on the efficacy of the various treatment options. Currently, none of the available treatment options show consistent responses or a clear superiority to other modalities, the evidence on efficacy being restricted to a few case series.

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Melasma is one of the most common pigmentary disorders worldwide with a still unresolved pathogenesis and treatment continues to be challenging. Increased sun exposure and genetic factors are considered the two most important etiological factors. Estrogens, progesterones and increased melanocyte stimulating hormone are also involved. Melasma treatment can be very frustrating as many modalities can turn out to be ineffective. Dermal and mixed variants are quite resistant to therapy. Most patients seek medical help much after the onset of the condition, making treatment even more difficult. Sunscreens and topical depigmenting agents remain mainstay of therapy. Chemical peels and light sources are beneficial as adjuncts. There have been numerous advances in the understanding and management of melasma. This review attempts to look at these newer vistas in melasma. Literature search for the review was done from PubMed, the Cochrane Library, MEDLINE and Embase using the key word "melisma," "melasma pathogenesis" and "melasma treatment."

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Skin is an easily accessible source of various sub population of stem cells including epidermal stem cells, hair follicle stem cells (HFSCs) and dermal mesenchymal stem cells. The outer root sheath (ORS) of the hair follicle is a rich source of a type of HFSCs called the melanocytes stem cells (MelSCs). These HFSCs have a vast, unexplored potential in the treatment of vitiligo as initial re-pigmentation often occurs around the hair follicles. Common therapeutic modalities such as tacrolimus, phototherapy and dermabrasion acts through MelSCs. Newer cellular techniques have explored the use of ORS hair follicle suspension in surgical treatment of vitiligo. Advancement in melanocyte and stem cell research has identified various cytokines, growth factors and regulators involved in proliferation and differentiation of melanoblasts, which can be used for autologous in situ melanocyte regeneration. In this review, we briefly discuss the current position and future prospects of stem cells in vitiligo.

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In today’s world, physical appearance and the desire to look young are very important. Skin and hair play a powerful role in this as they impart much information, not only about our race, ethnicity, and health but also about gender and age. We experience a significant change in pigmentation during our journey of life from birth to puberty and then to young adulthood, middle age, and beyond. Graying of hair is a conspicuous sign of aging. It is said that 50% of the people have 50% gray hair by the age of 50. Premature graying or premature canities is defined as graying that occurs before the age of 20 in Caucasians, before 25 in Asians, and before 30 in Africans. The pathogenesis of premature canities is not yet clear but various hypotheses have been suggested including alteration in pH and cysteine levels in melanosomes, the role of trace metal ions, vitamin B₁₂ and folic acid, vitamin D₃, and oxidative stress. Along with increased awareness, there is an increased demand for treatment modalities but the options are limited and unsatisfactory. Various topical preparations containing phytic acid, amino acids, peptides, acetyl hexapeptide-1, melitane, capixyl, pea proteins, etc. are already available in the market. Currently, research is focusing on topical liposome targeting melanins, genes, and proteins selective to hair follicles for therapeutic and cosmetic modification of hair.

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Vitiligo is the most common depigmentary disorder that has been affecting human lives across centuries. Despite its high prevalence, not much can be said precisely about its pathogenesis. Over the years, several theories based on a lot of research have been put forward and many more are coming up each day. This article aims to summarise the various theories put forward so far and highlight the Recent updates in each of them.

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Nevus depigmentosus is a congenital disorder of pigmentation which occurs in all sexes and races. It commonly presents in childhood and is mostly nonprogressive. It is a form of cutaneous mosaicism with functionally defective melanocytes and abnormal melanosomes. Localized solitary lesions need to be differentiated from conditions like nevus anemicus, ash leaf macule, vitiligo, etc., and generalized lesions from hypomelanosis of Ito. Treatment is usually not required although cosmetic camouflage, phototherapy, grafting, and other modalities may be tried.

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We report a case of lichen planus pigmentosus (LPP) that developed in a linear pattern, that too over nonsun-exposed areas. The patient presented with linear dark brown macules and patches on the back in the midline. Skin biopsy showed features consistent with a diagnosis of LPP. LPP should be considered in the clinical differentials of linear hyperpigmented skin lesions.

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Background: Melasma is a common, acquired and symmetrical hypermelanosis characterized by more/less dark brownish macules, with an irregular contour, but clear limits, on photoexposed sites. The pathogenesis is unknown, but several clinical patterns and etiological factors have been implicated. Aims: Our present study aims to elucidate the epidemiology, clinical patterns and etiological factors in the causation of melasma in North Indians. Methods: A total of 200 consecutive patients attending the out-patient clinic from September 2013 to February 2104 with the clinical diagnosis of melasma were enrolled for the study. Photographic record was kept to study the clinical patterns. Results: The mean age of patients with melasma was 32.9 years, ranging from 18 to 60 years. Female patients out-numbered male patients, and ratio of female to male patients was 6.14:1. Patients sought medical treatment on an average of 1.79 years after appearance of melasma. 48.84% of female patients and 78.57% of males reported exacerbation with sun exposure. 36.4% of the females reported onset of melasma during pregnancy. Family history was observed in 29.07% of our female patients and 14.28% of males. History of use of mustard oil either for massage or for cooking was given by 54.07% of females and 32.14% of males, while 45.35% of females and 32.14% of males used topical corticosteroids or over-the-counter products for the treatment of melasma. Centro-facial was the most common pattern observed in 76.74% of the female patients while the malar pattern was seen in 85.71% of males. Other patterns we observed were mandibular (3.5%), lateral cheek (1.5%) and brachial (1%). Conclusion: The exact pathogenesis of melasma is unknown. Here in we have tried to elucidate the epidemiology, clinical patterns, and etiological factors in the causation of this pigmentary imperfection.

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Background: Several factors have been implicated in the etiology of melasma which include ultraviolet radiation, genetics, pregnancy, skin type, and drugs. However, there is a paucity of literature regarding the role of endocrine factors. Aim: To study the clinical and hormonal correlation in female patients with melasma. Methods: A total of 30 untreated female patients with melasma were included in the study. The control group included an equal number of age-matched females. Assays of free testosterone, total testosterone, dehydroepiandrosterone sulfate, 17-hydroxyprogesterone, luteinizing hormone (LH), follicle stimulating hormone, prolactin, 17β-estradiol (E2), progesterone, free triiodothyronine, free tetraiodothyronine, thyroid stimulating hormone were done on the 5^th or 6^th day of the menstrual cycle in the midfollicular phase. Results: The difference between means of free testosterone, total testosterone, LH, estradiol, progesterone, and free thyroxine of melasma cases and controls was found to be statistically significant. No correlation was found between the severity of melasma and the mean hormone levels. Conclusion: It can be inferred that these hormonal alterations may represent a subclinical evidence of a suppressed hypothalamic-gonadal axis and preclude the role of hormones in the pathogenesis of melasma.

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Background: Melasma is a known, acquired, pigmentary disorder among females. It is very difficult to treat because of its variable response to treatment and rapid recurrence. Dermoscopy is an essential tool, by which, we can classify melasma based on its colour pattern and other findings. Aims and Objectives: To classify melasma by dermoscopic examination and correlate dermoscopic findings with the clinical diagnosis. Materials and Methods: A total of 100 patients attending the out patient department of skin department were included in the study. After obtaining the consent, the patients were examined in detail. The dermoscopic examination was performed, and findings were noted. Results: Out of 100 patients, who enrolled in this study, 80 patients were females, and 20 patients were males. On dermoscopy, 46 patients showed epidermal pattern, out of which 13 were males and 34 were females. Eighteen patients showed dermal pattern and 36 patients showed mixed pattern on dermoscopy. Between dermoscopic analysis and colour, a significant association was observed (Cramer’s V value = 0.534; P value = 0.000). We found that epidermal pattern was more associated with a light brown colour, whereas, the dermal pattern and mixed pattern were associated with ash grey colour and dark brown colour, respectively. Statistical analysis was performed by using percentage and bar diagrams. Both descriptive and inferential statistics were employed. Cramer’s V test was applied to find out the association using the Statistical Package for the Social Sciences software (SPSS Inc., Chicago, IL, USA). Conclusion: Dermoscopy can be used to assess the type of melasma by analysing colour pattern, as well as depth of pigmentation and to differentiate between melasma and exogenous ochronosis. From our observations, we conclude that dermoscopy can be used as a tool in the management of melasma and other dermatological disorders.

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Background: Lichen planus (LP) is a unique inflammatory papulosquamous disorder that affects the skin, hair, nail and mucous membranes, and is associated with a relapsing and remitting course. Aim: To study the clinicopathological profile in patients diagnosed with LP. Methods: A cross-sectional prospective study of 100 freshly diagnosed cases of LP over a period of 1 year, wherein following patient enrolment, they underwent a thorough clinical evaluation followed by a biopsy, that was carefully studied and evaluated. Results: A male preponderance (60%) was observed. Majority of the patients were in the 21–40 years age group (60%). Pruritus was witnessed in 84% of the patients. The morphological types of cutaneous LP encountered were classical (58.9%), hypertrophic (28.4%), linear (4.2%), lichen planopilaris (LPP) (4.2%), bullous (2.1%) and LP pigmentosus (2.1%). Out of the 42 patients with oral LP, reticulate type was present in 85.7% patients and erosive variant in the remaining 14.3%. Spotted hypergranulosis was a finding seen in 100% of the cutaneous biopsies taken. Hyperkeratosis was identified in 92.6%, pigmentary incontinence in 93.7% and subepidermal band like lymphocytic infiltrate in 92.6%. In none of the patients of LPP were the characteristic microscopic findings identifiable. In oral mucosal biopsies, dysplastic changes were evident in 50% of the participants. Conclusion: LP is a disorder more common in males usually manifesting in the 3^rd to 4^th decade of life, with the classical type of cutaneous LP and reticular variant of oral LP being most commonly encountered. Dysplastic changes in oral LP demonstrated a value of 50% in our study, a value much higher when compared to previous reports, thus mandating vigilant identification of the same for appropriate patient management.

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Postinflammatory hyperpigmentation (PIH) is a common pigmentary disorder that is distressing to patients, particularly those with skin of color, and can be very difficult to treat. Part of this difficulty arises from the dermal melanosis in addition to the epidermal hyperpigmentation. This article reviews the mechanisms that induce the hyperpigmentation including inflammatory mediators such as metabolites of arachidonic acid and reactive oxygen species (ROS) and how these may influence prevention and treatment strategies. Treating the inflammatory cause and sun protecting are crucial to effective therapy. Although common, few studies have been done focusing on prevention and treatment of this disease. Topical therapies are the mainstay of treatment for PIH, but have shown poor efficacy for the dermal hyperpigmentation component. Hydroquinone in combination with topical steroids, retinoids, glycolic acid, and lactic acid have been augmented with numerous emerging natural therapies such as kojic acid, arbutin, ascorbic acid, soy, and niacinamide. Although efficacious for hyperpigmentation, most of the natural therapies have not been studied specifically for PIH. Salicylic acid and glycolic acid chemical peels, as well as the quality-switched (QS) neodymium-doped yttrium aluminum garnet (Nd: YAG), QS Ruby, 1550 nm erbium fiber fractional thermolysis, and 1927 nm fractional thulium fiber lasers have shown good efficacy for the treatment of facial hyperpigmentation.

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Amyloidosis cutis dyschromica (ACD) is a very rare and distinctive variant of primary cutaneous amyloidosis, clinically characterized by the appearance of hyperpigmented and hypopigmented or depigmented macules on normal looking skin before puberty in generalized distribution. We herein report a 30-year-old male with ACD involving whole body except hands, feet, palm, soles, genitalia, and mucosa since 10 years of age and positive family history. His 25-year-old younger sister also had the similar mottled pigmentary lesions since 8 years of age. On histopathological examination (HPE) of the hyperpigmented macules, increased melanin in the basal layer, pigmentary incontinence, and amorphous eosinophilic deposits were seen in the papillary dermis. HPE of depigmented lesions demonstrated a significant decrease in the number of melanocytes and melanin in the basal layer along with deposition of eosinophilic amyloids in papillary dermis. Based on these HP findings, diagnosis of ACD was made.

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Background: Vitiligo has a complex etiopathogenesis. The role of nutritional factors (including Vitamin B₁₂and folic acid) has been recently proposed in its causation, which needs to be confirmed further. Aims: The study was conducted: (1) To estimate the serum levels of Vitamin B₁₂, folic acid, and homocysteine in patients of vitiligo and control group. (2) To determine the relationship between serum levels of Vitamin B₁₂, folic acid, homocysteine and the extent and activity of vitiligo. Methods: A cross-sectional, observational study consisting of 50 patients with vitiligo, and 35 age and sex matched controls was conducted. Serum homocysteine was estimated by Diazyme homocysteine enzymatic assay kit, and serum Vitamin B₁₂and folic acid levels were estimated by chemiluminescence using the Access Immunoassay System. Results: The mean serum Vitamin B₁₂and folate levels were found to be significantly lower in vitiligo patients than controls (157.18 ± 68.95 pg/mL vs. 306.6 ± 169.73 pg/mL and 4.18 ± 3.55 ng/mL vs. 7.3 ± 3.67 ng/mL, respectively), while serum homocysteine levels were significantly higher in cases (15.39 ± 7.2 μmol/L) as compared to controls (11.88 ± 4.81 μmol/L) (P < 0.05). There was a significant positive correlation of serum homocysteine levels with the duration of disease, Vitiligo Area Scoring Index (score), and type of vitiligo (higher levels in patients with universal vitiligo). Conclusions: Long standing vitiligo (especially universal and generalized variants) may show deranged serum homocysteine, Vitamin B₁₂, and folic acid levels. Supplementation with Vitamin B₁₂/folic acid may have a therapeutic role in improving the treatment outcome.

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Background: Vitiligo prevails to be a skin disease with endless possibilities but no promises. Despite substantial research in pathogenesis and therapeutic modalities, the literature is deplete with technologies to predict the probabilities for repigmentation with or without therapy in the common generalized vitiligo. Aim: To correlate pretreatment melanin index in skin patches of nonsegmental vitiligo to probable extent of repigmentation following 6 months of monotherapy with a topical corticosteroid. Methods: A prospective study was conducted including thirty patients of vitiligo and their melanin index (melanin value; pigmentation index) in representative skin lesion was determined using Mexameter^® MX 18. Patients were studied under three groups (A, B, and C) based on the obtained melanin indices. The extent of repigmentation following 6 months of topical therapy with mometasone furoate 0.1% cream was correlated with pretreatment melanin indices. Results: Repigmentation in Group C (mean melanin index >200) was significantly higher in terms of number of patients (P = 0.000) and area of patch coverage (P = 0.00) as against the other two groups with lower melanin indices. Conclusion: Melanin index in depigmented lesions is a useful indicator in the management of nonsegmental vitiligo to predict the repigmentation and to choose the appropriate treatment option. Mexameter is a simple, noninvasive, low cost staging, and monitoring device to estimate the melanin reservoir in vitiligo.

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Progressive macular hypomelanosis (PMH) is a common and often misdiagnosed disorder characterized by numerous nummular, coalescing hypopigmented macules on the trunk of adolescents, and young adults. It was originally described in patients with Fitzpatrick skin types V-VI from tropical countries, but is now understood to have a worldwide distribution in a variety of skin types. The pathogenesis of PMH is unknown, but is thought to involve Propionibacterium acnes, which has been found in abundance in the pilosebaceous units of lesional skin. Biopsies of lesions demonstrate normal architecture of epidermis and dermis, but exhibit decreased melanin content. It is important to note that this is different from vitiligo, which has a total absence of melanin. Many patients with PMH often times go misdiagnosed for tinea (pityriasis) versicolor, postinflammatory hypopigmentation, and other dyschromias. Topical antifungal and corticosteroid therapy have proven ineffective in PMH, but successes have been reported with topical and systemic antibacterial treatment modalities and even phototherapy. Given the increasing prevalence of patients with skin of color, it is important to better understand the nature of this condition, along with its diagnosis, management, and treatment.

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