mart-1-antigen and Hypopigmentation

Treatment of mixed melasma remains challenging. Promising results have been achieved with low-fluence 1064-nm Q-switched Nd-YAG laser; however, multiple sessions are necessary with occurrence of complications especially in dark skin types. So, combination methods may be recommended.. To compare efficacy of Q-switched Nd-YAG laser alone or with modified Jessner's peel in mixed melasma in dark skin.. Nineteen patients with mixed melasma received 6 sessions of laser on left side of face and alternating laser and modified Jessner on right side. Evaluation was carried out clinically through modified melasma area and severity index at 1 month after last session. Using histopathological, immunohistochemical, and computerized morphometric analysis, objective evaluation of melanin particle surface area and MART-1-positive cells was performed for pre- and post-treated skin biopsies.. There was significant clinical improvement on both sides of face (P < .001), without significant difference (P > .05). At the sixth laser session on left side of face, ill-defined mottled hypopigmentation was observed in 21.05% of patients. Histopathologically, melanin particle surface area and number of MART-1-positive cells (total, epidermal, and dermal) were significantly decreased after two treatment modalities (P < .001), without significant difference in their reduction percentage between both sides of face (P > .05).. Low-fluence Q-switched Nd-YAG laser alone and with modified Jessner's peel are equally effective regimens for mixed melasma clinically, histopathologically, and immunohistochemically. However, combined method is preferred, especially in dark skin, for obtaining better cosmetic result with fewer side effects of multiple laser sessions and decreasing cost rate of laser.

Topics: Adult; Biopsy; Chemexfoliation; Combined Modality Therapy; Female; Humans; Hypopigmentation; Lasers, Solid-State; MART-1 Antigen; Melanosis; Middle Aged; Severity of Illness Index; Skin; Skin Pigmentation; Treatment Outcome

As reported in the mass media on July 2013, numerous consumers who had used the cosmetic ingredient containing rhododendrol (4-(4-hydroxyphenyl)-2-butanol, Trade name; rhododenol), which is a melanin inhibitor isolated from Acer nikoense Maxim, released from Kanebo Cosmetics Inc. (Tokyo, Japan) noticed leukoderma patches on their face, neck and hands. We have experienced 32 cases that developed leukoderma after using such cosmetics so far and skin biopsy samples in some cases were obtained from both leukoderma and pigmented lesions. A histopathological analysis for skin lesions obtained from such patients notably showed basal hypo-pigmentation, melanin incontinence, and remaining melanocytes in most patients which is not relevant in vitiligo vulgaris. Subsequently, we comprehensively carried out immunohistochemical analyses of immune-competent cells infiltration to assess the effect of the cellular immune response to inducible hypopigmentation. Furthermore, detailed morphological observations performed by electron-microscopy notably showed the presence of melanocytes with only a small number of melanosomes, dermal fibroblasts containing melanosome globules and melanophages whereas no damage associated with melanosome transfer and the basal layer apparatus. These findings provide a cue to diagnose as rhododenol-induced leukoderma differentiate from vitiligo vulgaris and for rhododendrol to induce local immunity in addition to melanocyte damage.

Topics: Butanols; CD4-CD8 Ratio; Cosmetics; Fibroblasts; Humans; Hypopigmentation; MART-1 Antigen; Melanocytes; Microphthalmia-Associated Transcription Factor; Skin; T-Lymphocytes, Regulatory

Topics: Butanols; Cosmetics; Genotype; HLA-A24 Antigen; Humans; Hypopigmentation; MART-1 Antigen; Melanocytes; Monophenol Monooxygenase; T-Lymphocytes, Cytotoxic

Patients with melanoma may develop skin depigmentation spontaneously or following therapy, referred to as melanoma-associated leucoderma (MAL). As clinical presentation of MAL may precede primary/metastatic melanoma detection, recognition of MAL is important to prevent its misdiagnosis as vitiligo and the subsequent application of immunosuppressive treatment. To reveal the immunity involved in MAL development, we investigated the presence of antibody and T-cell immune responses directed against the melanocyte-differentiation-antigens MART-1 (Melan-A), tyrosinase and gp100 in patients with MAL, as compared to patients with vitiligo. Autoantibodies to gp100 and tyrosinase were commonly found in both diseases. Interestingly, MART-1 antibodies were only present in patients with MAL. Melanocyte antigen-specific T cells were found in all patients, with relatively more specific T cells in patients with active vitiligo. Although MAL and vitiligo may appear clinically similar, our results indicate that the humoral immune responses against MART-1 differ between these diseases, which can help to differentiate MAL from vitiligo.

Topics: Adolescent; Adult; Aged; Antibody Formation; Antibody Specificity; CD8-Positive T-Lymphocytes; Demography; Female; Humans; Hypopigmentation; Male; MART-1 Antigen; Melanocytes; Melanoma; Middle Aged; Vitiligo; Young Adult

Hypopigmentation is a recognized side effect of CO2 laser resurfacing. Pigment abnormalities are a major side effect of facial laser procedures and can cause much emotional distress. We report a case of a patient who, after receiving laser treatment, developed persistent hypopigmentation that has defied a variety of treatment attempts. Results of histologic and immunohistochemical studies support the hypothesis that suppressed melanogenesis rather than just destruction of melanocytes is important in the etiology of the alabaster skin side effect.

Topics: Antigens, Neoplasm; Carbon Dioxide; Humans; Hypopigmentation; Lasers; Male; MART-1 Antigen; Melanocytes; Middle Aged; Neoplasm Proteins; Photosensitivity Disorders; Skin

Lichen sclerosus (LS) shares with vitiligo a milky-white appearance. By biopsy, pathognomonic dermal sclerosis readily distinguishes LS from vitiligo and other causes of leukoderma. To determine what the mechanism of hypopigmentation is in LS, we examined samples from LS cases for alterations in melanin content (Fontana-Masson stain) and melanocyte number (HMB-45 [PMEL-17/gp100], Mel-5 [TRP-1], Mart-1 [Melan A]) and compared these findings with those in controls of normal skin, acute scars, vitiligo, and lichen planus (LP; a common inflammatory cause of hyperpigmentation). The degree and extent of melanization found in LS overlapped with that in acute scars showing predominantly hypomelanized keratinocytes, with that in LP containing regions with numerous melanophages, and with that in vitiligo exhibiting focal regions of keratinocytes devoid of melanin pigment. By hematoxylin-eosin staining and immunocytochemistry for Mel-5 and Mart-1, LS had a lower mean count of melanocytes than acute scars, LP, and normal skin per 200 basal keratinocytes. In addition, a few LS cases had a significant loss of melanocytes comparable to that of vitiligo. Surprisingly, Mart-1 identified rare melanocytes in 67% of vitiligo cases and a significantly larger pool of melanocytes in LS and controls other than those labeled by Mel-5. Furthermore, LP and evolving lesions of LS contained the highest Mart-1 counts. HMB-45-immunoreactive melanocytes were found in the majority of acute scars and in LP and late-stage LS lesions at significantly lower levels than Mel-5- and Mart-1- labeled melanocytes, but they were not found in vitiligo or normal skin. We propose that several mechanisms may play a role in the production of leucoderma in LS: 1) decreased melanin production; 2) block in transfer of melanosomes to keratinocytes; and 3) melanocyte loss. The latter finding may be the pathogenic connection (lichenoid dermatitis of LS triggering an autoimmune reaction to melanocytes) that underlies the documented association of LS with vitiligo.

Topics: Antigens, Neoplasm; Cell Count; Cicatrix; Glycoproteins; Humans; Hypopigmentation; Immunohistochemistry; Lichen Sclerosus et Atrophicus; MART-1 Antigen; Melanins; Melanocytes; Melanoma-Specific Antigens; Monophenol Monooxygenase; Neoplasm Proteins; Skin; Vitiligo

Reports of vitiligo associated with metastases and rare cases of spontaneous regression of disease have fueled enthusiasm for immunologic approaches to the treatment of advanced melanoma. More recent strategies have focused on using antigen-presenting dendritic cells as vaccines.. We observed 3 cases of leukoderma associated with a novel adenovirus-mediated gp100/MART-1-transduced dendritic cell (MART indicates melanoma antigen recognized by T cells). All 3 patients had advanced metastatic melanoma. Despite the development of this leukodermic response, all patients experienced disease progression while under treatment.. We provide the initial evidence for effective induction of a leukodermic response with a gp100/MART-1-transduced dendritic cell vaccine.

Topics: Adenoviridae; Adult; Aged; Antigens, Neoplasm; Biopsy, Needle; Cancer Vaccines; Female; Follow-Up Studies; gp100 Melanoma Antigen; Humans; Hypopigmentation; Male; MART-1 Antigen; Melanoma; Membrane Glycoproteins; Neoplasm Proteins; Neoplasm Staging; Risk Assessment; Skin Neoplasms