mart-1-antigen and Hyperpigmentation

Psoriatic lesions may resolve with hypo- or hyperpigmentation. The involvement of melanocytes in this dichotomous clinical outcome is not fully investigated.. Qualitative and quantitative assessment of melanocytes in untreated lesional and non-lesional psoriatic skin (n = 15) and healthy controls (n = 10).. Skin biopsies were labelled immunohistochemically (APAAP technique) with the antimelanocyte monoclonal antibodies (MoAbs) HMB45, Melan A, tyrosinase and microphthalmia-associated transcription factor (MITF). The labelled melanocytes were evaluated by an independent investigator with a digital image analyser.. Lesional melanocytes, in contrast to those in non-lesional and healthy skin, exhibited features of activation in the form of dilatation, prominent and long dendrites and intense labelling. The number of melanocytes was significantly increased in psoriatic lesions in comparison with non-lesional psoriatic and healthy skin as shown by counts of cells labelled with the MoAbs HMB45 (3-fold; p < 0.001), Melan A (1.6-fold; p < 0.01) and tyrosinase (1.5-fold; p < 0.01). In contrast, labelling with MITF revealed no significant difference (1.2-fold increase; p > 0.05). Likewise, no significant difference between non-lesional psoriatic and healthy skin control was found (p > 0.05). Furthermore, no positively labelled dermal cells were detected, apart from few only detected with Melan A.. Epidermal melanocyte activity and numbers are increased in the epidermal compartment of psoriatic lesions providing an explanation for postinflammatory hyperpigmentation.

Topics: Adult; Aged; Biopsy; Cell Count; Disease Progression; Epidermis; Female; gp100 Melanoma Antigen; Humans; Hyperpigmentation; Immunohistochemistry; Keratinocytes; Male; MART-1 Antigen; Melanocytes; Melanoma-Specific Antigens; Middle Aged; Monophenol Monooxygenase; Psoriasis

Tyrosinase is a key enzyme in the biosynthetic pathway of melanin pigments. Abnormal accumulation of melanin pigments causes melasma, freckles, and senile lentigo, which can be substantially ameliorated by treatment with arbutin or other tyrosinase inhibitors. In this study, roots of Angelica koreana Maxim. (Umbelliferae) inhibited melanin production in α-melanocyte stimulating hormone ( α-MSH)-activated B16 melanoma cells or melan-a melanocytes. To elucidate the hypopigmenting principle of A. koreana, the plant extracts were subjected to bioassay-guided phytochemical analysis, resulting in the identification of bisabolangelone. Bisabolangelone dose-dependently inhibited α-MSH-induced melanin production in B16 or melan-a cells with IC(15) values of 9-17 µM. The positive control arbutin also inhibited melanin production in B16 cells with an IC(50) value of 317 µM. Bisabolangelone suppressed α-MSH-inducible protein levels of tyrosinase in B16 cells but could not significantly inhibit the catalytic activity of cell-free tyrosinase. Taken together, this study indicates that bisabolangelone is the primary hypopigmenting principle of A. koreana and may have pharmacological potential in the melanin-associated hyperpigmentation disorders.

Topics: alpha-MSH; Angelica; Animals; Cell Line; Cell Line, Tumor; Dermatologic Agents; Dose-Response Relationship, Drug; Hyperpigmentation; Inhibitory Concentration 50; MART-1 Antigen; Melanins; Melanocytes; Melanoma, Experimental; Monophenol Monooxygenase; Phytotherapy; Plant Extracts; Plant Roots; Sesquiterpenes; Skin

We encountered recently 3 cases with a histopathologic diagnosis of melanoma in situ on sun-damaged skin (male = 2, female = 1; median age: 59 years; range: 52-60 years). The diagnosis was based mainly on the finding of actinic elastosis in the dermis and increased number of melanocytes in the epidermis and was confirmed by strong positivity for Melan-A in single cells and in small nests ("pseudomelanocytic nests"), located at the dermoepidermal junction. Indeed, examination of slides stained with hematoxylin and eosin revealed the presence of marked hyperpigmentation and small nests of partially pigmented cells at the dermoepidermal junction, positive for Melan-A. The histologic and especially the immunohistochemical features were indistinguishable from those of melanoma in situ on chronic sun-damaged skin. In addition, a variably dense lichenoid inflammation was present. Clinicopathologic correlation, however, showed, in all patients, the presence of a lichenoid dermatitis (phototoxic reaction, 1 case; lichen planus pigmentosus, 1 case; and pigmented lichenoid keratosis, 1 case). Our cases clearly show the histopathologic pitfalls represented by lichenoid reactions on chronic sun-damaged skin. Immunohistochemical investigations, especially if performed with Melan-A alone, may lead to confusing and potentially disastrous results. The unexpected staining pattern of Melan-A in cases like ours raises concern about the utility of this antibody in the setting of a lichenoid tissue reaction on chronic sun-damaged skin. It should be underlined that pigmented lesions represent a paradigmatic example of how immunohistochemical results should be interpreted carefully and always in conjunction with histologic and clinical features.

Topics: Antigens, Neoplasm; Biopsy; Dermatitis, Phototoxic; Diagnosis, Differential; Diagnostic Errors; Female; Humans; Hyperpigmentation; Immunohistochemistry; Lichenoid Eruptions; Male; MART-1 Antigen; Melanocytes; Melanoma; Middle Aged; Neoplasm Proteins; Predictive Value of Tests; Skin; Skin Neoplasms; Sunlight