The pathogenesis of melasma has not been clearly elucidated. Using Fontana Masson; diastase-resistant periodic acid-Schiff stains; and immunohistochemistry to stem cell factor (SCF), its receptor c-kit, anti-mast cell tryptase, and anti-collagen type IV antibody, we evaluated melasma lesions and compared them with perilesional skin and photoprotected skin. Samples were taken from lesional and photoprotected nonlesional skin in 24 patients. In other 24 patients, we took biopsies of lesional and perilesional skin. With Fontana Masson, we observed many pigmented basal cells protruding into the dermis of the melasma skin. Periodic acid-Schiff stain and anti-collagen type IV showed damage on the basal membrane in 95.5% and 83%, respectively, in melasma lesion. The immunoreactivity of SCF and the prevalence of mast cells were increased in the dermis of melasma compared with perilesional dermis. The expression of c-kit was significantly increased at lesional epidermis; a frequent protrusion of c-kit-positive basal cells into the dermis was evident in 70% versus that in 29% of perilesional skin. The expression of c-kit was increased at lesional dermis of melasma compared with perilesional skin. We found a low correlation between c-kit expression and prevalence of mast cells; these were increased in melasma skin. The results may suggest a role of SCF, c-kit, and mast cells in the pathogenesis of melasma. We were surprised by the unexpected evidence of damage to basal membrane (BM), which could facilitate the fall or the migration of active melanocytes and melanin into the dermis allowing the constant hyperpigmentation in melasma.

Melasma is an acquired hypermelanosis on sun-exposed areas. Its pathogenesis has not been clearly elucidated. Using histochemistry (Giemsa, Verhoeff-van Gieson and Fontana-Masson staining), we evaluated melasma lesions and compared them with nonlesional skin. Skin samples were obtained from lesional and nonlesional facial skin of 27 patients with melasma, and biopsies were also taken from normal control subjects. Mast cells and solar elastosis areas were evaluated using a computer-assisted image-analysis program. Lesional skin had abundant elastotic material compared with nonaffected skin (13.3 +/- 2.8% vs. 10.2 +/- 2.9%, P < 0.001). Mast cells were more prominent in the elastotic areas of melasma skin (173 +/- 57% vs. 145 +/- 57%, P = 0.04). Melasma could be a result of a cumulative sun exposure, in a microenvironment of cutaneous photoageing in which inflammatory cells, particularly mast cells, play a key role.

Background. Multiple modalities have been used in the treatment of melasma with variable success. Niacinamide has anti-inflammatory properties and is able to decrease the transfer of melanosomes. Objective. To evaluate the therapeutic effect of topical niacinamide versus hydroquinone (HQ) in melasma patients. Patients and Methods. Twenty-seven melasma patients were randomized to receive for eight weeks 4% niacinamide cream on one side of the face, and 4% HQ cream on the other. Sunscreen was applied along the observation period. They were assessed by noninvasive techniques for the evaluation of skin color, as well as subjective scales and histological sections initially and after the treatment with niacinamide. Results. All patients showed pigment improvement with both treatments. Colorimetric measures did not show statistical differences between both sides. However, good to excellent improvement was observed with niacinamide in 44% of patients, compared to 55% with HQ. Niacinamide reduced importantly the mast cell infiltrate and showed improvement of solar elastosis in melasma skin. Side effects were present in 18% with niacinamide versus 29% with HQ. Conclusion. Niacinamide induces a decrease in pigmentation, inflammatory infiltrate, and solar elastosis. Niacinamide is a safe and effective therapeutic agent for this condition.

BackgroundAxillary hyperpigmentation is a frequent cause of cosmetic consultations in dark-skinned women from tropical areas, including Latin America. Currently, there is no widely accepted treatment for the disorder, but it is usually treated with bleaching agents because it is considered a variant of inflammatory hyperpigmentation. The purpose of this study was to assess the efficacy of niacinamide 4% and desonide 0.05% emulsions compared with placebo in the treatment of axillary hyperpigmentation.MethodsTwenty-four women aged 19–27 years with hyperpigmented axillae (phototype III–V) were randomly assigned to receive the study treatments in the axillary region. Improvement was assessed at baseline, then clinically and by colorimetry 9 weeks later. Quantitative evaluation including melanin, inflammatory infiltrates, NKI/Beteb, CD1a, CD68, and collagen type IV content was performed by histochemistry and immunohistochemistry, assisted by computerized morphometric analysis.ResultsBoth niacinamide and desonide induced significant colorimetric improvement compared with placebo; however, desonide showed a better depigmenting effect than niacinamide. A good to excellent response was achieved in 24% of cases for niacinamide, 30% for desonide, and 6% for placebo. We observed a marked disruption of the basal membrane in axillary hyperpigmentation and an inflammatory infiltrate that improved after treatment. Decreased pigmentation in the desonide-treated axillae was associated with recovery of disruption at the basal membrane.ConclusionNiacinamide and desonide showed depigmenting properties in women with axillary hyperpigmentation. These findings may be explained by their antimelanogenic and anti-inflammatory properties, respectively.

Using these factors, a prognostic scale was developed to predict high risk of recurrence in cases of completely resected CRC and to identify them as a subgroup of patients with potential benefit of adjuvant chemotherapy.