Epidemiological, clinical, histological, and immunohistochemical study on hypopigmented epitheliotropic T-cell dyscrasia and hypopigmented mycosis fungoides.

BACKGROUND: Hypopigmented dermatoses, more evident in dark-skinned people, are a frequent cause of consultation. Their etiology includes a wide range of dermatoses, from benign to malignant diseases. The clinical presentation appears very similar between them, making the correct diagnoses and management a challenge. METHODOLOGY: Clinical records and histopathological biopsies were identified and compared in patients of the "Dr. Manuel Gea González" General Hospital throughout a 16-year period with the presumptive diagnosis of hypopigmented epitheliotropic T-cell dyscrasia (HTCD) or hypopigmented mycosis fungoides (HMF). Immunostaining analysis was performed in each specimen, the panel of antibodies used was: CD3, CD4, CD7, CD8, CD20, and CD62L. RESULTS: Thirty cases of 81 patients found in the registries were included in this study. The main age group was formed by children younger than 15 years old. The main clinical differences between both entities were gender, presence of plaques, and neck lesions. The most significant histopathological parameters used to differentiate both diagnoses were: severity of lymphocytic infiltration, the extent of epidermotropism, folliculotropism, presence of Pautrier's microabscesses, lymphocytes with cerebriform nuclei, and dermal fibroplasia. No immunohistochemical differences were found between them. CONCLUSION: The clinical distinction between HTCD and HMF continues to be a challenge, therefore an extensive clinicopathological correlation must be performed. AbCD7 and AbCD62L were not useful to differentiate both dermatoses. This paper suggests that HTCD and HMF should be considered as the beginning and the end of the same clinical spectrum.

Serum of Patients with Psoriasis Modulates the Production of MMP-9 and TIMP-1 in Cells of Monocytic Lineage.

Psoriasis is triggered by several stimuli that share a systemic production of interferon (IFN)-γ and other inflammatory mediators, which are key to regulate the production of matrix metalloproteinase (MMP)-9 and its inhibitor (TIMP)-1 by cells of monocytic lineage. This study evaluates the effect of the sera of 55 patients with psoriasis and 41 non-psoriatic individuals on the production of MMP-9 and TIMP-1 in cultured monocytes from a single healthy blood donor and in U937 cells. The effect of IFN-γ stimulation was also evaluated. Serum and supernatant concentrations of IFN-γ, MMP-9, and TIMP-1 were measured by enzyme-linked immunoassays, and the MMP-9/TIMP-1 ratios were calculated. In monocytes, incubation with psoriasis' sera increased the production of MMP-9 and TIMP-1 in comparison with both baseline and monocytes incubated with non-psoriatic sera. Although the MMP-9/TIMP-1 ratio was significantly higher compared to the baseline, no differences between groups were observed. In contrast, IFN-γ stimulation in monocytes previously exposed to psoriasis' sera increased MMP-9 levels and decreased TIMP-1 levels, whereas stimulation in monocytes exposed to non-psoriatic sera did not further modify the levels of MMP-9 or TIMP-1. Consequently, the MMP-9/TIMP-1 ratio in cells exposed to psoriatic serum was significantly higher than in cells exposed to non-psoriatic sera (24.5 versus 16.7; P < 0.05). Similar results were observed in U937 cells. Therefore, our results suggest that soluble mediators in psoriatic sera may enhance the proteolytic phenotype of monocytes when stimulated with IFN-γ, which supports the existence of a primed state in the inflammatory cells of patients with psoriasis.