Estrogen regulates the expression of retinoic acid synthesis enzymes and binding proteins in mouse skin.

Topical 17-beta-estradiol (E2) regulates the hair cycle, hair shaft differentiation, and sebum production. Vitamin A also regulates sebum production. Vitamin A metabolism proteins localized to the pilosebaceous unit (PSU; hair follicle and sebaceous gland); and were regulated by E2 in other tissues. This study tests the hypothesis that E2 also regulates vitamin A metabolism in the PSU. First, aromatase and estrogen receptors localized to similar sites as retinoid metabolism proteins during mid-anagen. Next, female and male wax stripped C57BL/6J mice were topically treated with E2, the estrogen receptor antagonist ICI 182,780 (ICI), letrozole, E2 plus letrozole, or vehicle control (acetone) during mid-anagen. E2 or one of its inhibitors regulated most of the vitamin A metabolism genes and proteins examined in a sex-dependent manner. Most components were higher in females and reduced with ICI in females. ICI reductions occurred in the premedulla, sebaceous gland, and epidermis. Reduced E2 also reduced RA receptors in the sebaceous gland and bulge in females. However, reduced E2 increased the number of retinal dehydrogenase 2 positive hair follicle associated dermal dendritic cells in males. These results suggest that estrogen regulates vitamin A metabolism in the skin. Interactions between E2 and vitamin A have implications in acne treatment, hair loss, and skin immunity.

Oestrogen receptor-beta expression in melanocytic lesions.

Melanomas rarely occur before puberty, have a higher death rate for males, and tend to be more invasive during pregnancy. Prior to the discovery of a second oestrogen receptor (ERbeta), studies with the initial oestrogen receptor, ERalpha, showed no obvious role for oestrogen in the pathophysiology of benign or malignant melanocytic lesions. To investigate the specific immunostaining patterns of ERalpha and ERbeta, benign nevocytic nevi, dysplastic nevi with mild, moderate and severe cytological atypia, lentigo malignas and melanomas of varying depth (Clark) and thickness (Breslow) were studied. ERbeta but not ERalpha was the predominant oestrogen receptor we found in all types of benign and malignant melanocytic lesions. The most intense ERbeta immunostaining was seen in melanocytes in dysplastic nevi with severe cytological atypia and in lentigo malignas. ERbeta expression levels also correlated with the malignant tumor microenvironment; i.e., melanocytes in proximity with keratinocytes>deeper dermal melanocytes in contact with stroma>minimally invasive melanomas>Clark Level III/IV or thick melanomas (Breslow). Discovery that ERbeta expression varies in relation to the tumor microenvironment and increasing depth of invasion suggests its possible usefulness as a surrogate marker for neoplasia and prognosis in malignant melanoma.

Conjugal transformed mycosis fungoides: the unknown role of viral infection and environmental exposures in the development of cutaneous T-cell lymphoma.

The etiology of mycosis fungoides (MF) is uncertain, although infectious agents and other environmental exposures have been implicated. We describe what appears to be the first case in which both a husband and his wife were diagnosed with large-cell transformation of MF. After 10 years of having stage I MF, the wife developed tumors that showed sheets of large transformed cells with dysplastic nuclei on skin biopsies, leading to a diagnosis of transformed MF. Her husband was diagnosed 14 months later with transformed MF following a biopsy of his right arm and leg after a 15-year history of presumed psoriasis. The fact that this rare occurrence happened in a couple who had been married for more than 25 years points to a common environmental exposure. Future studies should aim to clarify the potential role of infectious agents, such as human T-lymphotropic virus I and II, cytomegalovirus, Epstein-Barr virus, and other environmental exposures, in the development of MF.

Lack of difference in the rates of hypopigmentation with 90-microsecond pulsed and longer dwell time carbon-dioxide laser resurfacing.

BACKGROUND: Hypopigmentation is an adverse outcome associated with carbon-dioxide (CO(2)) laser resurfacing. A 90-microsecond pulse produces a more favorable postoperative course of healing, erythema, and pain compared with a 900-microsecond dwell time. The rate of hypopigmentation after 90-microsecond pulsed CO(2) resurfacing may also be reduced. To date, there have been no comprehensive reports on the effect of varying pulse duration on the occurrence of hypopigmentation. OBJECTIVE: We sought to investigate the relationship between pulse duration and the occurrence of hypopigmentation after CO(2) laser resurfacing. METHODS: We conducted a retrospective review of 447 consecutive patients who were treated with a 90-microsecond pulsed CO(2) laser (n = 229) or a continuous wave CO(2) laser with a modifiable dwell time (100-950 microseconds, n = 218). Follow-up ranged from 8 to 61 months (median: 27). RESULTS: A series of 4 threshold dwell times (range: 90-950 microseconds) were used to divide patients into 2 treatment groups (above and below) at each threshold. The rates of hypopigmentation between groups were similar (range: 6.37%-9.09%) and serial chi-square testing revealed no statistical differences between groups for each dwell time tested (P < 1.0). CONCLUSION: No significant relationship between pulse duration and the occurrence of hypopigmentation was observed.