Skin, hair and beyond: the impact of menopause.

The skin is an endocrine organ and a major target of hormones such as estrogens, androgens and cortisol. Besides vasomotor symptoms (VMS), skin and hair symptoms often receive less attention than other menopausal symptoms despite having a significant negative effect on quality of life. Skin and mucosal menopausal symptoms include dryness and pruritus, thinning and atrophy, wrinkles and sagging, poor wound healing and reduced vascularity, whereas skin premalignant and malignant lesions and skin aging signs are almost exclusively caused by environmental factors, especially solar radiation. Hair menopausal symptoms include reduced hair growth and density on the scalp (diffuse effluvium due to follicular rarefication and/or androgenetic alopecia of female pattern), altered hair quality and structure, and increased unwanted hair growth on facial areas. Hormone replacement therapy (HRT) is not indicated for skin and hair symptoms alone due to the risk-benefit balance, but wider potential benefits of HRT (beyond estrogen's effect on VMS, bone, breast, heart and blood vessels) to include skin, hair and mucosal benefits should be discussed with women so that they will be able to make the best possible informed decisions on how to prevent or manage their menopausal symptoms.

Recent progresses in understanding pigmentation.

Human pigmentation involves production and dispersion of melanin by epidermal melanocytes to neighboring keratinocytes. Melanin synthesis or melanogenesis occurs within the specialized organelle termed melanosomes where the amino acid L-tyrosine serves as the starting precursor. Melanocytes from individuals of different pigmentary phenotypes differ in their rate and types of melanin synthesis, as well as in the rate and manner of melanosome transfer. Modern molecular biology methods and the use of transgenic animals have greatly advanced our understanding in the molecular and cellular mechanisms regulating human pigmentation and its disorders. This review examines recent advances in the regulation of human pigmentation and their implication in treatments for the pigmentary disorders.

Cellular mechanisms regulating human melanogenesis.

The major differentiated function of melanocytes is the synthesis of melanin, a pigmented heteropolymer that is synthesized in specialized cellular organelles termed melanosomes. Mature melanosomes are transferred to neighboring keratinocytes and are arranged in a supranuclear cap, protecting the DNA against incident ultraviolet light (UV) irradiation. The synthesis and distribution of melanin in the epidermis involves several steps: transcription of melanogenic proteins, melanosome biogenesis, sorting of melanogenic proteins into the melanosomes, transport of melanosomes to the tips of melanocyte dendrites and finally transfer into keratinocytes. These events are tightly regulated by a variety of paracrine and autocrine factors in response to endogenous and exogenous stimuli, principally UV irradiation.

DNA polymorphisms: what they are and their role in human pigmentation.

The color of the skin, hair and eye is controlled by multiple genes and is among the most visible examples of human phenotypic variation. Genetics correlate phenotypic with genotypic variation. Recent scientific work reveals DNA polymorphisms at least partially responsible for some of the differences observed in human pigmentation. These are the focus of this review.

Sunscreens--what's important to know.

The popularity of sunscreens dramatically increased since ultraviolet irradiation was implicated in the pathogenesis of skin cancer and skin ageing. The absorption properties, safety, photostability of different organic and inorganic filters are reviewed: para-aminobenzoic acid, salicylates, cinnamates, benzophenones, butylmethoxydibenzoylmethane (Parsol 1789), drometrizole trisulphonic (Mexoryl XL), terephthalydene dicamphor sulphonic acid (Mexoryl SX), methylene bisbenzotriazol tetramethylbutylphenol (Tinasorb M), anisotriazine (Tinasorb S), titanium dioxide and zinc oxide. Furthermore, this review discusses the optimal methods for measuring the protection that a sunscreen offers, the role of sunscreen use in melanoma prevention and future trends in sunscreen filters development.

The Greek experience with efalizumab in psoriasis from a University Dermatologic Hospital.

BACKGROUND: Efalizumab (anti-CD11a antibody) targets T cell-mediated steps important in the immunopathogenesis of psoriasis. As efalizumab is intended to be administered on a continuous long-term basis in psoriasis, it is important to share experience concerning issues commonly occurring during its use in real daily practice. OBJECTIVE: To evaluate the efficacy and safety of efalizumab treatment in Greek patients with moderate-to-severe plaque psoriasis, and to investigate whether there are specific characteristics that predict the clinical outcome of therapy. PATIENTS: Seventy-two patients with moderate-to-severe plaque psoriasis, who had failed to respond to, or had a contraindication to, or were intolerant to other systemic therapies, received efalizumab (1 mg kg(-1) per week) for 12 weeks or more. RESULTS: After 12 weeks of efalizumab treatment, 65% of patients achieved 50% or more improvement from baseline Psoriasis Area and Severity Index (PASI) and 39% achieved at least 75% reduction in PASI score. The mean percentage PASI improvement from baseline was 62%. The most common side effects were a flu-like syndrome, a transient localized papular eruption, leucocytosis and lymphocytosis. There was no correlation between the occurrence of these side effects and the clinical response. Patients with a past history of unstable types of psoriasis were likely poor responders to efalizumab, and at an increased risk of developing generalized inflammatory flare. CONCLUSION: These results confirm previous reports suggesting that treatment with efalizumab is an efficacious and safe option for patients with moderate-to-severe plaque psoriasis. A detailed previous history of psoriasis is important in order to select possible candidates for efalizumab therapy.

The role of telomeres in skin aging/photoaging.

Recent work has substantially elucidated the mechanisms of skin aging and photoaging. In particular, a central role for telomere-based signaling can be inferred. Intrinsic aging is largely controlled by progressive telomere shortening, compounded by low grade oxidative damage to telomeres and other cellular constituents, the consequence of aerobic cellular metabolism. In sun exposed skin, UV irradiation also damages DNA and accelerates telomere shortening. Aging and photodamage appear to share a common final pathway that involves signaling through p53 following disruption of the telomere. These telomere-initiated responses, in combination with UV-induced damage to critical regulatory genes, lead to the familiar picture of "photoaging." These and other insights into the molecular basis for skin aging/photoaging may lead to enhanced management options.

Mean platelet volume: a useful marker of inflammatory bowel disease activity.

OBJECTIVES: We investigated whether the mean platelet volume would be a useful marker in the evaluation of inflammatory bowel disease activity. METHODS: Complete blood count, C-reactive protein, erythrocyte sedimentation rate, serum thrombopoietin and erythropoietin, plasma beta-thromboglobulin, and platelet factor 4 were measured in 93 patients with ulcerative colitis, 66 patients with Crohn's disease, and 38 healthy blood donors. Disease activity was assessed by the Clinical Colitis Activity Index in patients with ulcerative colitis and by the Crohn's Disease Activity Index in patients with Crohn's disease. RESULTS: Mean platelet count was increased in patients with active compared to inactive ulcerative colitis (p < 0.05), and in patients with active compared to inactive Crohn's disease (p = 0.0002) or healthy controls (p < 0.0001). On the other hand, mean platelet volume was significantly decreased in patients with active compared to inactive ulcerative colitis (p = 0.02) or healthy controls (p < 0.0001), and in patients with active compared to inactive Crohn's disease (p = 0.0005) or healthy controls (p < 0.0001). Mean platelet volume was inversely correlated with the white blood cell count (r = -0.17, p = 0.02), C-reactive protein (r = -0.46, p = 0.009) and erythrocyte sedimentation rate (r = -0.28, p = 0.008). No significant correlations were found between mean platelet volume and serum thrombopoietin or erythropoietin levels; however, a strong negative correlation between mean platelet volume and beta-thromboglobulin (r = -0.34, p < 0.0001) and platelet factor 4 (r = -0.30, p = 0.0002) was observed. CONCLUSIONS: Mean platelet volume is significantly reduced in active inflammatory bowel disease and is negatively correlated with the known inflammatory bowel disease activity markers and the platelet activation products. We propose that mean platelet volume provides a useful marker of activity in inflammatory bowel disease.