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Stuttgart, Germany

Reichrath J.,Klinik fur Dermatologie
Dermato-Endocrinology | Year: 2012

The skin is the only tissue in the human body that represents both a target tissue for biologically active vitamin D compounds including 1,25-dihydroxyvitamin D (1,25(OH)2D) and has the capacity for the synthesis of 1,25(OH)2D from 7-dehydrocholesterol (7-DHC). Recent findings indicate that the vitamin D endocrine system (VDES), besides multiple other important functions, regulates aging in many tissues, including skin. This concept is strongly supported by several independent studies in genetically modified mice (including FGF23-/- and Klotho-/- mice) that are characterized by altered mineral homeostasis caused by a high vitamin D activity. These mice typically have phenotypic features of premature aging that include, besides short lifespan, retarded growth, ectopic calcification, immunological deficiency, osteoporosis, atherosclerosis, hypogonadism, skin and general organ atrophy. Notably, it has been demonstrated that these phenotypic features can be reversed by normalizing mineral homeostasis and/or vitamin D status. Interestingly, the aging phenotypes of mice suffering from hypovitaminosis D (VDR-/- and CYP27B1-/- mice) are quite similar to those suffering from hypervitaminosis D (including FGF-23-/- and Klotho-/- mice). Consequently, it has been hypothesized that thus, both hypo- and hypervitaminosis D may enhance aging. Aging seems to show a U-shaped response curve to vitamin D status, and, therefore normovitaminosis D seems to be important for preventing premature aging. Additionally, laboratory investigations have now convincingly shown that vitamin D compounds protect the skin against the hazardous effects of various skin aging-inducing agents, including UV (UV) radiation. In conclusion, these findings support the concept that UV-radiation exerts both skin aging -promoting and -inhibiting effects, the latter via induction of cutaneous vitamin D synthesis. Future studies will clarify the effect of vitamin D compounds on expression and function of potential key regulators of skin aging, such as TAp63 or the IGF-1 signaling pathway. Furthermore, the efficacy of topically applied vitamin D compounds in the prevention of skin aging has to be evaluated in future clinical trials. © 2012 Landes Bioscience. Source


Brasch J.,Klinik fur Dermatologie
Hautarzt | Year: 2012

Under favorable conditions even molds can cause skin infections. Fusarium spp. belong to this group of agents. Onychomycoses due to Fusarium spp. are regularly encountered and cannot be clinically distinguished from nail infections triggered by dermatophytes. They can occur in otherwise healthy persons. Skin lesions caused by Fusarium spp. may be necrotizing, ulcerating, pustular, vasculitis-like, panniculitis-like or granulomatous. Single lesions can develop after fungal inoculation into damaged tissue; multiple ones are often due to a septic dissemination of Fusarium in severely immunocompromised patients. An immediate verification of the agents can be life-saving in such cases. Pathogenic Fusarium spp. should be identified at the species level and need to be tested for their susceptibility to antimycotics. In case of multiple lesions, systemic therapy is required. Many strains of Fusarium spp. are susceptible to amphotericin B, voriconazole and posaconazole; itraconazole and terbinafine may be helpful in certain cases. © Springer-Verlag Berlin Heidelberg 2012. Source


Allergens are possible trigger factors of atopic dermatitis. The clinical importance of allergens as trigger factors of atopic dermatitis is still a matter of debate. The increase of knowledge of molecular mechanism of barrier defects in atopic dermatitis during the last years led to a challenge of the concept of allergen - driven atopic dermatitis. This short review summarizes selected aspects of the role of allergens in atopic dermatitis. In addition to "classical" allergens microbial antigens and autoantigens as potential allergens are also discussed in atopic dermatitis. Other trigger factors like climate, skin irritants or hormones can influence the allergic immune response in atopic dermatitis but are not focussed in this paper. Source


Zouboulis C.C.,Klinik fur Dermatologie
Hautarzt | Year: 2010

The development and function of the sebaceous gland in the fetal and neonatal periods appear to be regulated by maternal androgens and by endogenous steroid synthesis, as well as by other morphogens. The most apparent function of the glands is to excrete sebum. A strong increase in sebum excretion occurs a few hours after birth; this peaks during the first week and slowly subsides thereafter. A new rise takes place at about age 9 years with adrenarche and continues up to age 17 years, when the adult level is reached. The sebaceous gland is a target organ but also an important formation site of hormones, and especially of active androgens. Hormonal activity is based on an hormone (ligand)-receptor interaction, whereas sebocytes express a wide spectrum of hormone receptors. Androgens are well known for their effects on sebum excretion, whereas terminal sebocyte differentiation is assisted by peroxisome proliferator-activated receptor ligands. Estrogens, glucocorticoids, and prolactin also influence sebaceous gland function. In addition, stress-sensing cutaneous signals lead to the production and release of corticotrophin-releasing hormone from dermal nerves and sebocytes with subsequent dose-dependent regulation of sebaceous nonpolar lipids. Among other lipid fractions, sebaceous glands have been shown to synthesize considerable amounts of free fatty acids without exogenous influence. Atopic dermatitis, seborrheic dermatitis, psoriasis and acne vulgaris are some of the disease on which pathogenesis and severity sebaceous lipids may or are surely involved. © 2010 Springer-Verlag. Source


Zouboulis C.C.,Klinik fur Dermatologie | Rabe T.,University of Heidelberg
JDDG - Journal of the German Society of Dermatology | Year: 2010

Background: An enhanced sebaceous gland activity with production of proinflammtory sebaceous lipids belongs to the major pathogenetic factors of acne. Hormonal antiandrogen treatment targets the androgen-metabolizing cells of the pilosebaceous unit, i. e. follicular kertinocytes and sebocytes, and leads to sebostasis, with a reduction of the sebum secretion rate of 12.5 to 65 %. Concerning their mechanism of action, hormonal antiandrogens are classified in androgen receptor blockers, inhibitors of circulating androgens by affecting the ovarial function (oral contraceptives), inhibitors of circulating androgens by affecting the pituitary (gonadotrophin-releasing hormone agonists and dopamin agonists in hyperprolactinemia), inhibitors of the adrenal function, and inhibitors of peripheral androgen metabolism (5α-reductase inhibitors, inhibitors of other enzymes). Methods: In this study, all original and review publications on hormonal antiandrogen treatment of acne as monotherapy or in combination included in MEDLINE, EMBASE and COCHRANE libraries were extracted by using the terms "acne", "seborrhea", "polycystic ovary syndrome", "hyperandrog*" and "treatment" and classified according to their level of evidence. Results: Antiandrogen treatment is overall active on acne lesions. The combinations of ethinyl estradiol with cyproterone acetate chlormadinone acetate, dienogest desogestrel and drospirenone have shown the strongest antiacne activity. Gestagens or estrogens as monotherapy, spironolactone, flutamide, gonadotrophin-releasing hormone agonists and inhibitors of peripheral androgen metabolism are not recommended according to the current stand of knowledge. Low dose prednisolone is to only be administered at late onset congenital adrenal hyperplasia and dopamine agonists at hyperprolactinemia. Treatment with hormonal antiandrogens requires missing of any contraindications. Conclusions: Hormonal antiandrogen treatment is limited to female patients who present additional signs of peripheral hyperandrogenism or hyperandrogenemia. In addition, females with acne tarda, persistent acne recalcitrant to treatment, with parallel wish of contraception, and as a requirement for a systemic isotretinoin treatment can be treated with hormonal antiandrogens. Hormonal antiandrogen treatment is not a primary monotherapy for uncomplicated acne. © Blackwell Verlag GmbH. Source

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