EMC - Dermatologie-Cosmétologie最新文献

Purpura is the consequence of a dermal extravasation of red cells. The purpura presentation is relevant for the diagnostic orientation: petechial purpura, ecchymoses, infiltrated or necrotic purpura. Thrombocytopenia is a frequent cause of purpura and induces petechial purpura or ecchymoses. Thrombocytopenia with normal medullar analysis may be due to infection (viral or bacterial), drugs, auto-immune disease or is idiopathic (idiopathic thrombocytopenic purpura). Thrombocytopenia may be one of the elements of severe disseminated intravascular coagulation or purpura fulminans. Decreased production of platelets may be due to diverse bone marrow diseases, congenital or acquired. Abnormal platelet functions are less frequently observed. Skin aging, vitamin C deficiency, or prolonged corticoid therapy may induce ecchymotic purpura due to frail vascular walls. Necrotic purpura, generally associated with inflammatory livedo and skin necrosis, may be due to microvascular thrombosis (platelet plugs (heparin, myeloproliferative diseases with thrombocytosis), occlusion due to infective agents growing in vessels, alterations in coagulation control (protein C or S deficiency, antiphospholipids)) or embolization (fat embolization, cholesterol emboli, myxoma). Palpable (infiltrated) and inflammatory pupuras require skin biopsy seeking leukocytoclastic vasculitis. Chronic pigmented purpuras represent a group of characteristic anatomo-clinical entities, of chronic but benign evolution. Pathogenesis is unknown. Some dermatosis may be purpuric (urticaria, drug reactions, erysipelas, pityriasis lichenoides). Some purpuras are characterized by their topography (socks and gloves syndrome) or their context (Gardner-Diamond syndrome). Pediatric entities are neonatal purpura fulminans (protein S or C deficiency), Henoch-Schonlein purpura, acute hemorrhagic oedema of childhood.

A foreign body granuloma is a chronic lesion predominantly made of cells which belong to the monocyte-macrophage lineage. The phagocytic function is usually well developed. Such a reaction can be induced by various xenobiotic macrostructures and cristalline or amorphous exogenous micro particles, as well as by some structures of endogenous origin. The distinction between a genuine xenic reaction and a granuloma with immunogenic contribution is not easy to define in some clinical settings.

Sarcoidosis is a systemic granulomatous disease of unknown aetiology. Sarcoidosis skin manifestations are proteiform. They are classically separated in specific lesions which show histological granuloma and are often chronic, or non specific lesions, most typically erythema nodosum, which is most of the time an acute process. They are observed in about 25% of patients with sarcoidosis. Skin involvement may be inaugural. For the clinician, the diagnosis of skin sarcoidosis induces three problems: screening for systemic involvement, evaluating the prognosis, implementing a management combining a long-term follow-up and a treatment when skin lesions lead to disfigurement or functional disability.

The skin provides a complex microenvironment where several cell populations actively participate in the initiation and regulation of inflammatory and immune responses. Cutaneous dendritic cells serve as dominant antigen-presenting cells in the induction of T-cell mediated immune responses and subsequent reactivation of T cells. Under homeostatic conditions, however, dendritic cells are primarily involved in the maintenance of immune tolerance to self- and innocuous non-self antigens. T lymphocytes with specificity for antigens penetrating through the skin acquire the propensity, by virtue of the expression of specific homing receptors, to recirculate in the skin. Keratinocytes have the capacity to secrete an array of cytokines and chemokines very important for the regulation of dendritic cell functions, and the recruitment and activation of inflammatory cells; in addition, keratinocytes can directly modulate T cell activation by expressing on their surface adhesion molecules and major histocompatibility complex class II molecules. Mast cells and peptidergic nerve endings form an integrated unit which can readily release factors involved in the initiation of the vascular phase of acute inflammation, but, together with endothelial cells, they also regulate cell-mediated immune responses.

Cutaneous manifestations of parasitosis are numerous and related to various mechanisms. When parasites are located at the inoculation site (Leishmania spp), in dermis (Onchocerca volvulus), live on skin or hair (ectoparasites) diagnosis is mainly made by direct examination. PCR (polymerase chain reaction) is a sensible diagnostic method for cutaneous leishmaniaisis and allows a rapid identification of causative species. Other cutaneous symptoms of parasitosis are general allergic manifestations. In this case, specific demands must be selected after clinical and epidemiological data. Allergic reactions are particularly intense during the invasive stage of some helminthiasis (trichinellosis, schistosomiasis, fasciolasis) or in visceral larva migrans (toxocariasis). In these cases, the parasitologic diagnosis relies on serologic assays.

Melanin is synthesized by the melanocytes which are specialized dentritic cells originating from the neural crest. The melanocytes are located in the basal layer of the epidermis and in the hair bulb and the follicular wall. The melanin is produced within specialized organelles that share characteristics with lysosomes, and called melanosomes. Two kinds of melanin are produced, the black – brown eumelanins, and the yellow – red phaeomelanins which are the less photoprotective ones. Three key enzymes for melanogenesis are identified: tyrosinase and tyrosinase related proteins 1 and 2. A significant number of genes control the embryogenesis of melanocytes, the biogenesis of melanosomes, their transport within melanocytes and their final transfer to keratinocytes. Many factors of melanogenesis regulation have been identified (ultraviolet, melanotropic hormones, cytokines…). The mechanisms of cell signalling involved in the melanogenesis are progressively analysed. These recent data will allow bettering understanding the genetic mechanisms of the melanin photoprotection of the skin. They have allowed identifying new targets for the treatment of hyper- and hypo-melanosis.

Cutaneous chronologic aging is a complex phenomenon which is genetically programmed, with a deleterious effect due to free oxygen radicals generated in the organism. The clinical presentation consists of skin atrophy with cutaneous weakness, dryness, elasticity loss, marked wrinkles and numerous functional modifications associated with a decreased immune response. Histologically, chronologic aging induces a decrease in epidermal thickness with a flattening of dermo-epidermal junction, a dermal atrophy with collagen decrease, elastic fibre elastolysis and microcirculation alterations.

For many years, urban atmospheric pollution and tobacco intoxication have significantly increased, generating more and more cutaneous and pulmonary lesions. People complain about sensitive and irritable skin. Despite obvious short-term deleterious effects of pollution, long-term effects are more imperceptible, making necessary to consider the insidious role of moderate but often repeated pollutions. The aim of this chapter is to review the different types of those "environmental aggressors" that induce cutaneous aging: tobacco, ozone, air pollution.