La correction du vieillissement cutané et facial est le motif essentiel des consultations en dermatologie esthétique. Cette demande des patients, devenue un phénomène de société, s’est accrue avec les progrès remarquables des thérapeutiques non chirurgicales, moins invasives, lasers, toxine botulique, comblement. Mais pour les appliquer au mieux et de façon personnalisée, car chaque visage vieillit différemment, une analyse faciale globale, statique et dynamique est indispensable. En effet, le vieillissement ne se limite évidemment pas à la peau, mais concerne aussi les tissus sous-jacents : muscles, tissu adipeux, support osseux. Dans cet article, le vieillissement cutané et ses différents types, chronologique, hormonal, environnemental avec le rôle majeur des ultraviolets et aussi du tabac et peut-être de la pollution sont envisagés sur le plan clinique et physiopathologique. La description du vieillissement cutané concerne non seulement le visage où domine le photovieillissement, mais aussi le reste du corps. Ensuite sont décrites les modalités générales du vieillissement facial des structures sous-cutanées, celles des muscles peauciers, qui compensent leur atrophie par une hypercontraction permanente responsable de rides dynamiques, celles du tissu adipeux qui se ptôse et parfois s’atrophie faisant perdre au visage les courbes harmonieuses et la plénitude de la jeunesse, celles du support osseux et de ses zones de résorption préférentielles qui sont aussi celles où le vieillissement des parties molles est le plus marqué. Les tiers supérieur, moyen et inférieur du visage ne vieillissent pas de la même façon et les principes de correction y sont différents. Enfin, l’orientation thérapeutique est brièvement envisagée, en tenant compte des attentes, souvent très raisonnables, des patientes qui souhaitent un rajeunissement modéré et naturel, respectant leur personnalité, supprimant les expressions négatives liées au vieillissement et ne veulent ni visage figé, ni « clonage esthétique ».Correction of cutaneous and facial ageing is the key reason for consultations in aesthetic dermatology. This demand on the part of patients, which has become a social phenomenon, has increased thanks to the remarkable progress made in nonsurgical and less invasive therapies such as lasers, botulinum toxin and fillers. But in order to optimise their use and to provide a personalised touch, since each face ages differently, an overall facial analysis, both static and dynamic, is essential. Indeed, ageing is obviously not restricted to skin but also concerns underlying tissue such as muscle, fat tissue and supporting bone. In this article, we provide a clinical and physiopathological analysis of the ageing of skin and of the various types of ageing, whether chronological, hormonal or environmental, and we examine the major role played by UV radiation, as well as tobacco smoke and, in certain cases, pollution. The description of cutaneous ageing covers not only the face, in which photoaging is the predominant factor, but also ageing of skin throughout the rest of the body. Next we describe the general modes of facial ageing for the subcutaneous structures, first those of the skin muscles, which compensate for their atrophy by means of permanent hypercontraction that result in dynamic wrinkles, then those of fat tissue in which ptosis can occur, coupled in some cases with atrophy and loss of the fullness and harmonious facial curves of youth, and those of supporting bone structures and preferential areas of resorption, which are also where the most pronounced ageing of soft tissue is discernible. The upper third, middle and lower third of the face do not age in the same way and the relevant methods of correction thus differ. Finally, we briefly discuss the therapeutic choices available, taking into account the generally extremely reasonable expectations of patients, who tend to seek moderate and natural rejuvenation in keeping with their personality, as well as the elimination of negative expressions associated with ageing, and who want neither a rigid face nor aesthetic cloning.

The authors report a patient who developed systemic polyarteritis nodosa two months after hepatitis B vaccination and review the literature concerning this vaccination and the development of autoimmune conditions, mainly vasculitis. A 14-year-old boy who had no relevant previous history and who was not taking any drugs presented with a livedo reticularis, fever, loss of weight, testicular pain, and paresthesias two months after receiving the third dose of a hepatitis B vaccination. Inflammatory parameters (ESR and CRP) were high. The patient met the ACR diagnostic criteria for polyarteritis nodosa. He received corticosteroids and immunosuppressants and showed improvement. After reviewing the 27 cases of vasculitis after hepatitis B vaccination reported in the current literature, the authors suggest that, in some cases, vaccination may be the triggering factor for vasculitis in individuals with a genetic predisposition. Physicians should be aware of this possible association.

Le syndrome KID est un syndrome rare associant kératite, ichtyose et surdité (deafness), probablement dû à une anomalie congénitale de l'ectoderme affectant la cornée, la peau et l'oreille interne. Des manifestations cliniques associées telles que la sensibilité aux infections et l'atteinte des phanères peuvent aider à poser le diagnostic. Il n'y a pas d'anomalies biologiques spécifiques. La plupart des cas sont sporadiques mais il a été décrit des cas familiaux dont le mode de transmission reste mal précisé. Le traitement des atteintes cutanées, ophtalmologiques et auditives est décevant. La prise en charge passe donc essentiellement par le dépistage précoce des complicationsKeratitis, ichthyosis and deafness are the dominant signs of KID syndrome. The lesions involving cornea, epidermis and internal ear are probably the result of a congenital ectodermal abnormality. Associated signs such as increased sensitivity to infections, and dermoskeleton dystrophies are also useful for the diagnosis. There are no specific biological signs. Most cases are sporadic but familial cases have been described with unclear mode of inheritance. Treatment is disappointing. Thus management mainly relies upon early detection of complications

POEMS syndrome is an acronym defined by Bardwick (Polyneuropathy, Organomegaly, Endocrinopathy, Monoclonal component and Skin changes). Other various clinical and biological features are reported: edema, cachexia, microangiopathic glomerulopathy, most rarely pulmonary hypertension, cutaneous necrosis. Thrombocytosis or polycythemia may be a prominent feature. POEMS syndrome is sometimes associated with lymphoproliferative disorder. Castelman-like disease is frequently observed as pathologic findings on lymph nodes. Distinction between POEMS syndrome and osteosclerotic myeloma is delicate. The rate of the monoclonal protein is modest-always less than 30 g/L and is almost of the lambda light chain class. In contrast to multiple myeloma this syndrome is rarely associated with hypercalcemia, skeletal fracture, renal involvement and increasing of M component during evolution. Bone marrow plasmocytosis is usually less than 15% and the kinetic phenotype and genetic characteristics of the plasma cell remain those found in monoclonal gammopathy of undetermined significance. The pathophysiology of this syndrome remains largely unknown but overproduction of pro-inflammatory cytokines are reported especially TNF alpha, IL-6 and IL-1 beta. Some clinical manifestations seem to be cytokine related. Polyneuropathy and cachexia are the main cause of death. A part corticosteroid and cure of solitary bone lesion, treatment is disappointing and survival is 60% at five years.

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POEMS syndrome is a multisystemic disorder characterized by the association of polyneuropathy, organomegaly, endocrinopathy, M protein, skin changes and various other systemic clinical signs. The pathophysiology of this syndrome remains largely unknown. In order to gain insight into its pathophysiology, we studied the clinical characteristics and performed serum analysis (auto-antibodies, cytokine levels) and phenotypic and cytogenetic studies of bone marrow plasma cells (BMPC) in six patients with unequivocal POEMS syndrome. Two unusual clinical signs were present in these patients: pulmonary hypertension (two patients) and diffuse cutaneous necrosis (one patient). No auto-antibodies against peripheral nerve (PN) antigens (SGPG and SGLPG glycolipids, GM1, GD1a, GD1b and GT1b gangliosides) were found. Sequential evaluations of serum cytokines (IL-1-beta, IL-6 and TNF-alpha) showed a moderate to marked elevations of IL-6 and TNF-alpha in all patients (up to six-fold for TNF-alpha and 16-fold for IL-6). Using in situ hybridization of these cytokines mRNAs on lymph node specimens of two patients who had an angiofollicular lymph node hyperplasia, a strong positivity was found with the IL-1-beta antisense probe in lymph node macrophages. On skin biopsy a high number of cells expressing TNF-alpha mRNA was observed in the dermis. The biological features of BMPC: phenotype (expression of CD19 and CD56 antigens), kinetics (Ki-67 index), karyotype, DNA content and chromosomal in situ hybridization remained those of BMPC found in monoclonal gammopathy of undetermined significance. We conclude that POEMS syndrome is a hypercytokinemic syndrome in which BMPC are not of malignant type. Macrophages are involved in this syndrome and their role has to be further investigated as well as treatments which act through an anticytokine mechanism.