931 resultados para skin defect


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Objective: To develop a new endoscopic approach to the correction of a myelomeningocele-like defect in fetal sheep. Methods: The fetuses of 9 pregnant ewes, with an average gestational age of 115 days, were subjected to a 3.0 x 2.0 cm removal of the skin over the lumbar spine, performed through hysterotomy. The uterus was closed, and three 5-mm endoscopic cannulas, without valve mechanisms, were inserted. In the pilot phase (2 animals), we initially worked exclusively in the amniotic fluid space. In the study phase, we partially withdrew the fetus from the amniotic fluid to completely expose its back. By simply allowing air to enter the amniotic cavity (without gas injection), a working space was created using a uterine lift device. The skin around the defect was dissected, and a biosynthetic cellulose material was applied to cover the area. A continuous suture of the skin was performed to completely hide the material. Results: The combined air/fluid space allowed the skin to be successfully closed in 6 out of 7 cases in the study phase. All fetuses were alive at the end of the procedures. Time to complete the endoscopic part of the procedure fell from 3 to 1 h by the end of this series. Premature birth occurred in 2 of the 4 cases allowed to continue with the pregnancy. Conclusion: A new gasless fetoscopic surgery technique was developed as an alternative to current techniques used for fetal endoscopic surgery. Copyright (C) 2008 S. Karger AG, Basel.

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Objective: This is a clinical study of our experience using pedicle perforator flaps to cover skin defects in the middle and distal segment of the leg. Design: Prospective study. Setting: University hospital. Patients/Intervention: Twenty-four patients underwent treatment of a skin defect in the middle or distal segment of the leg by means of pedicled flaps based on perforating arteries. The perforating arteries were located before the operation by means of echo-Doppler examination. The flaps were planned in propeller fashion (21 cases) and as advancement (three cases). Main Outcome Measurements: The results were evaluated according the origin of perforator flap, size of the flap, and donor area and viability of the flap. The success rate of the echo-Doppler to identify the location of perforator vessel was also evaluated. Results: In nine cases, the perforating vessels originated from the fibular artery, in 10 the posterior tibial artery, and in five the anterior tibial artery. The mean size of the flaps was 5 cm in width by 12 cm in length. The success rate using an echo-Doppler was 87%. The flaps were fully viable in 20 cases and partially viable in four cases. Conclusion: On the basis of these results, it is concluded that perforating flaps are a good choice of treatment for skin losses, especially in the distal segment of the leg, and could be an alternative option for the use of free microsurgical flaps.

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Objective: To assess the ability of a three-layer graft in the closuse of large fetal skin defects. Methods: Ovine fetuses underwent a large (4 x 3 cm) full-thickness skin defect over the lumbar region at 105 days` gestation (term = 140 days). A bilaminar artificial skin was placed over a cellulose interface to cover the defect (3-layer graft). The skin was partially reapproximated with a continuous nylon suture. Pregnancy was allowed to continue and the surgical site was submitted to histopathological analysis at different post-operative intervals. Results: Seven fetuses underwent surgery. One maternal/fetal death occurred, and the remaining 6 fetuses were analyzed. Artificial skin adherence to the wound edges was observed in cases that remained in utero for at least 15 days. Neoskin was present beneath the silicone layer of the bilaminar artificial skin. Conclusions: Our study shows that neoskin can develop in the fetus using a 3-layer graft, including epidermal growth beneath the silicone layer of the bilaminar skin graft. These findings suggest that the fetus is able to reepithelialise even large skin defects. Further experience is necessary to assess the quality of this repair.

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INTRODUCTION: Excision of large dermatofibrosarcoma protuberans in the anterior aspect of the trunk often results in large surgical defects that frequently dictate the need for microsurgical reconstruction. However, this option is not always available. PRESENTATION OF CASE: The authors describe two patients with very large anterior trunk dermatofibrosarcoma protuberans: one in the epigastric region and the other in the hypogastric region. In the patient with the hypogastric tumor, a classical abdominoplasty flap associated with umbilical transposition was used to cover the skin defect after muscle and fascial plication, and placement of a polypropylene mesh. In the patient with the epigastric tumor, a synthetic mesh was also placed, and the skin and subcutaneous defect was reconstructed with a reverse abdominoplasty flap and two thoraco-epigastric flaps. In both cases, complete closure was possible without immediate or late complications. DISCUSSION: The local options described in this paper present several potential advantages compared to microsurgical reconstruction, namely they are easier and faster to perform and teach; they provide a good skin color and texture match; they are not associated with distant donor site morbidity; follow-up is usually less cumbersome; the post-operative hospital stay tends to be shorter; they are less costly; they are less prone to complete failure. CONCLUSION: The authors believe that these two patients clearly show that local flaps, although frequently neglected, continue to be valid options for reconstructing large anterior trunk defects, even in the current era of microsurgery enthusiasm.

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Calendula officinalis L. and S. barbadetiman are used in Brazil for the treatment of a number of aliments. The healing properties of these substances are well known, mainly in domestic or sun burn. In order to establish a pharmacological rationale for the traditional use of these plants as a cicatrizant or antiinflammatory remedy, we used ethanol extracts or gel from stem bark of the S. barbadetiman and inflorescence of the Calendula. We selected four groups of patients; two groups shown varicose ulcer (I, II) and two groups shown skin lesions (III and IV). Groups I and III were treated with Calendula and group II and IV were treated with Calendula plus barbadetiman. The data in this study suggest that the treatment with Calendula or Calendula plus barbadetiman are effective in the process that brings wounds to a close. These findings provide basis to an alternative treatment of varicose ulcer.

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Background: Sporotrichosis is a granulomatous fungal infection caused by Sporothrix schenckii, which frequently causes cutaneous or lymphocutaneous lesions and rarely has oral manifestations. Case: A 38-year-old, white, HIV-positive man complained of a 5.0-cm, symptomatic, ulcerated lesion with thin, superficial granulation in the soft palate extending to the uvula. Exfoliative cytology of this oral lesion showed chronic granulomatous inflammatory alterations and extracellular fungal structures consisting of periodic acid-Schiff-positive budding cells and spherical or elongated (cigar bodies) free spore forms. Conclusion: The clinical and cytologic findings allowed the diagnosis of sporotrichosis, demonstrating the importance of cytodiagnosis in fungal diseases. © The International Academy of Cytology.

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Autoimmune bullous dermatoses are diseases in which blisters and vesicles are the primary and fundamental types of skin lesion. Their classification is based on the location of the blister: intraepidermal and subepidermal. Patients produce autoantibodies against self-specific structures of the skin detectable by immunofluorescence techniques, immunoblotting and ELISA. Recent advances in molecular and cellular biology have brought to knowledge these self-antigens, against which patients are sensitized, and which are found in epidermis or in the dermo-epidermal junction. These are low incidence, but high morbidity diseases that may be fatal. The aim of this article is to review and describe the progress of four autoimmune vesiculobullous disorders: endemic pemphigus foliaceous (wild fire), pemphigus vulgaris, bullous pemphigoid and dermatitis herpetiformis. ©2009 by Anais Brasileiros de Dermatologia.

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Ticks are hematophagous ectoparasites which can transmit several diseases to the host during their feeding process. When ticks mechanically damage the tissue, they eventually induce inflammatory responses on the skin spot where they are fixed. One of the alternatives to control these ectoparasites is the use of chemical substances like selamectin - the active principle of Pfizer's antiparasitic Revolution® - a macrocyclic lactone capable of doing neurotoxic damage to the tick and eventually eliminating infestation in dogs and cats. The purpose of this study was to analyze, using histological and histochemical techniques, the occurrence of morphophysiological alterations in the skin of the host rabbits exposed to selamectin and infested with Rhipicephalus sanguineus (Acari: Ixodidae). Histologically, the exposed and infested rabbits showed a partial and/or total decrease in the stratum corneum and the epithelium decreased in the number of cell layers, consequently reducing the stratification (thinning) and quite pronounced formations of sub-epidermal edemas with consequent disorganization of collagen fibers in the dermal layer's connective tissue. Histochemical tests showed strong periodic acid-Schiff-positive reaction in the hair follicle and some regions of the dermis, besides resynthesis of collagen fibers detected by Mallory's trichrome technique. The obtained results showed that selamectin acts like a toxicant agent when in contact with the skin of the rabbit infested with ticks, inducing morphophysiological alterations in the acute inflammatory process in the animal's tegument. Selamectin is a chemical substance which has a dose-dependent action since higher concentrations cause greater morphophysiological damage in the skin of rabbits. © 2013 Springer-Verlag Berlin Heidelberg.

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An 8-year-old female neutered Siamese cat was presented with a recent history of incomplete excision of an apocrine gland adenocarcinoma from the palmar aspect of the right antebrachium, just proximal to the carpal joint. There was no evidence of metastasis. Wide surgical excision of the previous surgery site was performed resulting in a soft tissue defect. Partial reconstruction was achieved using digital pad transposition of the first digit (dewclaw), forming a local axial pattern flap that was transposed into the adjacent defect. The remaining defect was closed by primary apposition. The skin flap healed successfully. Some breakdown of the skin closed by primary apposition necessitated open wound management. The cosmetic and functional result of the first digital pad transposition was considered excellent, rendering it a useful means to reconstruct soft tissue defects in the carpal region.

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The authors report a case of diffuse cutaneous leishmaniasis, with longstanding evolution and presenting with diffuse infiltrated lesions rich in amastigotes in the absence of mucosal involvement. In situ characterization with monoclonal antibodies revealed Leishmania amazonensis. Large regional lesions have presented spontaneous healing without specific therapy. Considering that DCL presents with a defect in the cellular immune response, thisfact demonstrate that this patient may develop a regional cellular immune response enough to destroy the parasites and to produce clearing of some lesions.

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Résumé : La voie de signalisation Notch est essentielle pour la différentiation de l'épiderme lors du développement embryonnaire de la peau. Il a été démontré que l'inactivation de Notch1 dans la peau de souris conduit à une hyperplasie de l'épiderme ainsi qu'à la formation subséquente de carcinomes basocellulaires ainsi que de plaques cornéennes. L'inactivation de Notch1 dans la cornée combinée à des lésions mécaniques démontre que les cellules progénitrices de la cornée se différentient en un épithélium hyperplasique et kératinisé comme la peau. Ce changement de destinée cellulaire conduit à une cécité cornéenne et implique des processus non-autonomes aux cellules épithéliales, caractérisés par la sécrétion de FGF-2 par l'épithélium Notch1-/- suivi d'une vascularisation et d'un remaniement du stroma sous-jacent. La déficience en vitamine A est connu comme cause de lésions cornéennes humaines (xérophtalmie sévère). En accord, nous avons trouvé que la signalisation Notch1 était liée au métabolisme de la vitamine A par la régulation de l'expression de CRBP1, nécessaire pour générer un pool de rétinol intracellulaire. La perte de Notch1 dans l'épiderme, l'autre récepteur de la famille présent dans la peau marine, ne conduit pas à un phénotype manifeste. Cependant, l'inactivation dans l'épiderme de Notch1 et Notch2 ensemble, ou de RBP-J, induit une dermatite atopique (DA) sévère chez les souris. De même, les patients souffrants de DA mais pas ceux souffrant de psoriasis ou de lichen plan, ont une réduction marquée de l'expression des récepteurs Notch dans la peau. La perte de Notch dans les keratinocytes conduit à une activation de la voie NF-κB, ce qui ensuite induit la production de TSLP, une cytokine profondément impliquée dans la pathogenèse de la DA. Nous démontrons génétiquement que TSLP est responsable de la DA ainsi que du développent d'un syndrome myéloprolifératif non-autonome aux cellules induit par le G-CSF. Cependant, ces souris avec une inactivation dans l'épiderme de Notch1 et Notch2 et aussi incapables de répondre au TSLP développent des tumeurs invasive sévères caractérisées par une haute activité de signalisation ß-catenin. TSLPR est identifié comme un potentiel suppresseur de tumeur non-autonome aux cellules tumorales; la transplantation de cellules hématopoïétiques TSLPR-/- dans des souris déficientes pour Notch est suffisant pour causer des tumeurs. Summary : The Notch pathway is essential for proper epidermal differentiation during embryonic skin development. It has previously been demonstrated that Notch1 inactivation in marine skin results in epidermal hyperplasia and subsequent formation of basal cell carcinoma-like (BCC-like) tumors as well as corneal plaques. Inducible ablation of Notch1 in the cornea combined with mechanical wounding show that Notch1 deficient corneal progenitor cells differentiate into a hyperplasic, keratinized, skin-like epithelium. This cell fate switch leads to corneal blindness and involves cell non-autonomous processes, characterized by secretion of FGF-2 through Notch1-/- epithelium followed by vascularisation and remodelling of the underlying stroma. Vitamin A deficiency is known to induce a similar corneal defect in humans (severe xerophthalmia). Accordingly, we found that Notch1 signaling is linked to vitamin A metabolism by regulating the expression of CRBP1, required to generate a pool of intracellular retinol. Epidermal loss of Notch2, the other Notch receptor present in marine skin, doesn't lead to any overt phenotypes. However, postnatal epidermis-specific inactivation of both Notch1 and Notch2, or of RBP-J, induces the development of a severe form of atopic dermatitis (AD) in mice. Likewise, patients suffering from AD, but not psoriasis or lichen planas, have a marked reduction of Notch receptor expression in the skin. Loss of Notch in keratinocytes leads to an activation of NF-κB signaling which in turn induces the production of Thymic stromal lymphopoietin (TSLP), a cytokine deeply implicated in the pathogenesis of AD. We genetically demonstrate that TSLP is responsible for AD as well as the development of a cell non-autonomous G-CSF induced myeloproliferative disorder (MPD) in mice. However, these mice with conditional epidermal inactivation of Notch1 and Notch2 as well as incapable to respond to TSLP develop severe invasive tumors characterized by high ß-catenin signaling activity. TSLPR is identified as a potential cell non-autonomous tumor suppressor; transplantation of TSLPR-/- hematopoietic cells into epidermal Notch deficient mice is sufficient to cause tumors.

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Abstract In humans, the skin is the largest organ of the body, covering up to 2m2 and weighing up to 4kg in an average adult. Its function is to preserve the body from external insults and also to retain water inside. This barrier function termed epidermal permeability barrier (EPB) is localized in the functional part of the skin: the epidermis. For this, evolution has built a complex structure of cells and lipids sealing the surface, the stratum corneum. The formation of this structure is finely tuned since it is not only formed once at birth, but renewed all life long. This active process gives a high plasticity and reactivity to skin, but also leads to various pathologies. ENaC is a sodium channel extensively studied in organs like kidney and lung due to its importance in regulating sodium homeostasis and fluid volume. It is composed of three subunits α, ß and r which are forming sodium selective channel through the cell membrane. Its presence in the skin has been demonstrated, but little is known about its physiological role. Previous work has shown that αENaC knockout mice displayed an abnormal epidermis, suggesting a role in differentiation processes that might be implicated in the EPB. The principal aim of this thesis has been to study the consequences for EPB function in mice deficient for αENaC by molecular and physiological means and to investigate the underlying molecular mechanisms. Here, the barrier function of αENaC knockout pups is impaired. Apparently not immediately after birth (permeability test) but 24h later, when evident water loss differences appeared compared to wildtypes. Neither the structural proteins of the epithelium nor the tights junctions showed any obvious alterations. In contrary, stratum corneum lipid disorders are most likely responsible for the barrier defect, accompanied by an impairment of skin surface acidification. To analyze in details this EPB defect, several hypotheses have been proposed: reduced sensibility to calcium which is the key activator far epidermal formation, or modification of ENaC-mediated ion fluxes/currents inside the epidermis. The cellular localization of ENaC and the action in the skin of CAPl, a positive regulator of ENaC, have been also studied in details. In summary, this study clearly demonstrates that ENaC is a key player in the EPB maintenance, because αENaC knockout pups are not able to adapt to the new environment (ex utero) as efficiently as the wildtypes, most likely due to impaired of sodium handling inside the epidermis. Résumé Chez l'homme, la peau est le plus grand organe, couvrant presque 2m2 et pesant près de 4kg chez l'adulte. Sa fonction principale est de protéger l'organisme des agressions extérieures mais également de conserver l'eau à l'intérieur du corps. Cette fonction nommée barrière épithéliale est localisée dans la partie fonctionnelle de la peau : l'épiderme. A cette fin, l'évolution s'est dotée d'une structure complexe composée de cellules et de lipides recouvrant la surface, la couche cornée. Sa formation est finement régulée, car elle n'est pas seulement produite à la naissance mais constamment renouvelée tout au long de la vie, ce qui lui confère une grande plasticité mais ce qui est également la cause de nombreuses pathologies. ENaC est un canal sodique très étudié dans le rein et le poumon pour son importance dans la régulation de l'homéostasie sodique et la régulation du volume du milieu intérieur. Il est composé de 3 sous unités, α, ß et y qui forment un pore sélectif pour le sodium dans les membranes. Ce canal est présent dans la peau mais sa fonction n'y est pas connue. Des travaux précédents ont pu montrer que les souris dont le gène codant pour αENaC a été invalidé présentent un épiderme pathologique, suggérant un rôle dans la différentiation et pourrait même être impliqué dans la barrière épithéliale. Le but de cette thèse fut l'étude de la barrière dans ces souris knockouts avec des méthodes moléculaires et physiologiques et la caractérisation des mécanismes moléculaire impliqués. Dans ce travail, il a été montré que les souris mutantes présentaient un défaut de la barrière. Ce défaut n'est pas visible immédiatement à la naissance (test de perméabilité), mais 24h plus tard, lorsque les tests de perte d'eau transépithéliale montrent une différence évidente avec les animaux contrôles. Ni les protéines de structures ni les jonctions serrées de l'épiderme ne présentaient d'imperfections majeures. A l'inverse, les lipides de la couche cornée présentaient un problème de maturation (expliquant le phénotype de la barrière), certainement consécutif au défaut d'acidification à la surface de la peau que nous avons observé. D'autres mécanismes ont été explorées afin d'investiguer cette anomalie de la barrière, comme la réduction de sensibilité au calcium qui est le principal activateur de la formation de l'épiderme, ou la modification des flux d'ions entre les couches de l'épiderme. La localisation cellulaire d'ENaC, et l'action de son activateur CAPl ont également été étudiés en détails. En résumé, cette étude démontre clairement qu'ENaC est un acteur important dans la formation de la barrière épithéliale, car la peau des knockouts ne s'adapte pas aussi bien que celle des sauvages au nouvel environnement ex utero à cause de la fonction d'ENaC dans les mouvements de sodium au sein même de l'épiderme. Résumé tout public Chez l'homme, la peau est le plus grand organe, couvrant presque 2m2 et pesant près de 4kg chez l'adulte. Sa fonction principale est de protéger l'organisme des agressions extérieures mais également de conserver l'eau à l'intérieur du corps. Cette fonction nommée barrière épithéliale est localisée dans la partie fonctionnelle de la peau : l'épiderme. A cette fin, l'évolution s'est dotée d'une structure complexe composée de cellules et de lipides recouvrant la surface, la couche cornée. Sa formation est finement régulée, car elle n'est pas seulement produite à la naissance mais constamment renouvelée tout au long de la vie, ce qui lui confère une grande plasticité mais ce qui est également la cause de nombreuses maladies. ENaC est une protéine formant un canal qui permet le passage sélectif de l'ion sodium à travers la paroi des cellules. Il est très étudié dans le rein pour son importance dans la récupération du sel lors de la concentration de l'urine. Ce canal est présent dans la peau mais sa fonction n'y est pas connue. Des travaux précédents ont pu montrer que les souris où le gène codant pour αENaC a été invalidé présentent un épiderme pathologique, suggérant un rôle dans la peau et plus particulièrement la fonction de barrière de l'épiderme. Le but de cette thèse fut l'étude de la fonction de barrière dans ces souris mutantes, au niveau tissulaire et cellulaire. Dans ce travail, il a été montré que les souris mutantes présentaient une peau plus perméable que celle des animaux contrôles, grâce à une machine mesurant la perte d'eau à travers la peau. Ce défaut n'est visible que 24h après la naissance, mais nous avons pu montrer que les animaux mutants perdaient quasiment 2 fois plus d'eau que les contrôles. Au niveau moléculaire, nous avons pu montrer que ce défaut provenait d'un problème de maturation des lipides qui composent la barrière de la peau. Cette maturation est incomplète vraisemblablement à cause d'un défaut de mouvement des ions dans les couches les plus superficielles de l'épiderme, et cela à cause de l'absence du canal ENaC. En résumé, cette étude démontre clairement qu'ENaC est un acteur important dans la formation de la barrière épithéliale, car la peau des mutants ne s'adapte pas aussi bien que celle des sauvages au nouvel environnement ex utero à cause de la fonction d'ENaC dans les mouvements de sodium au sein même de l'épiderme.

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We report a case of abdominal eventration associated with cystic fibrosis, diagnosed by mid-trimester ultrasonography. The defect concerned the abdominal muscles and their aponevrotic sheath, but respected the skin. There was no associated malformation. The outcome was favorable after surgery, and the infant is well at the age of 6 months.

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INTRODUCTION: Hidradenitis suppurativa of the groin is a chronic, relapsing inflammatory disease of the skin and subcutaneous tissues. Radical surgical excision is the treatment of choice. Often split-skin grafting or wound healing by secondary intention are used for defect closure, sometimes with disfiguring results. We describe our experience with radical excision of localised inguinal hidradenitis suppurativa and immediate defect closure with a medial thigh lift. PATIENTS AND METHODS: Our hospital database was searched for all patients presenting to our institution for surgical treatment of hidradenitis suppurativa between 2001 and 2006. Only patients with hidradenitis confined to the groin were included. Exclusion criteria were simple abscess incisions, recurrence after previous grafting or flap surgery and extension of the disease outside the groin and presence of clinical signs of infection at the time of surgery. We documented patient demographics, sizes of defects, complications, time of follow-up, recurrences and patient satisfaction. RESULTS: A total of 8 patients with localised inguinal hidradenitis suppurativa were identified and 15 thigh lifts were performed. Defect size assessed on pathologic examination of the excised specimens averaged 15.9 cm x 4.3 cm x 1.3 cm (length x width x depth). All wounds but one healed primarily. Functional and aesthetic results were satisfactory. No major complications and no irritations of the genital area were observed. No recurrences were observed either. CONCLUSION: We propose the medial thigh lift to be considered for immediate defect closure after radical excision of localised inguinal hidradenitis suppurativa provided that no perifocal signs of infection are present after debridement.