Home About us Contact | |||
Affected Skin (affected + skin)
Terms modified by Affected Skin Selected AbstractsSurgical Treatment of Chronic Gluteal Hidradenitis Suppurativa: Reused Skin Graft TechniqueDERMATOLOGIC SURGERY, Issue 2 2003Hung-wen Kuo MD BACKGROUND The treatment of chronic lesions in hidradenitis suppurativa (HS) remains a challenge for dermatologists. In most cases, wide surgical excision of the affected skin reduces the recurrence rate to a minimum. Split-thickness skin grafts have usually been applied to resurface large postoperative defects. OBJECTIVE The aim of this study is to introduce an alternative method of skin grafting, called "reused" or "recycled" skin graft, for the reconstruction of the large skin defect with chronic gluteal HS. METHODS The study consisted of six patients (two females and four males) with gluteal HS. After a wide en bloc excision, the wound was immediately recovered with meshed-skin graft, made from the resected skin itself. Thus, the sacrifice of the skin donor is spared. The drum dermatome (Padgett-Hood) is suitable to take the split-skin graft from the resected skin of the affected buttock. The thickness of grafts was set between 12/1,000 and 20/1,000 inches, and all grafts were meshed with 1.5 times the expansion. The skin grafts were secured in place on the wound and a tie-over dressing was applied. RESULTS Postoperative complications were usually minor ones, such as hematoma, discharge, and small areas of graft skin necrosis (less than 1 cm2), although one patient developed a 3×4 cm2 graft necrosis and wound infection. The follow-up period after surgery ranged from 8 to 36 months. No patient experienced any functional disabilities or recurrence during follow-up years. CONCLUSION When the epidermal involvement remains mild to moderate, this reused skin graft technique is an alternative choice to resurface the surgical defect of gluteal HS. It is superior to the conventional procedure, which requires fresh skin donor site. [source] Deposition of chromatin-IgG complexes in skin of nephritic MRL-lpr/lpr mice is associated with increased local matrix metalloprotease activitiesEXPERIMENTAL DERMATOLOGY, Issue 8 2010Annica Hedberg Please cite this paper as: Deposition of chromatin-IgG complexes in skin of nephritic MRL-lpr/lpr mice is associated with increased local matrix metalloprotease activities. Experimental Dermatology 2010; 19: e265,e274. Abstract:, Chromatin-IgG complexes appear as electron dense structures (EDS) in glomerular basement membranes in lupus nephritis. Here, we present results of comparative analyses of the composition of EDS in murine lupus dermatitis and nephritis. One focus was to perform an analytical approach to understand why such complex structures bind skin basement membrane components. Transcription of skin membrane-encoding genes was analysed to see if expression of such genes was increased, eventually indicating that binding capacity of immune complexes increased when dermatitis developed. Variations in matrix metalloprotease 2 (MMP2), MMP9 and Dnase1 mRNA levels and enzymatic activities were correlated with circulatory chromatin-IgG complexes and deposition in skin. We also examined if glomerular deposits of EDS predicted similar deposits in skin of (NZB × NZW)F1 or MRL-lpr/lpr mice, as we observed chromatin-IgG complexes in capillary lumina in skin and glomeruli in both strains. EDS consisting of chromatin fragments and IgG were found sub-epidermally in skin with LE-like lesions of end-stage nephritic MRL-lpr/lpr mice. Dermal MMP-encoding genes were up-regulated during disease progression, and gelatinolytic activity was increased in affected skin. Dnase1 mRNA level and total nuclease activity remained stable in skin during the disease, in contrast to progressive loss of renal Dnase1 mRNA and total renal nuclease activity during development of nephritis. Loss of renal Dnase1 may explain release of chromatin fragments, while increased MMP activity may disrupt membranes making them accessible for chromatin fragment-IgG complexes. Circulatory chromatin-IgG complexes, and up-regulated intradermal MMP activity may be crucial for deposition of immune complexes in skin of lupus-prone mice. [source] Mosaic Chromosome 6 Trisomy in an Epidermal NevusPEDIATRIC DERMATOLOGY, Issue 2 2007Glenda J. Sobey F.C.Derm. Mosaicism for chromosome 6 in skin fibroblasts of affected skin was discovered. Trisomy 6 has not been previously implicated as an isolated finding in epidermal nevi or cutaneous mosaicism. [source] Tumor necrosis factor , blockade exacerbates murine psoriasis-like disease by enhancing Th17 function and decreasing expansion of Treg cellsARTHRITIS & RHEUMATISM, Issue 2 2010Hak-Ling Ma Objective Patients with psoriasis and psoriatic arthritis respond well to tumor necrosis factor , (TNF,) blockers in general; however, there is now mounting evidence that a small cohort of patients with rheumatoid arthritis who receive TNF, blockers develop psoriasis. This study was undertaken to explore the mechanisms underlying TNF, blockade,induced exacerbation of skin inflammation in murine psoriasis-like skin disease. Methods Skin inflammation was induced in BALB/c scid/scid mice after they received CD4+CD45RBhighCD25, (naive CD4) T cells from donor mice. These mice were treated with either anti,interleukin-12 (anti,IL-12)/23p40 antibody or murine TNFRII-Fc fusion protein and were examined for signs of disease, including histologic features, various cytokine levels in the serum, and cytokine or FoxP3 transcripts in the affected skin and draining lymph node (LN) cells. In a separate study, naive CD4+ T cells were differentiated into Th1 or Th17 lineages with anti-CD3/28 magnetic beads and appropriate cytokines in the presence or absence of TNF,. Cytokine gene expression from these differentiated cells was also determined. Results Neutralization of TNF, exacerbated skin inflammation and markedly enhanced the expression of the proinflammatory cytokines IL-1,, IL-6, IL-17, IL-21, and IL-22 but suppressed FoxP3 expression in the skin and reduced the number of FoxP3-positive Treg cells in the draining LNs. TNF, also demonstrated a divergent role during priming and reactivation of naive T cells. Conclusion These results reveal a novel immunoregulatory role of TNF, on Th17 and Treg cells in some individuals, which may account for the exacerbation of skin inflammation in some patients who receive anti-TNF treatments. [source] Dapsone suppresses human neutrophil superoxide production and elastase release in a calcium-dependent mannerBRITISH JOURNAL OF DERMATOLOGY, Issue 5 2005T. Suda Summary Background, Dapsone (4,4,-diaminodiphenyl sulphone) is a powerful therapeutic tool in many skin diseases including neutrophilic dermatoses. The drug has an outstanding therapeutic efficacy against many skin diseases characterized by neutrophil-rich infiltrates; however, mechanisms of its action are poorly understood. Objectives, We investigated the effects of dapsone on respiratory and secretory functions of human neutrophils triggered by the chemotactic peptide N -formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP), the physiological agonist C5a, and phorbol myristate acetate (PMA). Methods, Human neutrophils were isolated from venous blood obtained from healthy donors. We detected extracellular production of superoxide (O2,) by cytochrome C reduction assay, and intracellular production of O2, by flow cytometry. Neutrophil elastase release was measured by the cleavage of the specific elastase substrate N -methoxysuccinyl-Ala-Ala-Pro-Val- p -nitroanilide. Measurement of cytosolic free calcium concentration was performed using the calcium-reactive fluorescence probe, Fluo-3. Results, Dapsone suppressed intra- and extracellular production of O2, and elastase release triggered by fMLP and C5a, but not by PMA. Both fMLP and C5a signalled the above pathways by inducing calcium influx, but PMA functions bypassed calcium influx. Dapsone was capable of antagonizing the induction of calcium influx. Conclusions, These findings suggest that one mechanism of the anti-inflammatory action of dapsone is inhibition of calcium-dependent functions of neutrophils including release of tissue-damaging oxidants and proteases in the affected skin. [source] Comparison of the 308-nm excimer laser and a 308-nm excimer lamp with 311-nm narrowband ultraviolet B in the treatment of psoriasisBRITISH JOURNAL OF DERMATOLOGY, Issue 4 2005K. Köllner Summary Background, Psoriasis is a chronic, genetically determined inflammatory disease, characterized by an immunomediated pathogenesis, which affects approximately 1,3% of the population. Various modalities have been used for psoriasis treatment, including ultraviolet (UV) radiation. Narrowband UVB (311 nm) phototherapy is a well-established, widely used and highly efficient treatment for psoriasis, but a big disadvantage is that large areas of unaffected skin are irradiated along with the psoriatic lesions. Objectives, This investigation evaluates a 308-nm excimer laser and a 308-nm excimer lamp in comparison with 311-nm narrowband UVB in the treatment of patch psoriasis by using two different dose-increase schemes. Materials and methods, Fifteen patients with plaque psoriasis were enrolled in the study (first regime). Three different psoriatic lesions were treated with the 308-nm excimer laser, the 308-nm excimer lamp or 311-nm narrowband UVB three times per week. UVB doses were increased slowly and stepwise (1, 1, 2, 2, 3, 3, ,multiple MEDs). Sixteen patients were enrolled in the second regime. Two plaques were treated with the 308-nm excimer laser or with the 308-nm lamp with an accelerated scheme (2, 2, 4, 4, 6, 6, ,multiple MEDs) three times per week. We increased the UVB doses every second treatment (first and second regime) during the whole treatment. If blistering occurred, the blistered plaque was not treated on the next scheduled treatment. At every third visit and 1, 2 and 4 months after the last treatment a Psoriasis Severity Index (PSI) score was assigned in both regimes. Results, Using Friedman analysis, the PSI scores did not show a statistically significant difference (P > 0ˇ05) comparing 308-nm laser therapy, 308-nm lamp therapy and 311-nm narrowband therapy after 10 weeks in the first regime. The mean number of treatments to achieve clearance was 24. With the accelerated scheme, clearance could be achieved with fewer treatments and with half the cumulative dose of the first regime. Nevertheless, the side-effects such as blistering and crusting were also increased. Conclusions, Both 308-nm light sources can clear patch psoriasis in a similar manner to standard phototherapy, with the advantage of the ability to treat exclusively the affected skin and with a reduced cumulative dose, thus perhaps reducing the long-term risk of carcinogenicity. [source] A Japanese case of segmental Darier's disease caused by mosaicism for the ATP2A2 mutationBRITISH JOURNAL OF DERMATOLOGY, Issue 1 2003T. Wada Summary Darier's disease is an autosomal dominant skin disorder that is characterized by multiple keratotic papules, focal loss of adhesion and abnormal keratinization. Mutations in the ATP2A2 gene encoding sarco/endoplasmic reticulum calcium pumping ATPase type 2 have been identified as the molecular basis of Darier's disease. Segmental Darier's disease is a rare type of Darier's disease in which there is characteristic localization of the keratotic papules in a linear pattern following Blaschko's lines. In this study we examined ATP2A2 mutations in a Japanese patient with segmental Darier's disease. The samples from affected skin, unaffected skin and peripheral leucocytes were subjected to polymerase chain reaction (PCR). Direct sequencing of the PCR products was performed. Sequence analysis revealed that the patient had 160A,G substitution mutation which predicts I54V. This novel mutation was present in the affected skin, but not in the unaffected skin or peripheral leucocytes. This is the first report of segmental Darier's disease caused by mosaicism for an ATP2A2 mutation in Japan. [source] Expression of cyclin D1 and p16 in psoriasis before and after phototherapyCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 7 2010M. Abou EL-Ela Summary Background., Psoriasis vulgaris (PV) is characterized by keratinocyte hyper-proliferation. Altered expression of cell-cycle regulatory genes involved in the cyclin D1/p16 INK4,pRb pathway may contribute to this epidermal hyperproliferation. Aim., To assess the expression of cyclinD1 and p16 in psoriasis, and to evaluate the effect of phototherapy on their expression. Methods., The study population comprised 25 patients with PV and 10 healthy controls. Patients were treated with 24 sessions of either narrowband ultraviolet (UV) B or psoralen UVA. Skin biopsies were taken from the affected skin of each patient before and after treatment, and from the healthy controls, to examine cyclin D1 and p16 expression. Results., Before phototherapy, the mean value of cyclin D1 concentration in patients was significantly greater than that in controls and the mean value of p16 concentration in patients was significantly lower than that in controls. Following treatment, we detected a significant decrease in cyclin D1 and a significant increase in p16. Conclusion., Cyclin D1 upregulation and p16 downregulation may play a role in the pathogenesis of psoriasis. Normalization of the levels of both parameters may be a mechanism by which phototherapy induces remission in psoriasis. [source] A double-blind placebo-controlled trial of UVA-1 in the treatment of dyshidrotic eczemaCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 6 2003M. C. A. Polderman Summary We carried out a randomized, double-blind, placebo-controlled study to examine the therapeutic effect of UVA-1 irradiation on dyshidrotic hand eczema. Twenty-eight patients were randomised to receive UVA-1 irradiation (40 J/cm2) or placebo, five times a week for 3 weeks. Evaluated by the DASI and the VAS, UVA-1 was significantly more effective after 2 and 3 weeks. Also, desquamation and area of affected skin improved significantly more after UVA-1. We did not find any difference regarding the response of patients with increased IgE blood levels (> 100 IU/mL) compared with those having normal IgE levels. No side effects were observed. This study indicates that UVA-1 can cause a significant improvement of both objective and subjective signs of dyshidrotic eczema. [source] |