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It is generally acknowledged that the first morphological change of hidradenitis suppurativa/acne inversa (HS/AI) consists of infundibular plugging of the folliculosebaceous apocrine apparatus, which is followed by acute and chronic inflammation, cysts with sinus formation, and fibrosis. Alternatively, it has been hypothesized that HS/AI is primarily a neutrophilic autoinflammatory disease and that the follicular plugging typical of this disease is secondary to inflammation.To review the sequence of the changes that mark the disease development, we have performed a histopathologic study on the surgical material from a series of axillary and inguinal/perineal cases.The histologic material from surgery on Hurley's second and third stage HS/AI was retrieved and collected with the patients' clinical images. The virtually uninvolved skin peripheral to the lesions was studied together with the main inflammatory foci on vertical sections stained with hematoxylin-eosin and immunohistochemistry for the follicle sheaths.The fully developed lesions showed acute and chronic, suppurative and granulomatous inflammation overlapping fibrosis, cysts, and sinuses. Instead, the skin adjacent to florid inflammation showed plugging and dysmorphic alterations of the hair follicles associated with immunopathological changes of the inner root sheath keratin expression.Our observations coincide with the classical pathological studies on the progressive changes of HS/AI; however, in our specimens, the virtually normal skin peripheral to the fully developed lesions show seemingly initial follicular changes that suggest development error. This finding would support the hypothesis of combined mutation-induced epithelial differentiative defects and immunological derangement in HS/AI pathogenesis.GRUNDLAGEN: Es wird allgemein akzeptiert, dass die ersten morphologischen Veränderungen einer Hidradenitis suppurativa/Acne inversa (HS/AI) infundibuläre Keratosen des apokrinen follikulosebaceösen Apparates darstellen. Dieser Verschluss der Ostien wird gefolgt von akuter und chronischer Entzündung, Zysten mit Sinusformationen und Fibrose. Alternativ wird die HS/AI als eine primär neutrophile autoinflammatorische Erkrankung angesehen, bei der die Infundibulumkeratosen als Sekundärphänomen auftreten.Wir führten eine histopathologische Untersuchung an chirurgischen Gewebeproben axillärer und anogenitaler HS/AI durch, um die Reihenfolge morphologischer Veränderungen im Verlauf der Erkrankung zu erfassen.Das Gewebematerial stammte von Patienten mit HS/AI im Hurley-Stadium II und III, die sich einer chirurgischen Behandlung unterzogen hatten. Klinische Abbildungen lagen ebenfalls vor. Wir analysierten sowohl klinisch gesunde Haut in der Peripherie der Exzidate als auch die verschiedenen inflammatorischen Läsionen mittels vertikaler Gewebeschnitte. Hierzu wurden Hämatoxylin-Eosin und immunhistologische Färbungen der Haarscheiden verwendet.Die vollausgebildeten Läsionen zeigten akute und chronische, suppurative und granulomatöse Entzündungszeichen, die sich mit Fibrose, Zysten und Sinusen überlappten. Die benachbarte scheinbar gesunde Haut wies Infundibulumverschlüsse und dysmorphe Veränderungen der Haarfollikel auf. Es fanden sich immunpathologische Alterationen der Keratinexpression der inneren Haarwurzelscheiden.Unsere Beobachtungen stimmen mit den klassischen Studien zu progredienten entzündlichen Veränderungen der HS/AI überein. Wir konnten jedoch auch initiale Alterationen der Haarfollikel in der scheinbar gesunden Haut finden, die auf eine Entwicklungsstörung hinweisen. Diese Befunde stützen die Hypothese einer Kombination von durch Mutationen bedingten Störungen der epithelialen Differenzierung und immunologischen Komponenten in der HS/AI-Pathogenese.

Background Pityriasis rosea (PR) is a common, self-limited, inflammatory papulosquamous skin disease with a possible viral etiology. Objective The goal of this study was to evaluate skin biophysical properties in patients with PR compared with uninvolved skin to better understand the pathogenesis of PR. Methods Stratum corneum hydration, transepidermal water loss, surface friction, pH, sebum, melanin, erythema, temperature, elasticity parameters (R0, R2, R5), thickness, and echodensity of the epidermis and dermis were measured on lesions of classic PR in 21 patients and compared with control sites (average of uninvolved perilesional and symmetrical skin) with a paired t test. Results Stratum corneum hydration (p

BACKGROUND Some skin diseases may modify epidermal barrier function. Psoriasis is a chronic multi-systemic inflammatory disease that affects the epidermal barrier. Phototherapy is an option for treating psoriasis, but little is known about how epidermal barrier function is modified by phototherapy in psoriatic patients. OBJECTIVES (a) To compare skin homeostasis between involved and uninvolved skin in psoriatic patients with healthy controls (b) To evaluate changes in the epidermal barrier function in psoriatic patients treated with phototherapy. METHODS Sixty patients with plaque-type psoriasis and sixty gender and age-matched healthy controls were enrolled. Temperature, transepidermal water loss (TEWL), stratum corneum hydration (SCH), pH, elasticity, erythema and melanin index were measured using non-invasive tools in the healthy control and involved and uninvolved psoriatic skin before and after phototherapy. RESULTS Healthy controls had lower TEWL and erythema index and higher SCH than psoriatic patients, both at uninvolved psoriatic skin and psoriasis plaques. TEWL was higher at psoriasis plaques than at uninvolved skin (19.20 vs 11.57 g/h/m2 ; P

Idiopathic scrotal calcinosis is a rare condition, characterized by the idiopathic deposition of calcium in the scrotal dermis leading to the formation of a single nodule or multiple nodules of different sizes. Surgical excision of the nodules reduces symptoms and improves cosmesis. We present a case of idiopathic scrotal calcinosis that had an en bloc excision of scrotal skin nodules and primary closure of the scrotal skin. Handling each hemiscrotum as a separate entity and preserving the median raphe with its uninvolved skin improved the cosmesis. Reported outcomes of surgery were satisfactory with no postoperative complications. At 30 months of follow-up, the residual scrotal skin had regained its laxity and the scrotum its normal configuration. There is the risk of recurrence of the calcific nodules post excision, but these may be smaller in size and with regained scrotal configuration that could be amenable to excision with further preservation of the native scrotal skin.

Keratinocyte stress-response of the uninvolved psoriatic epidermis is known to be altered compared to healthy cells. Therefore, we aimed to reveal potential mechanisms underlying this alteration. We compared the expression of annotated cell-stress-related proteins between uninvolved psoriatic and healthy skin using the protein array method. Data were analyzed by the Reactome over-representation test. We found that p27/CDKN1B and cytochrome C showed at least a two-fold increase, while cyclooxygenase-2, indolamine-2,3-dioxygenase-1, serum paraoxonase 1, serum paraoxonase 3, serine-46-phosphorylated tumor protein p53, and superoxide-dismutase-2 showed a two-fold decrease in expression in the uninvolved skin. Over-representation analysis suggested the Forkhead-box protein O (FOXO)-mediated transcription as the most significant pathway affected by the differently expressed cell-stress-related proteins (DECSRPs). DECSRPs indicate increased FOXO-mediated transcription of cell-cycle genes and reduced interleukin-signaling in the psoriatic uninvolved skin. Nuclear positivity of the FOXO-signaling-related p27/CDKN1B and FOXO1 are negatively correlated with the disease severity and showed increased expression in the uninvolved epidermis and also in healthy primary keratinocytes, which were grown on cartilage oligomeric matrix protein-coated surfaces. Our results indicate a cell-cycle inhibitory process, as a stress-related compensatory mechanism in the uninvolved epidermis, that could be responsible for blocking keratinocyte hyperproliferation in the psoriatic uninvolved skin, thus maintaining the symptomless skin phenotype.

In recent years, a growing interest in the characterization of the molecular basis of psoriasis has been observed. However, despite the availability of a large amount of molecular data, many pathogenic mechanisms of psoriasis are still poorly understood. In this study, we performed an integrated analysis of 23 public transcriptomic datasets encompassing both lesional and uninvolved skin samples from psoriasis patients. We defined comprehensive gene co-expression network models of psoriatic lesions and uninvolved skin. Moreover, we collected, curated and exploited a wide range of functional information from multiple public sources in order to systematically annotate the inferred networks.The integrated transcriptomics analysis of public datasets shed light on a number of genes which are frequently deregulated in the psoriatic lesion compared with the unaffected skin in a large number of studies. In particular, CRABP2, LCN2, S100A12 and PDZK1IP1 were found to be deregulated in all of the datasets analyzed.Furthermore, the analysis of co-expression networks highlights genes showing aberrant patterns of connectivity in the lesional network as compared to the network inferred from unaffected skin samples. For instance, we identified co-expression patterns of SERPINB4, KYNU and S100A12 as being the most affected by the disease. Network analysis allowed us to identify YPEL1 and HUS1 as plausible, previously unknown, actors in the expression of the psoriasis phenotype. In addition, by exploiting topological properties of the network models, we highlighted a set of 250 non-deregulated genes, 223 of which have never been associated with the disease before, including CACNA1A, HADH, ATP5MC1 and CBARP among others.Finally, we characterized specific communities of co-expressed genes sustaining relevant molecular functions and specific immune cell types expression signatures playing a role in the psoriasis lesion. Overall, integrating experimental driven results with curated functional information from public repositories represents an efficient approach to empower knowledge generation about psoriasis and may be applicable to other complex diseases.

Psoriasis affects more than 125 million people worldwide, and the diagnosis and treatment efficacy evaluation of the disease mainly rely on clinical assessments that could be subjective. Our previous study showed that the skin erythema level could be quantified using diffuse reflectance spectroscopy (DRS), and the hemoglobin concentration of most psoriatic lesion was higher than that of its adjacent uninvolved skin. While the compromised epidermal barrier function has been taken as the major cause of clinical manifestation of skin dryness and inflammation of psoriasis, very few methods can be used to effectively evaluate this function. In this study, we investigate the near infrared spectroscopic features of psoriatic (n = 21) and normal (n = 21) skin that could link to the epidermal barrier function. From the DRS measurements, it was found that the water bonding status and light scattering properties of psoriasis are significantly different from those of uninvolved or normal skin. The connection between these parameters to the epidermal barrier function and morphology will be discussed. Our results suggest that objective evaluation of epidermal barrier function of psoriasis could be achieved using a simple DRS system.

Background The ability of Cutibacterium acnes strains to form biofilms has been correlated with their virulence. Objective This study examined biofilm and skin microbiota in acne patients in order to understand their role in the development of acne lesions. Methods Thin sections of punch biopsy specimens of (i) uninflamed comedones, (ii) inflammatory lesions, and (iii) uninvolved adjacent skin of acne patients were examined. Epiflourescence and confocal laser scanning microscopy were used for biofilm detection, and pyrosequencing with taxonomic classification of 16s rRNA gene amplicons was used for microbiota analysis. Results Of the 39 skin specimens from patients with mild-moderate acne (n = 13) that were studied, nine (23%) contained biofilm. Among these specimens, biofilm was most frequently detected in comedones (55.6%) and less frequently in inflammatory papules (22.2%) and uninvolved skin (22.2%). Comedones demonstrated the highest mean alpha diversity of all the lesion subtypes. The relative abundance of Staphylococcus was significantly higher in comedones (11.400% ± 12.242%) compared to uninvolved skin (0.073% ± 0.185%, P = 0.024). Conclusions The microenvironment of the comedone differs from that of inflammatory lesions and unaffected skin. The increased frequency of biofilm in comedones may account for the lack of host inflammatory response to these lesions.

Pityriasis rubra pilaris (PRP) is a rare inflammatory skin disorder of unknown etiology, initially described in 1835. It is characterized by keratotic follicular papules, well-demarcated salmon-colored erythematous scaly plaques interspersed with distinct islands of uninvolved skin, and palmoplantar keratoderma. Is PRP a systemic disease? Skin is mainly affected in PRP. Despite its clinical heterogeneity, PRP could be associated with a variety of rheumatologic, infectious, neoplastic, and other extracutaneous manifestations. We accept the hypothesis of not only an association but also a causative relation between skin and systemic manifestations with possible common underlying pathomechanisms such as systemic immunologic processes and superantigen mimicry., SCOPUS: ar.j, info:eu-repo/semantics/published

Pseudoxanthoma elasticum (PXE) is a rare multisystemic autosomal recessive connective tissue disease. In most cases, skin manifestations of PXE are the first to develop, followed later by severe ocular and cardiovascular complications. In our present study, in addition to dermoscopy, we introduced novel techniques, autofluorescence (AF) and diffuse reflectance (DR) imaging for the assessment of affected skin sites of five PXE patients. PXE-affected skin areas in most skin sites showed a previously observed pattern upon dermoscopic examination. With the novel imaging, PXE-affected skin lesions displayed high AF intensity. During our measurements, significantly higher mean, minimum and maximum AF intensity values were found in areas of PXE-affected skin when compared to uninvolved skin. Conversely, images acquired with the use of 660 and 940 nm illumination showed no mentionable difference. Our results demonstrate that AF imaging may be used in the in vivo diagnostics and quantification of the severity of the skin lesions of PXE patients. In addition, it is a safe, fast and cost-effective diagnostic method. AF imaging may be also used to objectively monitor the efficacy of the possible novel therapeutic approaches of PXE in the future.

Whole-body phototherapy is limited in that there can be needless exposure of uninvolved skin and no benefit to unexposed skin (such as the hair-covered scalp). In the last decade, various portable and lightweight handheld phototherapy units have become available for the treatment of localized psoriasis in the office and at home. These handheld devices, as compared with full-body irradiance in a booth or by a panel, have the added benefit of limiting skin exposure to UV light. The handheld devices are useful for the treatment of scalp psoriasis, as well as recalcitrant localized psoriasis plaques.

HHS Public Access Author manuscript Author Manuscript J Invest Dermatol. Author manuscript; available in PMC 2015 May 01. Published in final edited form as: J Invest Dermatol. 2014 November ; 134(11): 2843–2846. doi:10.1038/jid.2014.205. Abnormal Epidermal Barrier Recovery in Uninvolved Skin supports the Notion of an Epidermal Pathogenesis of Psoriasis Li Ye 1 , Chengzhi Lv 1 , George Man 2 , Shunpeng Song 1 , Peter M. Elias 2 , and Mao-Qiang Man 2 1 Dalian Skin Disease Hospital, Liaoning, P.R. China 2 Dermatology Author Manuscript Services, Veterans Affair Medical Center and University of California San Francisco, CA, USA Keywords Psoriasis; Stratum Corneum; Permeability Barrier; Hydration; pH; Transepidermal Water Loss To The Editor Author Manuscript Psoriasis is generally considered to be an immunologically-initiated disorder, which shares certain common susceptibility loci with autoimmune diseases (Zhang, 2012). Yet, both clinical experience (Gottlieb et al.,1990; Griffiths et al., 1995; Volden et al., 2001;) and recent molecular studies (Bergboer et al., 2012; Kim et al., 2011; Mischke et al., 1996; Vermeij et al., 2011) support an emerging concept that psoriasis could be ‘driven’ by a primary defect in epidermal permeability barrier function. Clinicians know well that psoriasis predictably flares during winter months (Park and Youn, 1998; Kwon et al., 2012), when the barrier is under additional stress due to low stratum corneum hydration, which accelerates transepidermal water loss (TEWL) rates (Lin, 2009; Muizzuddin et al., 2013). They also appreciate that sites vulnerable to epidermal trauma, such as the extensors of the extremities and the scalp, are preferentially involved in psoriasis. The Koebner phenomenon offers an additional, eloquent example of how psoriasis can be provoked by external perturbations. Finally, improvement of epidermal permeability barrier function by occlusion alone often alleviates psoriasis (e.g., Friedman, 1987). Author Manuscript Among psoriasis susceptibility genes, PSORS4 is located on chromosome 1q21, within the epidermal differentiation complex, which encodes numerous proteins required for epidermal differentiation and the formation of the cornified envelope (Mischke et al., 1996), a structure that is critical for the permeability barrier (Vermeij et al., 2011). Additionally, deletion of differentiation-related proteins, such as keratin1, whose levels are reduced in psoriasis (Thewes et al., 1991; Bata-Csorgo and Szell, 2012), not only compromises the permeability barrier, but also leads to upregulation of inflammatory genes and altered cytokine production Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms Address Correspondence To: Mao-Qiang Man, MD, Dermatology Service (190), 4150 Clement Street, San Francisco, CA 94121, USA, Tel: (415)750-2091, Fax: (415)750-2106, mqman@hotmail.com Or Chengzhi Lv, MD, dlpfb@126.com. All authors declare no conflicts of interest

Background In chronic spontaneous urticaria (CSU) mast cell activation together with inflammatory changes in the skin are well documented and may play an important role in mechanisms of tissue oedema. Objectives To confirm and extend these observations by measuring microvascular markers, leucocytes and mast cell numbers in lesional and uninvolved skin and to compare findings with a control group. Methods Paired biopsies (one from 4–8-h spontaneous weals and one from uninvolved skin) were taken from eight patients with CSU and nine control subjects and studied using immunohistochemistry and confocal microscopy using the lectin Ulex europaeus agglutinin 1 (UEA-1). Results Lesional skin in CSU contained significantly more CD31+ endothelial cells; CD31+ blood vessels, neutrophils, eosinophils, basophils and macrophages; and CD3+ T cells than nonlesional skin. Increased vascularity was confirmed by confocal imaging using the lectin UEA-1. Uninvolved skin from CSU contained significantly more CD31+ endothelial cells, CD31+ blood vessels and eosinophils compared with the control subjects. There was a threefold increase in mast cell numbers when CSU was compared with controls but no difference was observed between lesional and uninvolved skin. Conclusions Increased vascular markers together with eosinophil and neutrophil infiltration are features of lesional skin in CSU and might contribute to tissue oedema. Eosinophils and microvascular changes persist in uninvolved skin, which, together with increased mast cells, suggests that nonlesional skin is primed for further wealing.

Lichen planus pemphigoides (LPP) is a rare autoimmune blistering disease. It appears to be combination of lichen planus and bullous pemphigoid. We describe four new cases of LPP and discuss the epidemiological, clinical, pathological, and therapeutic features of this singular association through a review of the 74 published cases within the English literature. We report four cases of LPP (three women aged respectively 47, 51, and 53 years old, and a 53-year-old man). All patients presented with bullae on lichenoid and normal skin, predominately on the extremities. The diagnosis was confirmed by immunohistological findings. Our patients were treated with oral corticosteroids with a good response. Our review of the literature of 78 cases of LPP (65 adults and 13 children) showed that it involved adults (mean age: 54 years), with a slight female preponderance. A mean lag time between LP and the development of LPP was 8.3 months. LPP is characterized by developing blisters on lichenoid lesions and on uninvolved skin with more acral distribution of bullous lesions. Involvement of palms and soles was more frequent in children. The diagnosis is based on pathological and immunological confrontation. LPP is usually idiopathic, but some cases were reported in association with various drugs. There have also been reports of association with internal malignancy. Most cases of LPP are successfully treated with systemic corticosteroids. In most cases, the prognosis was good.

SUMMARY A study of thirty-three patients with a clinical diagnosis of dermatitis herpetiformis (DH) referred to our DH clinic over the last 11 years is reported. Twenty-six were referred by other consultant dermatologists. The diagnosis had been made by the clinical features and response of the rash to dapsone. Seventeen patients were found to have IgA in the uninvolved skin (IgA positive) and in sixteen no IgA was found (IgA negative). The duration of the rash prior to referral to the DH clinic was 3 months to 19 years (mean 5.0 years) for the IgA negative patients and 2 months to 22 years (mean 5.2 years) for the IgA positive group. The length of follow-up was 3 months to 11 years (mean 5.0 years) for the IgA negative, and 2–11 years (mean 5.6 years) for the IgA positive group. During follow-up the rash cleared completely and required no treatment in seven of the sixteen IgA negative patients. Thirteen of these sixteen patients no longer required dapsone, but six patients were receiving alternative treatment. In the three patients still taking dapsone IgA has not been found on subsequent biopsy. Of the seventeen IgA positive patients only three were able to stop dapsone during follow-up and in these three the IgA was still detected in the skin. Small intestinal mucosa was abnormal in eight of eleven IgA positive patients, but was normal in all thirteen IgA negative patients in whom jejunal biopsies were performed. An alternative diagnosis to DH has subsequently been made in thirteen of the sixteen IgA negative patients. Although the significance of IgA in the skin in DH is not known it appears to be part of the disease process. Patients who have a rash suggestive of DH and which is dapsone responsive, but in whom IgA is not found in the uninvolved skin, usually turn out to have a dermatosis other than dermatitis herpetiformis. Referral to a unit with expertise in immunofluorescence techniques of skin biopsies would appear to be helpful.

SUMMARY IgA deposits in the skin in 53 patients with dermatitis herpetiformis (DH) have been studied in relation to treatment. In 19 patients the disorder was controlled by a gluten-free diet (GFD) alone, in 13 patients by dapsone and GFD and in 18 by dapsone alone. In 3 patients the skin disorder became insignificant and required no treatment. Of the patients taking a GFD alone, six had been clear of skin lesions for 7 years, 5 for 3–5 years, and 8 for periods of 6 months-3 years. IgA deposits were found in all patients in an initial biopsy and in a second biopsy after treatment for periods varying from I to 7 years. There was no difference in the quantity of IgA, as assessed by the amount of fluorescence, whether patients were controlled with a GFD alone, GFD and dapsone, dapsone alone, or in those in clinical remission. The C3 component of complement was present in the skin in 3 of the 19 patients (16%) controlled by a GFD alone, 6 of the 13 patients (46%) of those controlled by a GFD and dapsone, and in 12 of 18 (66%) of the patients taking dapsone alone, and in one of the patients in clinical remission.

Uninvolved skin of psoriasis may not be entirely normal. The object was to characterize healthy, uninvolved psoriatic skin and lesional skin by biophysical methods.Involved and uninvolved psoriatic and age-gender matched healthy skin was measured objectively with a colorimeter and evaporimeter and subjectively with visual assessment in 14 subjects.Visual assessment of erythema (E), scaling (S) and induration (I) as well as the target lesion score at the involved psoriatic skin sites were significantly elevated (p0.05) above uninvolved psoriatic or healthy skin sites. No difference between uninvolved psoriatic and healthy skin was measured visually. Transepidermal water loss at involved psoriatic skinuninvolved psoriatic skinhealthy skin (p0.05). Objective assessment of skin color in 3 color scales, L*, a*, and b*, differentiated involved and uninvolved psoriatic skin from healthy skin sites. Involved psoriatic skin demonstrated higher (p0.01) a-scale values and lower (p0.01) L* and b* scale values than uninvolved psoriatic skin. Further, colorimeter L* and a* scale values at uninvolved psoriatic skin sites were lower and higher (p0.05), respectively, than healthy skin. The individual chromameter parameters (L*, a*, b*) correlated well with the visual parameters (E, S and I). Composite colorimeter description (L*× b*)/a* significantly differentiated healthy skin from both involved and uninvolved psoriatic skin.These collective data highlight that even visually appearing uninvolved psoriatic skin is compromised compared with healthy skin. These objective, noninvasive but differential capabilities of the colorimeter and evaporimeter will aid in the mechanistic quantification of new psoriatic drug therapies and in conjuction with biochemical studies, add to understanding of the multifactorial pathogenesis of psoriasis.

Basal cell carcinoma (BCC) is the most common non-melanoma skin cancer. The incidence of BCC is rising. The nodular, superficial spreading, and infiltrating variants are the three most commonly encountered types of BCC in descending order of prevalence. Superficial spreading basal cell carcinoma (SSBCC) accounts for 15-26% of all cases of BCC. It usually occurs on the trunk and upper extremities, but may be seen on the face. Surgical excision is the most commonly used treatment for BCC. Topical chemotherapy agents such as imiquimod or 5-fluorouracil (5-FU) may be various alternatives or adjuvants in the treatment of SSBCC. characteristically shows areas of uninvolved skin between tumor nests.[7].

Background: Ideal treatment for warts should be effective, safe, have less morbidity and provide long-lasting immunity against human papilloma virus. This can optimally achieved by the stimulation of the immune system against the virus. The autoimplantation of warts, autowart injection and quadrivalent vaccines have been used for this purpose. Autoimplanatation is a simple technique where the subcutis deep wart tissue is harvested as a donor and implanted into the uninvolved skin. However, this led to two wounds, at donor and recipient sites. Aim: The aim was to evaluate the safety and efficacy of a novel modification of autoimplantation therapy in the treatment of multiple, recurrent and palmoplantar warts. Subjects and Methods: Thirty-three patients with multiple, recurrent and palmoplantar warts were enrolled. Instead of taking a bit of the wart tissue, the donor tissue was harvested by paring the wart. The pared tissue was implanted deep into the subcutis by stab incision done using the same surgical blade no. 11. The resolution of all warts within 3 months after the procedure was considered successful. Patients with complete clearance were followed up for 1 month for any recurrence. Results: Out of 35 patients, 27 patients were available for follow-up. A total of 20 (74.1%) patients showed a complete clearance of warts within 3 months. Partial clearance was seen in 1 patient. Erythematous nodules developed at the site of implantation in 3 (11.1%) patients. There was relapse in one patient. Conclusion: A modified technique of autoimplantation of warts employing the pared stratum corneum tissue from the wart is a simple, effective, less traumatic and rapid procedure in the treatment of multiple, recurrent and palmoplantar warts.

Lichen planus pemphigoides (LPP) is a rare and controversial disease. It is characterized clinically by tense bullae arising both on lichen planus papules and on uninvolved skin, histologically by the demonstration of subepidermal bullae and by linear deposits of immunoglobulin G and C3 along the basement membrane zone on immunofluorescence of peribullous skin. Some authors consider LPP as the combination of lichen planus and bullous pemphigoid. Others think that it most likely encompasses a heterogeneous group of subepidermal autoimmune blistering disorders occurring in association with lichen planus. We present a child case that supports the heterogeneous condition of this disease triggered by varicella.

Background: Recent studies have shown that human beta-defensin-1 (hBD-1) and (human beta-defensin-2 hBD-2), which are antimicrobial peptides produced by the skin, play a role in the pathogenesis of acne vulgaris (AV). Objective: The aim of this study was to determine the role of antimicrobial peptides in the pathogenesis of AV and enlighten the effects of doxycycline and isotretinoin in the expression of these defensins in AV. Materials and Methods: A total of 44 patients (22 patients in each group) with Grade 6 and 8 AV who were indicated doxycycline or isotretinoin for their treatment, and 20 healthy volunteers were included in this study. Pretreatment cutaneous samples were obtained from pustular lesions and uninvolved skin of AV patients and were repeated after the treatment. Only one biopsy was obtained from controls. Results: Cutaneous levels of hBD-1 and hBD-2 were significantly increased in AV patients when compared with healthy controls (P0.05). Conclusion: In the light of these results, it was reasonable to assume the role of hBD-1 and hBD-2 in the pathogenesis of AV. Our results showing a significant reduction in hBD-1 staining with doxycycline treatment and in hBD-2 with isotretinoin suggested that some part of their anti-acne effect worked through these mechanisms.