A randomized,controlled and blinded study of papulopustular lesions in Turkish Behçet’s patients

Background Papulopustular lesions (PPL), the commonest presentation of skin lesions in Behçet’s disease (BD) are cutaneous, sterile folliculitis or acne-like lesions on erythematous base. Our purpose was to determine the true frequency and anatomic location of the PPL and compare this with controls. We also sought to determine whether or not there was any relationship between PPL and either disease activity or other manifestations of BD. Methods Fifty patients with BD, diagnosed according to the criteria of the International Study Group for Behçet’s Disease, were enrolled in the study. The control group consisted of 100 patients with other dermatologic diseases (21 acne and 79 non-acne patients), selected randomly. A dermatologist counted the lesions, in a blind protocol, on seven anatomic locations: scalp, face, neck, trunk, upper and lower extremities and genitalia. Results The frequency of PPL in patients with BD was 96% and the most common location was the trunk, whereas in the control group the frequency was 89% and the most common location was the face. In acne and non-acne patients, the frequency was 100% and 86.1% respectively. The total mean number, and mean numbers of PPL on the location of trunk, upper and lower extremities, and genitalia were higher in patients with BD than in controls. When the PPL in BD patients with a positive pathergy test was compared with that in patients with a negative pathergy test, the difference was significantly higher. Conclusions Our results indicate that PPL appear to be non-specific. In the diagnosis of BD the mean number and anatomic location of the lesions are of more importance than the frequency.     

Immunoglobulin A-associated lymphocytic vasculopathy: a clinicopathologic study of eight patients

Introduction: Cutaneous IgA‐associated vasculitis can be a clue to Henoch–Schönlein purpura (HSP), which typically comprises renal and gastrointestinal tract disease and arthritis, whereby prominent and predominant IgA deposits within the cutaneous vasculature provoke a pustular leukocytoclastic vasculitis. Design: We describe eight patients with a novel expression of a cutaneous IgA vascular injury syndrome, namely a lymphoid vasculopathy which clinically and light microscopically resembled a pigmentary purpura (PP) in six, and correlate direct immunofluorescence (DIF) and clinical features to light microscopy. Results: Among associated diseases were prior viral infection, an HSP symptom complex, an undifferentiated connective tissue disease syndrome, lupus erythematosus profundus (LEP), Degos' disease and Berger's disease. Skin lesions comprised non‐palpable petechial lesions involving lower extremities in all cases and also the upper extremities in two. A superficial perivascular lymphocytic infiltrate unaccompanied by vascular fibrin deposits was associated with prominent erythrocyte extravasation including into the epidermis. Mural and extravascular fibrin deposition was seen in one biopsy from a PP‐like lesion and mural fibrinoid necrosis was seen in the cases of LEP and Degos' disease; in biopsies from these three cases, the presence of fibrin deposition warranted use of the appellation ‘lymphocytic vasculitis’. In all patients, DIF showed prominent and predominant IgA deposits. Conclusions: A non‐necrotizing lymphocytic purpuric vascular reaction is one manifestation of vascular IgA deposition in the skin. A subpopulation of human lymphocytes bear surface Fc receptor and/or C3 receptors (‘complement receptor lymphocytes’) which can bind circulating immune complexes (ICs) or C3 generated via activation of the alternative complement cascade. Thus, circulating ICs are a potential pathogenic basis of this eruption, the histologic differential diagnosis of which is idiopathic PP and PP of drug or viral etiology.     

Fas (CD95) and bcl-2 expression in active skin lesions of Behçet''s disease

Over‐expression of bcl‐2 in lymphocytes has an important role in some immunological and inflammatory diseases. Fas (CD95) is a cell surface molecule that mediates receptor‐triggered apoptosis in various cells including autoreactive T cells. In this study we investigated bcl‐2 and Fas (CD95) expression in dermal lymphocytes in active skin lesions of Behçet's disease (BD) and in skin biopsy samples with chronic, non‐specific inflammations. Tissue sections of 29 skin lesions of Behçet's disease and of 10 chronic non‐spesific inflammatory process cases from the archives of the Ondokuz May?s University's Pathology Department were immunohistochemically stained for bcl‐2 and Fas (CD95), and lymphocytes in the dermal infiltrate were evaluated for cytoplasmic staining. bcl‐2 staining was observed in the skin lesions of 22 cases (75.8%) of Behçet's disease. bcl‐2 staining was detected in two (20%) control skin biopsy samples with non‐specific chronic inflammation. Fas (CD95) positivity was not detected in lymphocytes in Behçet's disease‐related skin lesions. Fas (CD95) staining was observed in only three skin biopsy samples with non‐specific chronic inflammation. bcl‐2 and Fas (CD95) staining values in Behçet's and non‐specific inflammation groups were significantly different (P < 0.01); differences in the bcl‐2 staining values between Behçet's patients with mucocutaneous involvement only and mucocutaneous and other systemic involvements were not significant (P > 0.05). Expression of bcl‐2 and loss of Fas (CD95) expression in dermal lymphocytes may play a role in the development of skin lesions and may account for the chronic course with periodic exacerbations in BD.     

Investigation of Propionibacterium acnes in progressive macular hypomelanosis using real-time PCR and culture

Background Progressive macular hypomelanosis (PMH) is a dermatosis of unknown etiology. It has been concluded that it involves the presence of Propionibacterium acnes, a saprophyte of the pilosebaceous follicles. In our study, we investigated the presence of P. acnes in lesional and non‐lesional skin of patients with PMH through quantitative real‐time polymerase chain reaction (PCR) and bacterial culture from a skin fragment. Materials and methods An observational, exploratory study, with laboratory comparison of lesional (study group) and non‐lesional skin (comparison group), in patients with PMH, was carried out with 36 patients, seen in the dermatology outpatient setting at the Oswaldo Cruz University Hospital (OCUH), Recife, Pernambuco, Brazil, between March and May 2008. All patients were submitted to a Wood’s lamp examination, mycological research, and biopsies of lesional and non‐lesional skin from the back. Skin fragments were submitted to a histopathology test, bacterial culture, and a quantitative real‐time PCR test. The program Statistical Package for Social Sciences, version 12.0, was employed for relationship analysis with the Wilcoxon and McNemar tests. Results There was a significant predominance of P. acnes on lesional skin, in comparison to non‐lesional skin (P < 0.001), as demonstrated by culture and quantitative real‐time PCR. Conclusion Although P. acnes is a saprophyte, the hypothesis may be raised that this microorganism participates in the development of PMH.     

IgD immune complex vasculitis in a patient with hyperimmunoglobulinemia D and periodic fever

We describe a 27-year-old Dutch woman with the hyperimmunoglobulinemia D and periodic fever syndrome. During febrile attacks she occasionally presented with skin lesions on the distal parts of her upper and lower extremities, with the histologic picture of a leukocytoclastic vasculitis. Clear perivascular deposits of IgD and C3 were presented in early lesional skin on immunofluorescence investigation. Circulating IgD immune complexes were demonstrated on several occasions, both during and in between clinical attacks. These findings are consistent with an IgD immune complex-mediated pathogenesis for the skin lesions. In 10 patients with other forms of immune complex vasculitis of the skin, minimal perivascular deposits of IgD were found in four cases. In these cases, however, IgD was never found as the solitary immunoglobulin class.     

Steroid acne vs. Pityrosporumfolliculitis: the incidence ofPityrosporum ovaleand the effect of antifungal drugs in steroid acne

Background Steroid acne is a folliculitis that can result from systemic or topical administration of steroid, and has been described as showing a similar clinical picture to Pityrosporum folliculitis, but there have been few reports about the incidence of Pityrosporum ovale and the effect of antimycotic drugs in steroid acne and other acneiform eruptions. Our purpose was to describe the association between steroid acne and P. ovale, and to confirm the superior efficacy of oral antifungal drugs over anti-acne drugs in the treatment of steroid acne. Methods The history, clinical features direct microscopy, histopathologic analysis, and therapeutic results of 125 cases with steroid acne or other acneiform eruptions were described and compared. Results Over 80% of patients with acneiform eruption receiving systemic steroid revealed significant numbers of P. ovale in the lesional follicle. Furthermore, oral antifungal drug (itraconazole) showed significantly better clinical and mycologic effects than any other group of medications used in this study. Conclusions Steroid acne and other acneiform eruptions showing discrete follicular papules and/or pustules localized to the upper trunk and acneiform facial skin lesions associated with multiple acneiform lesions on the body in the summer period should be suspected as Pityrosporum folliculitis. In addition, oral antifungal drugs recommended for Pityrosporum folliculitis; however, it will require a larger case-control study to confirm the superiority of antifungal therapy over anti-acne treatment.     

Immunophenotyping of inflammatory cells in subacute prurigo

Background Subacute prurigo (SP) is a relatively common disease of papular cutaneous lesions that itch intensely. However, there is a lack of systematic clinical and histological studies on SP. Objectives We aimed to immunophenotype inflammatory cells in SP using immunohistochemistry and flow cytometry. Methods Lesional and non‐lesional skin of 21 patients with SP was investigated. Immunohistochemical staining for CD1a, CD3, CD4, CD8, CD15, CD34, CD68, and anti‐human tryptase (AHT) was performed. In order to evaluate the absolute counts and percentages of CD4+ and CD8+ lymphocytes in the peripheral blood of SP patients, flow cytometric methods were used. Results Compared to non‐lesional skin, there was a significant increase of the median percentage of CD3+, CD4+, and CD8+ cells in the lesional dermis (12.6% vs. 19.7%, P = 0.044; 0.8% vs. 3.7%, P = 0.016; and 1% vs. 15.6%, P = 0.0039, respectively). The mean ± SD CD4+/CD8+ ratio was 0.58 ± 0.6. Median percentage of CD15+ cells was significantly increased in lesional skin as compared to non‐lesional skin (11.7 vs. 1%, P = 0.027). Median percentage immunoreactivity of CD68+ cells was significantly increased in lesional dermis as compared to non‐lesional skin (32.5% vs. 9.4%, P = 0.0005). CD1a, CD34, and AHT positive cells did not significantly differ between lesional and non‐lesional skin. T lymphocyte subsets in the peripheral blood of SP patients did not show significant pathologies. Conclusions We observed that the inflammatory cell infiltrate in SP mainly consists of T lymphocytes, particularly CD8+ cells, CD15+ neutrophils, and CD68+ macrophages.     

Annular lesions of cutaneous sarcoidosis with granulomatous vasculitis

Sarcoidosis is known to be involved in diseases with vasculitis as sarcoid vasculitis. However, vasculitis in cutaneous sarcoidal lesions is extremely rare. Here we describe a case of sarcoidosis with multiple annular skin lesions with granulomatous vasculitis. A 62‐year‐old female was diagnosed with sarcoidosis by chest‐abdominal computed tomographic examination and laboratory tests. The skin lesions had appeared on her lower limbs 2 years before. Physical examination showed multiple infiltrated annular eruptions on the lower extremities. A skin biopsy of an area of erythema showed multiple non‐caseating epithelioid cell granulomas in the dermis and subcutaneous fat and granulomatous vasculitis with fibrinoid degeneration in the subcutaneous fat. There are two types of vasculitis in sarcoidosis: leukocytoclastic and granulomatous vasculitis. Ulcers and livedo were more common in granulomatous vasculitis than in leukocytoclastic vasculitis. The present case had unique annular skin lesions of sarcoidosis with granulomatous vasculitis.     

Fractionated aminolevulinic acid–photodynamic therapy provides additional evidence for the use of PDT for non-melanoma skin cancer

Background Photodynamic therapy (PDT) is an accepted treatment for superficial basal cel carcinoma (sBCC) and Bowens disease. In Rotterdam, extensive preclinical research has lead to an optimized twofold illumination scheme for aminolevulinic acid–PDT (ALA‐PDT). Objective To provide additional evidence of ALA‐PDT for sBCC, Bowens disease (BD), nodular BCC (nBCC) and actinic keratosis (AK) using a 2‐fold illumination scheme after a single application of ALA. Methods Five hundred fifty‐two lesions (430 sBCC, 20 nBCC, 32 BD, 70 AK) were treated with ALA‐PDT using a twofold illumination scheme. ALA was applied topically for 4 h. Lesions were treated with two light fractions of 20 and 80 J/cm² separated by a 2‐h dark interval. Results After a minimum follow‐up of 12 months, in average follow‐up of 2 years, an overall complete response of 95% was seen for all lesions. For sBCC, the complete response at 2 years was 97% (for AK 98%, for BD 84% and for nBCC 80% after 2 years). A sub‐analysis of the results of lesions larger than 2 cm showed CR at 2 years of 89% for all lesions (n = 57). Cosmetic outcome was good to excellent in 95% of the treated lesions. Conclusion ALA‐PDT using a twofold illumination scheme of 20 plus 80 J/cm² separated by a 2‐h dark interval leads to high complete response rates at 2 years and can be regarded as an evidence‐based treatment modality for superficial growing non‐melanoma skin cancer and the (pre)malignant AK. The Rotterdam fractionated approach should be included in future guidelines.     

Expression of bcl-2 protein in active skin lesions of Behçet's disease

Abstract Background Expression of bcl‐2 protein has been shown to play an important role in the pathogenesis of some inflammatory as well as neoplastic disorders. In this study we have investigated the presence of bcl‐2 protein in active skin lesions of Behçet's disease and compared these results with normal skin samples of Behçet's disease (BD) patients and BD unrelated leukocytoclastic vasculitis. Methods Active skin lesions of 23 Behçet's disease patients, normal skin samples of seven Behçet's disease patients, and archival biopsy specimens of 23 cutaneous leukocytoclastic vasculitis were investigated for the presence of bcl‐2 protein by immunohistochemical methods. Results of staining were assessed semiquantitatively. Chi‐square tests were used for statistical analysis. Results Expression of bcl‐2 protein were demonstrated in 16 of 23 (69.5%) and 8 of 23 (34.7%) patients with Behçet's disease and leukocytoclastic vasculitis, respectively. There were statistically significant difference between two groups (x² = 4.27, P < 0.05). None of the normal skin samples of Behçet's disease patients showed bcl‐2 expression. Conclusion Expression of bcl‐2 protein may play a particular role in the development of skin lesions in Behçet's disease by causing prolonged survival of infiltrating lymphocytes.     

Prolactin level is significantly elevated in lesional skin of patients with psoriasis

Background Accumulating data point to a potential role of prolactin in the pathogenesis of psoriasis. Methods We initiated a study including psoriasis patients (n = 15) and healthy volunteers (n = 15) as controls. Psoriasis area and severity index (PASI) score was evaluated, and prolactin levels in serum and blister fluid were assessed by enzyme‐linked immunosorbent assay (ELISA). Results Prolactin levels were significantly (P < 0.01) elevated in blister fluid of psoriatic lesional skin. Correlations between PASI score and different serum prolactin levels in lesional and non‐lesional skin were insignificant. Significant positive correlations of prolactin level were observed between lesional and non‐lesional skin in psoriasis (P < 0.05) and between serum and clinically normal skin in both psoriasis and control subjects (P < 0.05). Conclusions Locally produced prolactin may be involved in the pathogenesis of psoriatic lesions.     

某些粘附分子在皮肤血管炎中表达的研究

目的 研究某些细胞粘附分子（ＩＣＡＭ－１，ＶＣＡＭ－１，ＥＬＡＭ－１）在皮肤血管炎中的表达及其意义。方法 采用免疫组织化学方法研究皮肤血管炎皮损部和非皮损部细胞粘附分子的表达。结果 皮肤血管炎皮损部粘附分子表达均高于非皮损部及正常皮肤，ＶＣＡＭ－１与ＥＬＡＭ－１表达呈正相关。结论 患者皮损粘附分子（ＩＣＡＭ－１，ＶＣＡＭ－１，ＥＬＡＭ－１０表达上调，提示其参与皮肤血管炎的发病机制。     

Expression profiles of ProEx C and Ki67 in squamous cell carcinoma in situ of the skin and their relationship with human papillomavirus genotypes

Background: ProExC is a new marker for identification of precursor lesions of cervical carcinoma. Its utility in noncervical squamous cell carcinoma in situ (SCCIS) such as Bowen's disease (BD) and actinic keratosis (AK) where human papillomavirus (HPV) plays a role has not been elucidated. Our aim was to ascertain the immunohistochemical features and clinical utility of ProExC in SCCIS of the skin. Methods: HPV presence was tested in SCCIS (38 BD and 7 AK) using GP5+/6+ and Short PCR fragment (SPF) primers and subsequently genotyped. Histopathologic sections were stained for ProExC and Ki67. A set of non‐neoplastic skin proliferative lesions were included for immunohistochemical evaluation [14 psoriasis (PS) and 6 psoriasiform dermatitis (PSD)]. Results: HPV was detected in 18.9% BD. ProExC and Ki67 in the whole epidermis thickness was observed in 86.5 and 37.1% BD, respectively (p < 0.0001). ProExC and Ki67 were restricted to the lower third of the epidermis in PS and PSD. Conclusions: ProExC expression is not associated with HPV in SCCIS of the skin. Proliferating cells are better delineated in SCCIS by ProExC which may be useful to assess the extent of these lesions. Different immunohistochemical profiles seen in neoplasic and non‐neoplastic skin lesions suggest diverse alteration of cell‐cycle kinetics. Sánchez‐Hernández M, Conesa‐Zamora P, García‐Solano J, Corbalán‐Vélez R, Martínez‐Barba E, Pérez‐Guillermo M. Expression profiles of ProEx C and Ki67 in squamous cell carcinoma in situ of the skin and their relationship with human papillomavirus genotypes.     

Impaired sweating function in adult atopic dermatitis: results of the quantitative sudomotor axon reflex test

Summary Background Impaired sweating is thought to be a cause of barrier dysfunction in atopic dermatitis (AD). Objectives To examine the sweating function in AD in a quantitative manner. Methods We investigated the sweating response of lesional and non‐lesional skin of adult patients with AD by a quantitative sudomotor axon reflex test in which the axon reflex is stimulated by acetylcholine iontophoresis. Sweat volume on the volar aspect of the forearm was measured in 18 adult patients with AD and in 40 non‐atopic controls; five patients with Sjögren's syndrome were also studied as disease comparators. We also evaluated the sweating function in four AD patients after topical corticosteroid therapy. Latency time, direct (DIR) sweat volume and axon reflex‐mediated indirect (AXR) sweat volume were the variables studied. Results The latency time in AD patients was significantly prolonged and AXR sweat volume significantly reduced compared with those in non‐atopic control subjects. The latency time and AXR sweat volume of lesional AD skin were significantly more prolonged and reduced, respectively, than those of non‐lesional skin. In contrast, the DIR sweat volume of lesional or non‐lesional AD skin induced by direct stimulation with acetylcholine was only slightly reduced when compared with that in non‐atopic controls. Latency time and sweat volumes of lesional and non‐lesional AD skin improved after topical corticosteroid therapy. Conclusions These results suggest that the impaired sweat response in AD is attributable to an abnormal sudomotor axon reflex, which is reversed by topical corticosteroid administration.     

Panarteritis cutanea benigna – an entity limited to the skin or cutaneous presentation of a systemic necrotizing vasculitis? Report of seven cases and review of the literature

Objective In 1931 Lindberg described a limited and benign subcutaneous form of panarteritis nodosa, which, in contrast to systemic panarteritis, only affects the skin. The terms panarteritis nodosa cutanea benigna, cutaneous polyarteritis nodosa, apoplexia cutanea Freund as well as livedo with nodules are used synonymously for this vasculitis which predominantly affects women in the fifth decade of life. Cutaneous lesions characteristically comprise painful subcutaneous nodules or vasculitis racemosa at the lower extremities. The cutaneous panarteritis may be regarded as its own entity or an isolated skin manifestation within systemic panarteritis nodosa. Methods Seven patients (M = 3, F = 4) presented with subcutaneous, painful nodules (n = 2), erythema and edema (n = 2) or livedo racemosa (n = 3) on the lower extremities. Histological examination revealed perivascular lymphocyte inflammatory infiltrates with fibrinoid necrosis and bulging of endothelial cells. In a direct immunofluorescence examination neither immunoglobulin nor complement deposits could be found. Serological autoimmune parameters, abdominal ultrasound examination, and chest X-rays showed no systemic manifestation. Erythrocyte sedimentation rate was slightly raised, and hepatitis B/C serology was negative. Results Topical corticosteroids under occlusion (n = 3), oral methyl-prednisolone (n = 4) in combination with either azathioprine (n = 4) or mycophenolate mofetil (n = 2) showed no relapses [follow up 28.43 (6–82) months]. Conclusion The etiology of panarteritis nodosa cutanea is unknown in detail. Both focal infections and hypersensitivity reactions are discussed. Differential diagnosis includes systemic panarteritis, livedo reticularis, Sneddon's syndrome or erythema nodosum. Despite the prognostically favorable but prolonged chronic course of the disease over decades, patients should be regularly examined to exclude possible transition to systemic disease.     

Acral lesions of vitiligo: why are they resistant to photochemotherapy?

Background Acral lesions of vitiligo are usually resistant to conventional lines of treatment as well as surgical interventions. Objective To clarify causes underlying resistance of acral lesions to pigmentation in vitiligo by studying some of the factors associated with mechanisms of repigmentation following photochemotherapy. Methods The study included twenty patients with active vitiligo. Skin biopsies were taken from lesional and perilesional skin of areas expected to respond (trunk and proximal limb) and skin of acral areas, before and after PUVA therapy. Sections were stained with H and E, Melan‐A, MHCII, CD1a, SCF and c‐kit protein. Results Before treatment acral areas showed significantly lower hair follicle density, melanocyte density, Langerhans cell (LC) density, epidermal MHCII expression, lesional SCF expression and perilesional c‐kit expression. Following treatment with PUVA in both non‐responsive acral and repigmenting non‐acral lesions identical immunohistochemical changes in the form of significant decrease in LC density, epidermal MHC‐II and SCF expression were observed. Conclusion The surprisingly similar histochemical changes in response to PUVA in acral and non‐acral lesions did not manifest with clinical repigmentation except in non‐acral ones. Factors such as inherent lower melanocyte density, lower melanocyte stem cell reservoirs and/or lower baseline epidermal stem cell factor may be considered as possible play makers in this respect.     

Eosinophilic annular erythema: A late but complete response to hydroxychloroquine

A 69‐year‐old woman with a 12‐month history of asymptomatic erythematous, non‐scaly, annular and arciform plaques on her face, trunk and extremities is presented. The skin lesions had been unresponsive to treatment with systemic corticosteroids and antihistamines. Skin biopsy demonstrated superficial and deep dermal inflammatory infiltration consisting mainly of eosinophils and a few neutrophils. Dermal interstitial mucin deposition was also detected in the absence of vasculitis, flame figures or granulomatous reaction. The patient was diagnosed as having eosinophilic annular erythema and treated with hydroxychloroquine (2 × 200 mg/day, p.o.). Response to treatment was observed after 7 weeks and full recovery was achieved after 10 weeks. Eosinophilic annular erythema is rarely reported in the literature. Although hydroxychloroquine is a good choice for treatment, response time can vary between patients.     

Diagnostic, prognostic and pathogenic value of the direct immunofluorescence test in cutaneous leukocytoclastic vasculitis

BACKGROUND: No precise studies have been performed on cutaneous leukocytoclastic vasculitis (LV) to establish whether it is better to obtain a skin biopsy from lesional or from perilesional skin for direct immunofluorescence (DIF). There is no agreement on the immunoglobulins most frequently detected and the value of DIF for the classification of cutaneous vasculitis. METHODS: A prospective study of DIF in lesional and perilesional skin was performed in 50 leukocytoclastic vasculitis patients and 15 nonvasculitis patients. RESULTS: We detected a higher level of positivity in involved skin than in uninvolved skin for IgG, IgA, IgM, C3 and fibrinogen but not for C1q. In vasculitic patients, IgA was the immunoglobulin most frequently detected in lesional (82%) and perilesional skin (68%), followed by IgM (56 and 34%, respectively) and IgG (20 and 8%, respectively). Only IgA deposits were associated with the diagnosis of vasculitis, with a sensitivity of 82% in lesional and 68% in perilesional skin, and with a specificity of 73 and 66.7%, respectively. The presence of IgA in lesional skin was associated with renal involvement but there was no association with severity. The presence of IgG or IgM, or the absence of IgA in perilesional skin was related to the presence of cryoglobulins. The absence of IgA in lesional and perilesional skin was also related to hepatitis C virus infection. CONCLUSIONS: DIF findings in involved skin are more closely related to the diagnosis of vasculitis and can give more information about overall renal involvement than findings in uninvolved skin. However, findings in uninvolved skin are more closely related to the pathogenic factors that trigger the development of vasculitis.     

Immunopathogenic characterization of cutaneous inflammation in Behçet’s disease

Background Behçet’s disease (BD) is a recurrent multisystemic inflammatory disease characterized by recurrent oral aphthous and genital ulcers, ocular lesions and cutaneous lesions. Although many studies of cytokine levels in sera of BD patients have been conducted, there are only limited number of studies about the cytokine expression and cellular infiltration in the BD‐related skin lesions. Objectives To investigate the immunophenotypes and cytokine profiles of BD‐related skin lesions. Methods Twenty patients who fulfilled the diagnostic criteria for BD with BD‐related skin lesions were enrolled in this study. We assessed the histopathological features of BD‐related skin lesions by immunohistochemical studies with anti‐human CD4, CD8, CD68, FoxP3, CD‐11b, IFN‐γ and IL‐4 antibodies. Results Immunophenotyping of inflammatory infiltrating cells showed that CD68+ macrophages were the most common type of infiltrated cells in erythema nodosum‐like lesions, erythema multiforme‐like lesions and Sweet’s syndrome‐like lesions, whereas neutrophils were the main population of inflammatory infiltrating cells in papulopustular lesions. In all of the four types of BD‐related skin lesions, the percentage of CD8+ T cells was higher than that of CD4+ T cells (P < 0.05), and IL‐4 expression was stronger than IFN‐γ expression (P < 0.05). Conclusion In this study, we assessed the infiltrating inflammatory cells and cytokine expression of acute cutaneous lesions in BD through immunohistochemical staining of BD‐related skin lesions. Further studies about the disease activity and the molecular biology underlying the cutaneous inflammation are needed to understand the detailed pathogenesis of BD.     

Autoantigens ADAMTSL5 and LL37 are significantly upregulated in active Psoriasis and localized with keratinocytes,dendritic cells and other leukocytes

Psoriasis is a common immune‐mediated disease that affects 2%‐4% of individuals in North America and Europe. In the past decade, advances in research have led to an improved understanding of immune pathways involved in the pathogenesis of psoriasis and has spurred the development of targeted therapeutics. Recently, three psoriasis autoantigens have been described: cathelicidin (LL37), a disintegrin and metalloprotease domain containing thrombospondin type 1 motif‐like 5 (ADAMTSL5), and lipid antigens generated by phospholipase A2 (PLA2) group IVD (PLA2G4D). It is important to establish the expression, regulation and therapeutic modulation of these psoriasis autoantigens. In this study, we performed immunohistochemistry and two‐colour immunofluorescence on non‐lesional and lesional psoriasis skin to characterize ADAMTSL5 and LL37, and their co‐expression with T cells, dendritic cells, neutrophils and macrophages, which are the main immune cells that drive this disease. Our results showed that ADAMTSL5 and LL37 are significantly (P<.05) increased in lesional skin and are co‐expressed by many dendritic cells, macrophages and some T cells in the dermis. Gene expression analysis showed significant (P<.05) upregulation of LL37 in lesional skin and significant downregulation following treatment with etanercept. ADAMTSL5 and LL37 are also significantly decreased by IL‐17 or TNF‐α blockade, suggesting feed‐forward induction of psoriasis autoantigens by disease‐related cytokines.