Reduced induction of human ß-defensins is involved in the pathological mechanism of cutaneous adverse effects caused by epidermal growth factor receptor monoclonal antibodies.

Epidermal growth factor receptor inhibitors (EGFRIs) frequently cause cutaneous adverse effects such as papulopustular eruptions. However, the mechanism of the reactions remains unclear. To assess the pathological mechanism of cutaneous adverse reactions caused by EGFRIs, we investigated whether EGFRIs have an influence on the innate immune response of the skin. Levels of human ß-defensins (hBDs), which serve as the first line of defence against infection by pathogenic microorganisms, in the stratum corneum samples of patients treated with EGFR. monoclonal antibodies were measured before and after starting therapy. There were no obvious trends in hBD production in patients without eruptions, whereas a significant decrease in hBD1 and hBD3 production and a nonsignficant decrease in hBD2 production were observed in patients who developed papulopustular eruptions. Our results suggest that a reduction in hBD contributes to the increased incidence of papulopustular eruptions.

Bacillus cereus strain isolated from Demodex folliculorum in patients with topical steroid-induced rosaceiform facial dermatitis.

The aim of the study was to identify Bacillus species from the Demodex folliculorum of patients with topical steroidinduced facial rosaceiform dermatitis. Of the 75 patients examined, 20% had clinical spinulosis, while 18.66% had dermoscopic features of Demodex: follicular plugs and tails. Of the 17.33% positive patients identified upon microscopy for Demodex, samples for bacterial culture were plated on trypticase soy Colombia agar. Identification was performed by microorganisms grown method mass spectrometry. We identified a strain of Bacillus cereus.

Bacillus cereus strain isolated from Demodex folliculorum in patients with topical steroid-induced rosaceiform facial dermatitis

Abstract: The aim of the study was to identify Bacillus species from the Demodex folliculorum of patients with topical steroidinduced facial rosaceiform dermatitis. Of the 75 patients examined, 20% had clinical spinulosis, while 18.66% had dermoscopic features of Demodex: follicular plugs and tails. Of the 17.33% positive patients identified upon microscopy for Demodex, samples for bacterial culture were plated on trypticase soy Colombia agar. Identification was performed by microorganisms grown method mass spectrometry. We identified a strain of Bacillus cereus.

Cutaneous Granulomas Associated With Interferon Therapy.

Treatment with interferon (IFN) could be associated with variable cutaneous adverse reactions. The aim of this study was to describe the clinicopathological spectrum of cutaneous granulomas associated with IFN therapy and identify the causal relation between IFN therapy and granulomatous reactions. The study included 18 patients (16 males and 2 females) with an average age of 48 years. Clinically, most of the lesions were solitary (83.3%) and located on the face (44.4%) and/or trunk (38.9%). The lesions were commonly presented as nodules (33.3%) or plaques (27.8%) with a common size of 5-10 cm. Granulomatous reactions were localized to the injection site in 4 cases, distributed on other body areas (remote granuloma) in 11 cases, and associated with lung involvement (systemic granuloma) in 3 cases. Histologically, injection site granuloma showed suppurative reaction in 75% and sarcoidal reaction in 25%. Remote granuloma showed tuberculoid reaction in 27.3%, interstitial in 27.3%, and sarcoidal in 45.4%. Systemic granuloma showed sarcoidal reaction in all cases. After withdrawal of IFN, only 3 lesions showed spontaneous complete clearance, whereas most of the lesions (83.3%) showed only partial improvement. Our results suggested that IFN is not a causal agent of all associated cutaneous granulomas but it mostly provokes the appearance of granulomatous reactions in susceptible individuals. Findings that prove this concept include the formation of granuloma in body sites away from the injection site, the heterogeneous pattern of granuloma both clinically and histologically, and incomplete clearance of most of the lesions after withdrawal of IFN.

Nicolau syndrome following intramuscular diclofenac administration: a case report.

Nicolau syndrome (livedoid dermatitis) is a rare adverse reaction of a still largely unidentified pathogenesis at the site of intramuscular drug injection. The typical presentation is pain around the injection site soon after injection, followed by erythema, livedoid patch, haemorrhagic patch, and finally necrosis of skin, subcutaneous fat, and muscle tissue. The phenomenon has been related to the administration of a variety of drugs, including non-steroidal anti-inflammatory drugs, corticosteroids, and penicillin. We report a case of Nicolau syndrome following an intramuscular injection of diclofenac. The large ulceration over the right buttock was positive for Pseudomonas aeruginosa, and histology revealed subcutaneous fat necrosis and non-specific inflammation with no evidence of malignancy or vasculitis. The lesion required multiple debridements and a partial-thickness skin graft. Subcutaneous injection, rather than intramuscular injection, was found to be a determining factor in this case. Clinicians must be cautious in the use of proper injection procedures, including appropriate needle length, in order to minimise complications.

Assessment of Streptococcus pyogenes microcolony formation in infected skin by confocal laser scanning microscopy.

BACKGROUND: Streptococcus pyogenes and Staphylococcus aureus are often simultaneously detected from many cases of non-bullous impetigo with atopic dermatitis. OBJECTIVES: Using confocal laser scanning microscopy (CLSM), to investigate formation of S. pyogenes microcolonies in skin lesions. METHODS: The S. pyogenes cells in the stationary growth phase alone were strongly stained with fluorescein isothiocyanate-concanavalin A (FITC-ConA), and this staining was reduced by pretreatment with amylase. Although the components of sugars in glycocalyx produced by S. pyogenes cells are unknown, we suggested that the materials stained by FITC-ConA were consistent with the presence of ConA-reactive sugars in glycocalyx produced by S. pyogenes cells. RESULTS: S. pyogenes cells associated with streptococcal impetigo skin and croton-oil inflamed mouse skin formed microcolonies encircled by materials (glycocalyx) that stained strongly with FITC-ConA, and these findings were consistent with those in biofilms. In croton-oil inflamed mouse skin, polymorphonuclear leukocytes (PMNs) infiltrated to just below the epidermis in the cefdinir-treated group but only to the middle dermis in the cefdinir-non-treated group. In this case S. pyogenes and S. aureus cells formed separate microcolonies and existed independently in the outer walls of pustule lesions of streptococcal impetigo. CONCLUSION: In skin infections, S. pyogenes and S. aureus formed aggregates of microcolonies (similar to that in biofilms) encircled by glycocalyx, which can make the infection hard to eradicate using an antimicrobial agent alone. The effect of conventional antimicrobial agents against biofilm is mainly due to the increase of the invasion of PMNs into the biofilm.

Expression of interleukin-4 in the epidermis of transgenic mice results in a pruritic inflammatory skin disease: an experimental animal model to study atopic dermatitis.

Atopic dermatitis, a common, chronic, inflammatory skin disease that occurs with increasing prevalence, is characterized by hyperactivated cytokines of helper T cell subset 2 and is frequently associated with staphylococcal infection. An experimental animal model of atopic dermatitis induced by transgenically introduced cytokine is not available. We generated a transgenic mouse line expressing epidermal interleukin-4, a critical cytokine of helper T cell subset 2. Here we show that transgenic mice spontaneously developed a pruritic inflammatory skin disease reproducing all key features of human atopic dermatitis, including xerosis, conjunctivitis, inflammatory skin lesions, Staphylococcus aureus infection, histopathology of chronic dermatitis with T cell, mast cell, macrophage-like mononuclear cell, and eosinophil infiltration, and elevation of total serum IgE and IgG1. The onset and early progression of skin disease coincided with increased total serum IgE and IgG1. The mouse disease occurred at a 43% annual incidence rate and primarily affected the poorly haired skin: ear (100%), neck (65%), eye (53%), face (29%), tail (12%), leg (12%), and torso (6%). As a group the affected transgenic mice manifested with a skin disorder that fulfilled the clinical diagnostic criteria established for atopic dermatitis in human patients. Pending further characterization to authenticate it as a model of atopic dermatitis, this experimental animal model of pruritic inflammatory skin disease may facilitate investigations for the roles of interleukin-4 in cutaneous inflammation and skin infection in human patients.