Jin-Ok Baek

Chromoblastomycosis Caused by Phialophora richardsiae

Chromoblastomycosis is a chronic fungal disease of the skin and subcutaneous tissues caused by a group of dematiaceous (black) fungi. The most common etiologic agents are Fonsecaea pedrosoi and Cladophialophora carrionii, both of which can be isolated from plant debris. The infection usually follows traumatic inoculation by a penetrating thorn or splinter wound. Several months after the injury, painless papules or nodules appear on the affected area; these papules then progress to scaly and verrucose plaques. We report a case of chromoblastomycosis caused by Phialophora richardsiae, which has been rarely associated with chromoblastomycosis. The case involved a 43-year-old male, who for the past 2 months had noted an erythematous, pustulous plaque that was somewhat dark brown in color on his right shin; the plaque also had intermittent purulent discharge and crust formation. On histopathological examination, chronic granulomatous inflammation and sclerotic cells were seen. The tissue fungus culture grew out the typical black fungi of P. richardsiae, which was confirmed by polymerase chain reaction. The patient has been treated with a combination of terbinafine and itraconazole for 3 months with a good clinical response.

Oral tolerance inhibits atopic dermatitis‐like type 2 inflammation in mice by modulating immune microenvironments

Oral tolerance is immune unresponsiveness induced by oral administration of innocuous antigens. Oral administration of allergens has been shown to be effective for suppressing IgE production in allergic responses. However, whether oral tolerance has a role in protection from allergic skin inflammation has not been fully investigated. Here, we evaluated the potential protective role of oral tolerance in a murine model of atopic dermatitis (AD) and investigated the underlying immunologic mechanisms.

A novel homozygous keratin 14 mutation in a patient with autosomal recessive epidermolysis bullosa simplex and squamous cell carcinoma of the tongue

Epidermolysis bullosa simplex (EBS) is a group of inherited skin disorders characterized by lysis of basal keratinocytes leading to the development of intraepidermal blisters from mild trauma. 1 EBS is known to be an autosomal dominant disorder; however, a few recessive cases have been reported. In EBS, the risk of cutaneous malignancy is not higher than in the normal population. 2 We present a patient who showed generalized blistering after minor trauma followed by brownish reticulated hyperpigmentation and squamous cell carcinoma of the tongue. We identified a novel homozygous KRT14 mutation (E392X) inherited in an autosomal recessive fashion.

Oxidative stress and antioxidant strategies in dermatology

Oxidative stress results from a prooxidant-antioxidant imbalance, leading to cellular damage. It is mediated by free radicals, such as reactive oxygen species or reactive nitrogen species, that are generated during physiological aerobic metabolism and pathological inflammatory processes. Skin serves as a protective organ that plays an important role in defending both external and internal toxic stimuli and maintaining homeostasis. It is becoming increasingly evident that oxidative stress is involved in numerous skin diseases and that antioxidative strategies can serve as effective and easy methods for improving these conditions. Herein, we review dysregulated antioxidant systems and antioxidative therapeutic strategies in dermatology.

Treatment of patients with refractory atopic dermatitis sensitized to house dust mites by using sublingual allergen immunotherapy.

Even though atopic dermatitis (AD) is one of the most common chronic inflammatory skin diseases, its treatment remains a challenge in clinical practice, with most approaches limited to symptomatic, unspecific anti-inflammatory, or immunosuppressive treatments. Many studies have shown AD to have multiple causes that activate complex immunological and inflammatory pathways. However, aeroallergens, and especially the house dust mite (HDM), play a relevant role in the elicitation or exacerbation of eczematous lesions in many AD patients. Accordingly, allergen-specific immunotherapy has been used in AD patients with the aim of redirecting inappropriate immune responses. Here, we report three cases of refractory AD sensitized to HDM who were treated with sublingual immunotherapy.

N822K c-kit mutation in CD30-positive cutaneous pleomorphic mastocytosis after germ cell tumour of the ovary.

and scleroderma keratinocytes for 24 h, respectively. In normal keratinocytes, expression of integrin a5 was increased by TNF-a and IFN-c, but not altered by IL-17A and ET-1 (Fig. 2a). However, in scleroderma keratinocytes, integrin a5 was upregulated by IL-17A, and significantly so by ET-1, TNF-a and IFN-c (P < 0Æ05, Fig. 2b). It seems that scleroderma keratinocytes are more sensitive to IL-17A, ET-1, TNF-a and IFN-c than normal keratinocytes in production of integrin a5. Integrin b4 in normal keratinocytes was increased by IL-17A, ET-1, TNF-a and IFN-c (Fig. 2c), while in scleroderma keratinocytes no significant difference was observed as compared with controls (Fig. 2d). Our results suggested that the production of different molecules in keratinocytes varies with different status of cells, which may be affected differently by the same cytokine. The cellular environment may be critical for the response of cells to certain stimuli.

Oral tolerance modulates the skin transcriptome in mice with induced atopic dermatitis

Defective gut immune reactions have been implicated in the development of atopic dermatitis (AD), whereas oral tolerance (OT), that is, the immune unresponsiveness induced by oral antigen administration, protects mice against AD. To investigate this protective role of OT, the transcriptomic profiles of skin were obtained by RNA sequencing from mice that were epicutaneously sensitized, orally tolerized prior to epicutaneous sensitization, or neither (control). Oral tolerance inhibited the upregulation of keratin‐ and allergic inflammation‐associated genes that occurred in the epicutaneously sensitized group. Compared to the controls, mice that were orally tolerized and epicutaneously sensitized showed an upregulation of genes that regulate inflammation or keratinocyte differentiation. Knocking down two of those genes, SCGB1A1 and TSC22D3, upregulated Th2 inflammatory mediators and downregulated a cornified cell envelope‐related gene. Based on our findings, OT may protect skin against allergic inflammation by promoting the expression of genes that regulate Th2 inflammatory responses and skin barrier function.

Case of Gardner–Diamond syndrome after intramuscular stimulation

could involve multiple cranial nerves. Inflammation and edema of the multiple nerves might play a major role in the course of Ramsay–Hunt syndrome. These might be the reasons for the patient’s multiple cranial nerve involvement. Due to the early application of antiviral agents and glucocorticosteroid, or a younger age or the acupuncture and infrared physiotherapy, he recovered faster than many cases in the published work.

A Possible Case of Statin-Induced Ichthyosis in an Elderly Woman

Ichthyosis is a heterogeneous group of hereditary or acquired skin disorders, characterized by increased stratum corneum production. Several systemic diseases and many drugs can occasionally cause acquired ichthyosis. We report a case of statin-induced ichthyosis in which the causality between statin and ichthyosis was found possible by using the Naranjo scale. A 79-year-old woman presented with pruritic skin lesions on both legs that appeared erythematous, scaly, and cracked. A clinical diagnosis of acquired ichthyosis was made and the statin was suspected as the cause. The skin lesions improved after 6 weeks of dose reduction of the statin.

Optimization of Cytokine Milieu to Reproduce Atopic Dermatitis-related Gene Expression in HaCaT Keratinocyte Cell Line

Although atopic dermatitis (AD) is characterized by cytokine production predominantly mediated by T helper (Th) 2 cells, AD pathogenesis also involves innate immune and Th1 cells. To optimize the cytokine milieu required for accurate reproduction of AD-related gene expression profile in vitro, we evaluated the expression pattern of CCL22, CCL17, IL5, IL13, IL33, IL25, TSLP, FLG, and LOR in human lesional AD skin and cytokine-stimulated HaCaT cells. An increase in Th2 mediators (IL5, IL13, CCL22, CCL17, IL25, IL33, and TSLP) and a decrease in genes related to cornified cell envelope (filaggrin and loricrin) were observed in human AD lesions. Innate (tumor necrosis factor-α) and/or Th1/Th2 adaptive cytokines (interferon-γ/IL-4) were required for inducing these inflammatory changes in HaCaT cells, implying that a complex network of innate, Th1, and Th2 cytokines drives AD-like changes. Therefore, stimulation with various combinations of cytokines, beyond Th2 polarization, is necessary when HaCaT cell line is used to study genetic changes implicated in AD pathogenesis.