非特应性的湿疹皮炎患者皮肤马拉色菌携带情况

为探讨非特应性的湿疹皮炎患者皮肤马拉色菌携带情况，选取非特应性的温疹皮炎患者，参照Faergemann的方法取材，采用马拉色菌培养基培养。结果急性及慢性湿疹皮炎患者非脂溢部位皮损马拉色菌检出率显著高于正常人非脂溢部位，接触性皮炎及未分类湿疹患者非脂溢部位皮损马拉色菌检出率也显著高于正常人非脂溢部位。自身对照研究发现，慢性湿疹皮炎患者非脂溢部位皮损马拉色菌检出率显著高于自身正常非脂溢部位。结论示马拉色菌可能与一部分非特应性的湿疹皮炎有一定关系。     

Profiles of Foxp3+ regulatory T cells in eczematous dermatitis, psoriasis vulgaris and mycosis fungoides

Background It is well known that regulatory T cells (Tregs), identified by their expression of CD4, CD25 and Foxp3, play a crucial role in maintaining peripheral tolerance. Recently, it has been demonstrated that a Treg population resides in normal human skin. However, only a few studies have demonstrated the presence of Foxp3+ Tregs in inflammatory skin disorders. Objectives In this study, we immunohistologically examined the presence of CD4+ CD25+ Foxp3+ Tregs in the lesional skin of psoriasis vulgaris, mycosis fungoides and eczematous dermatitis. Methods We used immunohistochemistry to examine the presence of Foxp3+ Tregs in fixed sections of the lesional skin from 16 patients with psoriasis vulgaris, 17 patients with mycosis fungides and 18 patients with eczematous dermatitis in addition to 10 normal skin samples. Results In normal skin, epidermal and dermal Foxp3+ cells were rare. The psoriasis vulgaris, mycosis fungoides and eczematous dermatitis samples contained substantial numbers of epidermal and dermal CD3+, CD4+ and CD25+ Foxp3+ Tregs. The epidermis contained a higher percentage of CD3+, CD4+ and CD25+ Foxp3+ cells than the dermis. The percentage of Foxp3+ cells among CD3+ or CD4+ cells was significantly lower in eczematous dermatitis than in psoriasis vulgaris or mycosis fungoides, and that of dermal Foxp3+ cells was significantly lower in psoriasis vulgaris than in eczematous dermatitis or mycosis fungoides. Conclusions The lower percentage of epidermal or dermal Foxp3+ cells in eczematous dermatitis or psoriasis vulgaris, respectively, might contribute to their pathogenesis.     

Reduced skin threshold to irritation in the presence of allergic contact dermatitis in the guinea pig

The skin is more susceptible to irritation when an active eczematous process is present. This reduced threshold to irritation occurs in skin distant from the site of the eczematous skin. Data is presented to demonstrate the appearance of irritant dermatitis to lower concentrations of sodium lauryl sulfate during the presence of an allergic contact dermatitis in the guinea pig.     

Histamine helps development of eczematous lesions in experimental contact dermatitis in mice

Histamine is released from mast cells in the skin, causing urticaria and itching. However, little is known about the roles of histamine in development of eczematous lesions in contact dermatitis. Effects of histamine on development of eczematous lesions in contact dermatitis were assessed using histamine-deficient mice in which contact dermatitis was developed by repeated application of diphenylcyclopropenone. Development of eczematous lesions in contact dermatitis was suppressed in histamine-deficient mice compared to wild-type mice. H₁ agonist ((6-12-(4-imidazol)ethylamino)-N-(4-trifluoro- methylphenyl)hepatanecarboxamide) promoted development of eczematous lesions in histamine-deficient mice. H₁ receptor antagonist (loratadine) suppressed development of eczematous lesions in wild-type mice, whereas H₂ agonist (dimaprit) and receptor antagonist (cimetidine) were ineffective. These results suggest that histamine facilitates the development of eczematous lesions in a murine model of contact dermatitis via H₁ receptors.     

Periorbital dermatitis: Causes,differential diagnoses and therapy

Periorbital dermatitis is common and frequently difficult to treat. Patients with periorbital dermatitis often suffer severely because their disease is in such a visible location. Because of the variety of clinical appearance, the differential diagnostic considerations are often difficult. We examined the causes of periorbital dermatitis and compared the data of 88 patients from the Department of Dermatology, University Hospital Erlangen to those of the German IVDK (Information Network of the Departments of Dermatology). Between 1999 and 2004, predominant causes of periorbital dermatitis were allergic contact dermatitis (Erlangen 44 %, IVDK 32 %), atopic eczema (Erlangen 25 %, IVDK 14 %), airborne contact dermatitis (Erlangen 10 %, IVDK 2 %) and irritant contact dermatitis (Erlangen 9 %, IVDK 8 %). Less frequent causes for secondary eczematous periocular skin lesions were periorbital rosacea, allergic conjunctivitis or psoriasis vulgaris. Female gender, atopic skin diathesis and age of 40 years and older were identified as risk factors for periocular dermatitis. Common elicitors of periorbital allergic contact dermatitis were leave‐on cosmetic products (face cream, eye shadow) and eye drops with the usual allergens being fragrances, preservatives and drugs. Exact identification of relevant contact allergens and allergen elimination are essential for successful treatment. Calcineurin inhibitors are the first‐line therapy for facial atopic eczema. They may be also effective in periocular eczematous lesions of other origins although they are not approved for such use.     

Decisive role of tumor necrosis factor-α for spongiosis formation in acute eczematous dermatitis

Apoptosis of single keratinocytes (KC) is a characteristic feature of spongiosis formation, the histopathologic hallmark of acute eczematous dermatitis. In acute eczema, activated dermis-infiltrating T cells secrete several proinflammatory cytokines which might be decisive for KC apoptosis or survival. We analyzed the role of tumor necrosis factor alpha (TNF-α) in the determination of KC fate during spongiosis formation in acute eczematous dermatitis. Supernatants of activated human CD4⁺ T cells induced apoptosis in primary KC, which could be fully inhibited by individual blockade of interferon-γ (IFN-γ) and CD95 but not by neutralization of TNF-α activity. As compared to CD95-triggering alone, synchronous CD95 and TNF receptor cross-linking in the presence of IFN-γ only marginally enhanced KC apoptosis. Importantly, pre-treatment of KC with TNF-α followed by CD95 stimulation, but not vice versa, significantly amplified KC apoptosis as compared to CD95 stimulation alone. This TNF-α-mediated sensitization to CD95-induced KC cell death could be abrogated by blocking TNF receptor 1 (TNF-R1) but not TNF-R2 mAb. In eczematous dermatitis, the CD95 receptor was expressed throughout the epidermis, whereas immunohistological detection of TNF-R1 was rather restricted to KC around spongiotic vesicle formation. Thus, TNF-α primes KC for CD95-mediated signals which results in an increased susceptibility to apoptosis. TNF-R1 expression and spatial action of TNF-α restricted to spongiotic vesicles promote both CD95-induced KC apoptosis and limitation of spreading KC damage.     

Mango dermatitis: Allergic contact dermatitis to Mangifera indica

‘Mango Dermatitis’ is the common term given to allergic contact dermatitis to the sap or skin of the fruit of Mangifera indica. Four patients presented with urticaria and eczematous rash following exposure to mangoes or the trees. Patch testing with diluted sap, crushed leaf, crushed stem and fruit skin was strongly positive.     

Guidelines for Diagnosis and Treatment of Atopic Dermatitis in China (2020) #

Atopic dermatitis (AD) is a common disease clinically characterized by chronic recurrent eczematous lesions, dry skin, and pruritus. AD can negatively impact pa...     

In vitro reproduction of clinical hallmarks of eczematous dermatitis in organotypic skin models

Dermatitis is a group of highly pruritic chronic inflammatory skin diseases which represents a major public-health problem worldwide. The prevalence of dermatitis has increased in recent years affecting up to 20% of the general population. Acute skin lesions are characterized by extensive degrees of intercellular edema of the epidermis (spongiosis) and a marked perivenular inflammatory cell infiltrate in the dermis. Keratinocytes within eczematous lesions exhibit a modified expression of proinflammatory cytokines, chemokines and cell-surface molecules. The pathophysiological puzzle of dermatitis is far from being elucidated completely, but skin infiltration of activated memory/effector T cells are thought to play the pivotal role in the pathogeneses. The aim of this study was the set-up of organotypic models mimicking the symptoms of eczematous dermatitis to provide a tool for therapeutic research in vitro. Therefore activated T cells (ATs) were integrated in organotypic skin and epidermis equivalents (SE, EE). These models enabled the reproduction of several clinical hallmarks of eczematous dermatitis: (1) T cells induce keratinocyte apoptosis, which leads to a reduced expression of the adhesion molecule E-cadherin (E-cad) and disruption of the epidermal barrier. (2) Expression of intercellular adhesion molecule-1 (ICAM-1) allows the attachment of leukocytes to epidermal cells. (3) Upregulation of neurotrophin-4 (NT-4) in the epidermis is thought to mediate pruritus in lesions by supporting nerve outgrowth. (4) Elevated levels of pro-inflammatory cytokines (IL-1α and IL-6) and chemokines (IL-8, IP-10, TARC, MCP-1, RANTES and eotaxin) amplify the inflammatory response and lead to an influx of secondary immunocells into the skin. The therapeutics dexamethasone and FK506 markedly reduce cytokines/chemokines production and epidermal damaging in these models. These data underline that activated memory/effector T cells induce eczematous changes in this HaCaT cell based organotypic skin equivalent. Furthermore it can be concluded that these models make it possible to investigate targets of therapeutics in skin.     

Retrospective chart review in a cohort of patients with urticarial dermatitis

Urticarial dermatitis is a poorly understood skin condition while it seems to be much more common than the paucity of reports suggest. It manifests with severely pruritic papules and plaques that resemble eczematous and urticarial lesions morphologically. The key clues to diagnosis are the urticarial appearance and overlap with an eczematous reaction. Here, we present a series of 19 cases (13 women and six men) with urticarial dermatitis clinically and histologically. The patients' average age was 58 and most of the cases were idiopathic. Trunk and proximal extremities were the most common sites involved followed by the distal extremities. Poor response to potent topical corticosteroids and antihistamines was usual and many patients required oral prednisone or other immunosuppressant agents or phototherapy.     

Cobalt and nickel content of Asian cements

The total cobalt and nickel concentration of 11 brands of Asian cement ranged from 8.1 to 14.2 micrograms/g and 14.9 to 28.5 micrograms/g, respectively. These metals exist mainly as insoluble salts; the water-soluble concentration of cobalt and nickel in the cements ranged from 0.39 to 0.65 micrograms/g and from 0-1.2 micrograms/g, respectively. 1.5% (4/272) of construction workers in a prefabrication construction factory had cobalt sensitivity. All had allergic contact dermatitis from chromate in cement. No worker had isolated cobalt sensitivity and cement dermatitis. It appeared that sensitization to cobalt in cement occurs only secondarily to an existing cement dermatitis. 1.8% (5/272) workers had nickel sensitivity: 2 with allergic contact dermatitis to nickel in their watches, 2 were asymptomatic and 1 had allergic contact dermatitis to chromate and cobalt in cement. The low prevalence of cobalt and nickel sensitivity from cement was probably related to the low concentration of soluble cobalt and nickel salts in the cement. However, these insoluble salts can form soluble complexes with body fluids on eczematous skin and sensitize the skin.     

Evaluation of Langerhans' cells in normal and eczematous dermatitis skin by CD1a protein immunohistochemistry: preliminary findings

Background:  Langerhans' cells (CD1a positive, bone marrow–derived cells), are the antigen presenting cells of the skin. Our knowledge about the status of these cells in eczematous dermatitis is incomplete.
Aim:  This study tests the hypothesis that 'the development of eczematous dermatitis is associated with alterations of Langerhans' cells'.
Materials and methods:  Biopsy specimens from patients with eczematous dermatitis and normal skin (20 cases, each) were studied. Langerhans' cells were stained for CD1a using imunoperoxidase-staining methods and mouse monoclonal antibodies.
Results:  In normal skin, CD1a+ Langerhans' cells were seen in suprabasal position. In eczematous dermatitis skin, CD1a positive cells were seen scattered in the acanthotic epidermis. Compared with normal skin, the mean values of the Langerhans' cells were statistically significantly higher in eczematous dermatitis [epidermal Langerhans' cells: 1.20 (standard error of mean, SEM, 0.13) vs. 2.50 (SEM, 0.16); and dermal Langerhans' cells: 1.30 (SEM, 0.15) vs. 2.7 (SEM, 0.15); for normal and eczematous skin, respectively; p < 0.05].
Conclusions:  The higher Langerhans' cell counts in eczematous dermatitis suggest a possible link between antigen presenting capabilities of these cells, and development of these lesions.     

IgE-positive epidermal Langerhans cells in allergic contact dermatitis lesions provoked in patients with atopic dermatitis

Summary To see whether or not IgE-bearing epidermal Langerhans cells are specific to skin lesions of atopic dermatitis (AD), we performed immunohistochemical and immunoelectron microscopic examinations of dinitrochlorobenzene (DNCB) contact dermatitis lesions provoked in uninvolved skin of eight patients with AD. In all of the eight examined, IgE-positive epidermal Langerhans cells were observed in the DNCB dermatitis lesions. Typical staining of anti-IgE was absent in the epidermis of normal-appearing skin of five patients with AD. Thus, it is likely that IgE positive epidermal Langerhans cells non-specifically occur in different eczematous diseases provoked in patients with AD.     

Physical friction is under-recognized as an irritant that can cause or contribute to contact dermatitis

BACKGROUND: The role of physical friction as an irritant in the causation of contact dermatitis is under-recognized. Frictional dermatitis is defined as an eczematous process in which physical frictional trauma contributes to the induction of a dermatitis process. OBJECTIVES: To examine the clinical background of patients in whom friction was contributing to dermatitis. METHODS: Over a 30-month period during which 2700 new patients were seen, frictional irritancy was identified as playing a role in the dermatosis in 31 cases: in 27 of these, case notes were evaluated for a range of parameters. RESULTS: Physical friction was identified as causing or contributing to the dermatitis in 18 men and nine women, mean age at onset 42 years. The hands, usually the fingers of the dominant hand, were affected in all but two cases. Occupational frictional activities were found in 25 cases: commonly handling small metal components, paper, cardboard or fabric, and driving. Potential frictional activities in hobbies were noted in 12 cases. Wet work irritancy contributed in four cases (15%). Patch testing showed relevant contact allergies as cofactors in seven of 25 subjects tested (26%). Psoriasis was a cofactor in four (15%), and atopic dermatitis in 11. The study was selective, being based in a teaching hospital clinic with a special interest in contact dermatitis. Frictional irritancy is often one of several factors contributing to dermatitis. CONCLUSIONS: The contribution of friction to contact dermatitis is under-recognized probably because dermatologists do not think about the potential for physical forces to induce eczematous changes in the skin.     

角质形成细胞与特应性皮炎相关研究进展

角质形成细胞（keratinocytes，KCs）的异常导致角蛋白的表达出现异常，从而导致表皮屏障功能失调。在特应性皮炎(Atopic Dermatitis，AD)皮损中，KC大量表达胸腺淋巴基质生成素、肿瘤坏死因子α以及一些白细胞介素如IL-1α、IL-1β和IL-18等介导皮肤的炎症反应。在AD中KC还可表达模式识别受体，通过先天免疫系统，产生和维持炎症反应。另外，AD皮损中KC损伤导致抗菌肽的表达缺乏可能有助于增加AD患者皮肤对感染病毒、细菌和真菌的易感性。本文对角质形成细胞与特应性皮炎相关研究进展进行综述。     

Personalized Immunomodulatory Therapy for Atopic Dermatitis: An Allergist's View

The current standard medical therapy for atopic dermatitis (AD) mainly focuses on symptomatic relief by controlling skin inflammation with topical corticosteroids and/or topical calcineurin inhibitors. However, the clinical efficacy of pharmacological therapy is often disappointing to both patients and physicians. The terminology of AD contains a historical meaning of eczematous dermatitis caused by hypersensitivity reaction to environmental inhalant or food allergen. Complex interrelationships among genetic abnormalities, environmental triggers, skin barrier defects, and immune dysfunction resulting in a vicious domino-circle seem to be involved in the development and maintenance of AD. In the viewpoint of AD as an allergic disease, complete avoidance of clinically relevant allergen or induction of specific immune tolerance through administrations of allergen (allergen immunotherapy) can provide clinical remission by breaking the vicious domino-circle maintaining a chronic disease state. In recent clinical studies, monoclonal antibodies including the anti-interleukin-4 receptor antibody and anti-B cell antibody induced significant clinical improvements in patients with AD. The detailed characteristics of immune dysfunction are heterogeneous among patients with AD. Therefore, a personalized combination of immunomodulatory therapies to reduce hypersensitivity (allergen immunotherapy) and correct immune dysfunction (monoclonal antibody therapy) could be a reasonable therapeutic approach for patients with AD. Future immunomodulatory therapies for AD should be developed to achieve long-term treatment-free clinical remission by induction of immune tolerance.     

Phenotypes of atopic dermatitis

Atopic dermatitis (AD) is a common disease affecting both children and adults. AD develops from a complex interplay between environmental, genetic, immunologic and biochemical factors. Genetic factors predispose atopic subjects to mount exaggerated Th2 responses and to a poorly efficient epidermal barrier, which may be sufficient to initiate inflammation in the skin and may favor allergic sensitization. Thus AD can present with different clinical pheno‐types. AD is classically distinguished into an intrinsic and extrinsic form, which are clinically identical but the former lacks high level specific IgE and is not associated with respiratory atopy. Although in many cases AD presents with monotonous eczematous lesions on the face, neck and skin folds, it may also present with other features. Very common is nummular eczema, which in many instances may be the dominant expression of AD. In other patients, AD affects limited areas (periorificial eczema, nipple eczema, cheilitis, hand eczema) or its main presentation is with excoriated papules and nodules (atopic prurigo). In conclusion, AD is a multifaceted disease affecting patients with epidermal barrier dysfunction and dry and sensitive skin. The recognition of the less common AD phenotypes is essential for proper patient management.     

Advantages of histamine H4 receptor antagonist usage with H1 receptor antagonist for the treatment of murine allergic contact dermatitis

Histamine facilitates development of eczematous lesions in chronic allergic contact dermatitis. In addition to the well-known corticosteroid treatments, H1 receptor (H1R) antagonists also have been used. This study observed effects of histamine H4 receptor (H4R) antagonist usage with H1R antagonist in a murine chronic allergic contact dermatitis model, developed by repeated percutaneous challenge to the dorsal skin with 2,4,6-trinitro-1-chlorobenzene (TNCB). The H1R antagonist olopatadine hydrochloride and/or the H4R antagonist JNJ7777120 was then administered. Combination therapy was more effective than H1R antagonist monotherapy. Serum IgE and levels of interleukin (IL)-4, IL-5 and IL-6 (Th2 cytokines) in eczematous lesions decreased with combined therapy. Combined therapy with H1R and H4R antagonists counteracts the disadvantages of each as monotherapeutic agents and potentially represents a new strategy for the treatment of chronic allergic contact dermatitis.     

The successful use of topical tacrolimus treatment for a chronic actinic dermatitis patient with complications of idiopathic leukopenia

Chronic actinic dermatitis (CAD) is a photosensitivity disorder marked by severe eczematous lesions on exposed areas. Although associations with contact dermatitis, atopic dermatitis, and human immunodeficiency virus (HIV) have been suggested, its pathogenesis remains unknown. CAD is often refractory, and systemic administration of cyclosporin A has been the treatment of choice. Recently, topical tacrolimus therapy has been reported to be effective. We report the efficacy of topical tacrolimus treatment in a CAD patient who also had the complication of idiopathic leukopenia. A phototest showed marked suppression of erythema formation in the skin pre-treated with tacrolimus before UVB radiation but not in the skin treated after the irradiation. Therefore, it is suggested that tacrolimus may prevent UV-B induced erythema by suppressing a very early phase of the inflammatory process in CAD.     

Vasoconstrictor and the anti-inflammatory effects of 7 corticosteroids

The vasoconstrictor effect of 7 proprietary corticosteroid creams was compared with their effect on patches of allergic contact dermatitis provoked by patch testing in 20 subjects. A parallel between the blanching effect on the normal skin and the anti-inflammatory effect on the eczematous skin was generally found. A modified patch test method using the Finn chamber technique is described, which (with certain restrictions) offers an opportunity of studying the anti-inflammatory effect of corticosteroids on allergic dermatitis under standard conditions.