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.     

Histamine suppresses regulatory T cells mediated by TGF‐β in murine chronic allergic contact dermatitis

Regulatory T cells (Tregs) suppress effector T cells and ameliorate contact hypersensitivity (CH); however, the role of Tregs in chronic allergic contact dermatitis (CACD) has not been assessed. Repeated elicitation of CH has been used to produce CACD models in mice. We previously showed that the presence of histamine facilitates the creation of eczematous lesions in this model using histidine decarboxylase (HDC) (?/?) mice. Therefore, the effects of histamine on Tregs in the CACD model were investigated in this study. CACD was developed by repeated epicutaneous application of 2, 4, 6‐trinitro‐1‐chlorobenzene (TNCB) on HDC (+/+) and HDC (?/?) murine skin to assess the effects of histamine in CACD. Histamine aggravated CACD in the murine model and suppressed the number of Tregs in the skin. Histamine also suppressed the level of TGF‐β1 in this model. Recombinant TGF‐β1 or anti‐TGF‐β1 antibody was injected into the dorsal dermis of HDC (+/+) mice daily just before TNCB challenge to determine the effects of histamine‐regulated TGF‐β on the Treg population in CACD. Recombinant TGF‐β1 injection promoted the infiltration of Tregs in the skin and the production of IL‐10; however, anti‐TGF‐β1 antibody injection suppressed the number of Tregs in the skin and the production of IL‐10. Histamine suppresses the number of Tregs in CACD, and this effect is mediated by TGF‐β.     

Lack of preventing effect of systemically and topically administered histamine H(1) or H(4) receptor antagonists in a dog model of acute atopic dermatitis

As there is evidence for an anti‐inflammatory efficacy of histamine H₄ receptor (H4R) selective antagonists, we aimed at testing the efficacy of the H4R antagonists JNJ7777120 and JNJ28307474 in comparison with histamine H₁ receptor (H1R) antagonists hydroxyzine and cetirizine for skin lesion prevention in a canine model of acute atopic dermatitis. Six atopic Maltese‐beagle dogs experimentally sensitized to Dermatophagoides farinae (Df) house dust mites were selected for this study. Twenty‐four hours after challenge by epicutaneous application of Df, erythematous skin lesions were scored. In this blinded, placebo and active controlled study, topical JNJ7777120 or JNJ28307474 was applied as a 1% solution before allergen challenge. The latter was also given orally at 15 mg/kg before and after allergen challenge. A 0.015% triamcinolone acetonide solution was used as a positive control. The H1R antagonists hydroxyzine and cetirizine were administered orally before challenge in a second experiment. Twenty‐four hours after challenge, placebo‐treated animals had a median lesional score of 2. Treatment with topical and oral JNJ28307474 resulted in a median score of 2.5. After topical administration of JNJ7777120, the median lesional score was 2. Hydroxyzine and cetirizine did also not reduce the median score of the placebo treatment. Triamcinolone acetonide prevented all dogs from having any lesions. Determination of histamine in lesions revealed that only during the initiation increased concentrations of histamine were detected. In conclusion, the preventive administration of H1R or H4R antagonists has no impact on the development of acute skin lesions in this experimental canine atopic dermatitis model.     

The effectiveness of montelukast for the treatment of anti-histamine-resistant chronic urticaria

Many patients with chronic idiopathic urticaria are not sufficiently controlled with histamine H₁-receptor antagonists. Leukotriene receptor antagonists have been reported to be effective for certain cases of urticaria, although their proper application remains to be established. To study the effectiveness of montelukast, a leukotriene receptor antagonist, for the treatment of chronic urticaria that was not controlled by histamine H₁-receptor antagonists. Twenty-five patients with chronic idiopathic urticaria were treated with 10 mg of montelukast for one week or more, without changing any precedent treatment that they were using before the study including histamine H₁-receptor antagonists. The effectiveness of montelukast for each patient was evaluated and compared with clinical features and/or backgrounds of the patients. Twelve patients, including six who had been treated with corticosteroids, were evaluated as “markedly improved” or “improved” following treatment with montelukast. There was no statistically significant relation of the effectiveness to the complications with non-steroidal anti-inflammatory drugs (NSAIDs) intolerance, mechanical urticaria, or reactions to autologous serum skin test. However, the patients for whom montelukast was effective were younger (33.2±16.3 years, mean ± SD)(P<0.05, Mann-Whitney test) and their duration of illness shorter (15.9±18.3 months) (P<0.005, Mann-Whitney test) than those of patients for whom montelukast was ineffective (45.9±15.0 years, 89.6±71.7 months). Montelukast may be worth trying for patients with chronic idiopathic urticaria, when the condition is not sufficiently controlled with histamine H₁-receptor antagonists.     

Acquired cold urticaria: H1 and H2 antagonists versus cold induced histamine release

Three patients with idiopathic cold urticaria were treated with either or both cyproheptadine (Histamine H₁ receptor antagonist) and cimetidine (Histamine H₂ receptor antagonist). Cold induced histamine release (CIHR) was significantly higher in the patients (71.0 ± 23.8 pm/ml) than in normal volunteers (4.5 ± 1.0 pm/ml). Improvement of clinical manifestations with reduced CIHR was obtained by combination therapy using cyproheptadine and cimetidine but no favorable response was noted with either drug alone. The combined therapy with both drugs completely suppressed pruritis and edema but failed to suppress the erythematous reaction. Single cyproheptadine therapy was rather favored by the patients despite positive CIHR with the therapy. Histamine release from patients' leukocytes under three different conditions (37°C, 4°C→37°C, 4°C) was not significantly different.     

Increased expression of the histamine H4 receptor following differentiation and mediation of the H4 receptor on interleukin‐8 mRNA expression in HaCaT keratinocytes

Recent in vivo studies have demonstrated involvement of the histamine H4 receptor in pruritus and skin inflammation. We previously reported that an H4 receptor antagonist attenuated scratching behaviour and improved skin lesions in an experimental model of atopic dermatitis. We also reported the expression of the H4 receptor in human epidermal tissues. In this study, we investigated the expression of H4 receptor mRNA and the function of the receptor in a culture system that mimics in vivo inflammation on the HaCaT human keratinocyte cell line. Increased expression of the H4 receptor was observed in HaCaT cells following differentiation. Treatment of HaCaT cells with histamine and TNFα enhanced the mRNA expression of interleukin (IL)‐8. These increases in expression were significantly inhibited by the H4 receptor antagonist JNJ7777120. Our results indicate that IL‐8 mRNA expression might be enhanced by histamine and TNFα via H4 receptor stimulation in keratinocytes.     

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.     

Effect of epinastine hydrochloride on murine self-scratching behavior after skin-scratching stimulation

The itch–scratch cycle aggravates chronic inflammatory skin diseases. We have previously reported that mice begin to scratch themselves within several minutes after skin-scratching stimulation. This is associated with an increase in release of substance P (SP) from sensory nerve fibers in the skin, and the self-scratching behavior is suppressed by neurokinin-1 receptor (NK-1R) antagonist. Thus, SP may play a pivotal role in self-scratching behavior. The purpose of this study was to investigate the effect of second-generation histamine H₁-receptor antagonists on self-scratching behavior in mice. After oral administration of epinastine hydrochloride (epinastine) (total dose 50 ± 5 mg/kg for 7 days) or the vehicle only to ICR mice for 7 days, skin-scratching stimulation was administered to the dorsal skin for 10 min. Self-scratching behavior was recorded by video camera for 10 min. Twenty-four hours later, skin tissue was harvested and stained with toluidine blue. Immunohistochemical staining for SP was performed, and SP and nerve growth factor (NGF) concentrations were measured by enzyme-linked immunosorbent assay. Self-scratching behavior, mast cell degranulation, and NGF concentration decreased, and the length of SP-positive nerve fibers and SP concentrations increased significantly in the epinastine-treated group, when compared with the vehicle control group. We conclude that epinastine inhibits mast cell degranulation by attenuating SP release from sensory nerve fibers, which results in inhibition of self-scratching behavior. These results suggest that second-generation histamine H₁-receptor antagonists might efficaciously control itch–scratch cycle-related skin diseases.     

Selective Cannabinoid Receptor-1 Agonists Regulate Mast Cell Activation in an Oxazolone-Induced Atopic Dermatitis Model

BackgroundMany inflammatory mediators, including various cytokines (e.g. interleukins and tumor necrosis factor [TNF]), inflammatory proteases, and histamine are released following mast cell activation. However, the endogenous modulators for mast cell activation and the underlying mechanism have yet to be elucidated. Endogenous cannabinoids such as palmitoylethanolamide (PEA) and N-arachidonoylethanolamine (anandamide or AEA), were found in peripheral tissues and have been proposed to possess autacoid activity, implying that cannabinoids may downregulate mast cell activation and local inflammation.ObjectiveIn order to investigate the effect of cannabinoid receptor-1 (CB1R) agonists on mast cell activation, AEA-derived compounds were newly synthesized and evaluated for their effect on mast cell activation.MethodsThe effects of selected compounds on FcεRI-induced histamine and β-hexosaminidase release were evaluated in a rat basophilic leukemia cell line (RBL-2H3). To further investigate the inhibitory effects of CB1R agonist in vivo, an oxazolone-induced atopic dermatitis mouse model was exploited.ResultsWe found that CB1R inhibited the release of inflammatory mediators without causing cytotoxicity in RBL-2H3 cells and that CB1R agonists markedly and dose-dependently suppressed mast cell proliferation indicating that CB1R plays an important role in modulating antigen-dependent immunoglobulin E (IgE)-mediated mast cell activation. We also found that topical application of CB1R agonists suppressed the recruitment of mast cells into the skin and reduced the level of blood histamine.ConclusionOur results indicate that CB1R agonists down-regulate mast cell activation and may be used for relieving inflammatory symptoms mediated by mast cell activation, such as atopic dermatitis, psoriasis, and contact dermatitis.     

Eczematous dermatitis after vascular laser therapy: A report of two cases

Abstract

Eczematous dermatitis was found in two port wine stain (PWS) lesions in two different individuals following variable pulsed 532-nm laser therapy. Both of the individuals described in this report had received low-dose superficial X-ray several years prior to the development of the eczematous dermatitis. The eczematous dermatitis in the PWS lesions was characterized by oozing, crusting, and pruritus, which showed a tendency to expand to other sites when exacerbated. Treatment with topical corticosteroid ointments produced some temporary improvement, but the dermatitis in both cases recurred when the topical medications were stopped. The mechanism of action for the development of an eczematous dermatitis in a PWS remains unclear, but may be related to multiple factors including abnormal hemodynamic forces resulting from the malformed vessels, an abnormal production of cytokines, local pathophysiological and immunological changes resulting from either the X-ray therapy or the laser therapy, and atopic constitution inherent in these individuals. These hypotheses and ideas need further study for additional insight into this rare, but reported adverse event.     

Histamine H4 receptor antagonism reduces hapten-induced scratching behaviour but not inflammation

Abstract:  Effects of the histamine H₄ receptor antagonist JNJ 7777120 (1-[(5-chloro-1 H -indol-2-yl)carbonyl]-4-methylpiperazine) were tested in two models of allergic contact dermatitis. Dermatitis was induced by 2,4-dinitrochlorobenzene and toluene-2,4-diisocyanate, which differ in their Th1–Th2 profile in that way that 2,4-dinitrochlorobenzene is a classical contact allergen with a pronounced Th1-mediated inflammation, while the respiratory chemical allergen toluene-2,4-diisocyanate induces a Th2-dominated inflammation. JNJ 7777120 (15 mg/kg) administered 2 h and 30 min before and 1 h after challenge did not reduce the hapten-induced ear swelling determined 24 h after challenge. This was confirmed by histological evaluation of the ear skin. A repeated administration of the haptens to the rostral part of the back of sensitized animals resulted in a frequent scratching behaviour. An administration of JNJ 7777120 (15 mg/kg) 30 min before challenge reduced this hapten-induced scratching significantly. The H₁ receptor antagonist cetirizine also reduced the scratching bouts in sensitized mice. A combination of H₁ and H₄ receptor antagonists resulted in the strongest inhibition of scratching behaviour associated with allergic dermatitis. These results indicate that H₄ receptor antagonism fails to reduce the allergic inflammatory response but strongly inhibits allergen-induced itch. Thus, a combination of H₄ and H₁ receptor antagonism might be a new strategy to treat pruritus related to allergic diseases like atopic dermatitis.     

Histamine H1 and H2 receptor antagonists accelerate skin barrier repair and prevent epidermal hyperplasia induced by barrier disruption in a dry environment

Keratinocytes have histamine H1 and H2 receptors, but their functions are poorly understood. To clarify the role of histamine receptors in the epidermis, we examined the effects of histamine receptor antagonists and agonists applied epicutaneously on the recovery of skin barrier function disrupted by tape stripping in hairless mice. Histamine H2 receptor antagonists famotidine and cimetidine accelerated the recovery of skin barrier function, but histamine and histamine H2 receptor agonist dimaprit delayed the barrier repair. Application of compound 48/80, a histamine releaser, also delayed the recovery. Imidazole, an analog of histamine, had no effect. The histamine H1 receptor antagonists diphenhydramine and tripelennamine accelerated the recovery. Histamine H3 receptor agonist Nalpha-methylhistamine and antagonist thioperamide had no effect. In addition, topical application of famotidine or diphenhydramine prevented epidermal hyperplasia in mice with skin barrier disrupted by acetone treatment in a dry environment (humidity < 10%) for 4 d. In conclusion, both the histamine H1 and H2 receptors in the epidermis are involved in skin barrier function and the cutaneous condition of epidermal hyperplasia.     

Anti‐inflammatory effects of the GABAB receptor agonist baclofen in allergic contact dermatitis

Please cite this paper as: Anti‐inflammatory effects of the GABA_B receptor agonist baclofen in allergic contact dermatitis. Experimental Dermatology 2010; 19: 661–666. Abstract: The gamma amino butyric acid B (GABA_B) receptor is a G protein‐coupled receptor (GPCR) involved in synaptic transmission. Recent data indicate it to be also expressed on immune cells, along with chemokine receptors, which are also GPCRs. As GPCRs can undergo heterologous desensitization, we have examined the ability of baclofen, a GABA_B receptor selective agonist, to interfere with the function of pro‐inflammatory chemokine receptors known to be upregulated in cutaneous inflammation. In vitro, baclofen reduces chemotaxis of human peripheral blood mononuclear cells towards CCL2, CCL5, CXCL10, CXCL2 and CX3CL1 in a dose‐dependant manner. Protein kinase C inhibitors calphostin C and G0 6976 could reverse this effect, pointing towards the involvement of both calcium‐dependent and ‐independent protein kinase C in baclofen‐induced inhibition of chemokine receptors. In an in vivo model of contact hypersensitivity in C57BL/6 mice, intraperitoneal injection of baclofen markedly alleviated signs of inflammation as well as recruitment of neutrophils, monocytes and lymphocytes into the skin. This study demonstrates a new role for the GABA_B receptor in inflammation, making it a potential new therapeutic target to treat inflammatory skin diseases.     

A double blind trial of H1 and H2 receptor antagonists in the treatment of atopic dermatitis

Summary Eighteen patients with atopic dermatitis were randomly chosen for a clinical trial to compare the action of the H₂ receptor antagonist cimetidine in combination with the H₁ receptor antagonist chorpheniramine against chlorpheniramine alone and against placebo. Each treatment period lasted for 4 weeks. Intensity of puritus was recorded daily by the patient on an analogue scale. Global clinical assessment was graded on a 5-point scale every 2 weeks by the investigators and weekly by the patient himself. Further study parameters were: quantity of the corticosteroid ointment used for emergencies, immunoglobulin E level, and eosinophil count. The data of 16 patients was evaluated. These was no significant difference in any of the study parameters during the three treatment periods. On the basis of this study, the combined administration of H₁ and H₂ receptor antagonists is of no benefit in the treatment of atopic dermatitis.     

Effects of histamine on collagen synthesis by cultured fibroblasts derived from guinea pig skin

Summary Fibroblast-like cells derived from guinea-pig skin were cultured for 3 h in the presence of various concentrations of histamine. The total protein synthesized was determined by the incorporation of radioactive proline, and the collagenous protein synthesized was measured by the incorporation of labeled hydroxyproline in the cell layer and medium. Synthesis of both total and collagenous protein increased in the presence of histamine in the concentration range of 10¹–10³ g/ml. The ratio of collagen to total protein synthesized also increased at these concentrations. However, in no case was an increase found when H₁ antagonist (chlorpheniramine) and H₂ antagonist (cimetidine) were added with the histamine. DNA synthesis was not affected by histamine at the concentrations used. These results suggest that histamine increases the synthesis of collagen by fibroblast-like cells through H₁ and H₂-receptors.     

P物质在变应性接触性皮炎小鼠模型瘙痒中的作用

目的探讨P物质(SP)在变应性接触性皮炎(ACD)小鼠瘙痒中的作用。方法外用2,4-二硝基氟苯(DNFB)建立昆明小鼠ACD模型,观察激发后73h内小鼠的搔抓行为及神经激肽1(NK1)受体拮抗剂spantide和阿片受体拮抗剂纳洛酮对小鼠搔抓行为的影响,并用ELISA、免疫组化分别检测激发后48h小鼠颈背部皮损中SP含量、NK1受体表达。结果ACD小鼠模型在DNFB激发后48h出现搔抓高峰;搔抓高峰时,皮损中SP含量[(3873.40±291.58)pg/g]明显低于阴性对照组[(4349.90±502.83)pg/g](P<0.05),但NK1受体表达(6.13±1.25)明显高于阴性对照组(2.87±0.86)(P<0.05)。Spantide和纳洛酮均可抑制小鼠搔抓行为(P<0.01)。结论DNFB诱发的ACD小鼠模型搔抓行为是瘙痒相关反应;SP通过激活皮肤内NK1受体参与ACD小鼠模型瘙痒的发生。     

Mast cell histamine‐mediated transient inflammation following exposure to nickel promotes nickel allergy in mice

We previously reported that allergic responses to nickel (Ni) were minimal in mice deficient in the histamine‐forming enzyme histidine decarboxylase (HDC‐KO), suggesting an involvement of histamine in allergic responses to Ni. However, it remains unclear how histamine is involved in the process of Ni allergy. Here, we examined the role of histamine in Ni allergy using a murine model previously established by us. Mice were sensitized to Ni by intraperitoneal injection of a NiCl₂‐lipopolysaccharide (LPS) mixture. Ten days later, allergic inflammation was elicited by challenging ear‐pinnas intradermally with NiCl₂. Then, ear‐swelling was measured. Pyrilamine (histamine H1‐receptor antagonist) or cromoglicate (mast cell stabilizer) was intravenously injected 1 h before the sensitization or the challenge. In cell‐transfer experiments, spleen cells from Ni‐sensitized donor mice were intravenously transferred into non‐sensitized recipient mice. In both sensitized and non‐sensitized mice, 1 mm or more NiCl₂ (injected into ear‐pinnas) induced transient non‐allergic inflammation (Ni‐TI) with accompanying mast cell degranulation. LPS did not affect the magnitude of this Ni‐TI. Pyrilamine and cromoglicate reduced either the Ni‐TI or the ensuing allergic inflammation when administered before Ni‐TI (at either the sensitization or elicitation step), but not if administered when the Ni‐TI had subsided. Experiments on HDC‐KO and H1‐receptor‐KO mice, and also cell‐transfer experiments using these mice, demonstrated histamine's involvement in both the sensitization and elicitation steps. These results suggest that mast cell histamine‐mediated Ni‐TI promotes subsequent allergic inflammatory responses to Ni, raising the possibility that control of Ni‐TI by drugs may be effective at preventing or reducing Ni allergy.     

Effects of H1 antagonists on the cutaneous vascular response to histamine and bradykinin: a study using scanning laser Doppler imaging

Histamine plays an important part in the cutaneous weal and flare response which underlies many allergic skin conditions. It has a direct effect on the local vasculature to promote vasodilatation and increase microvascular permeability and may also initiate the more widely spread neurogenic flare. Quantification of these responses and studies of the mediator mechanisms underlying them have been limited by the lack of appropriate techniques to investigate them. To address this we have used two relatively new techniques, scanning laser Doppler imaging (LDI) and dermal microdialysis to measure changes in skin blood flow and the release of histamine within the weal and flare, following intradermal injection of histamine or bradykinin. These measurements have been made both in the absence and presence of the H₁ receptor blockers cetirizine and loratadine. Scanning LDI of the inflammatory response revealed marked differences in both the development and steady state responses to the intradermal injection of histamine (1–3 μmol/L) and bradykinin (1 μmol/L). The development of the flare and the weal response to both histamine and bradykinin was significantly reduced by cetirizine but not by loratadine. The histamine-induced flare area fell by 57 ± 4% (mean ± SEM, n = 10, P < 0.001) after cetirizine and the area of the weal fell by 73 ± 11% (P < 0.009). Bradykinin-induced inflammatory responses were similarly reduced by cetirizine, the weal by 60 ± 16% (P < 0.02) and the flare by 61 ± 4% (P < 0.005). Measurement of histamine concentration in skin using microdialysis, in six subjects, confirmed that histamine levels rose in the dialysate collected from the weal to 310 ± 16 nmol/L following injection of histamine. Histamine levels also rose following bradykinin injection in some subjects (mean 147 ± 46 nmol/L, range 18–336). Little increase in histamine concentration was seen in the dialysate from the flare following injection of either histamine or bradykinin. The histamine concentration in dialysate from unprovoked skin was 4.19 ± 0.75 nmol/L. These data reveal differences in the dermal responses to different mediators when assessed using scanning LDI. They confirm that histamine is released within the weal but not the flare response to the intradermal injection of both histamine and bradykinin and that its effects on the local vasculature to cause the oedematous weal and the axon reflex-mediated flare are significantly attenuated by the H₁ antagonist cetirizine and to a lesser extent by the H₁ antagonist loratadine.     

Leukocyte adherence in atopic dermatitis: diminished responses to histamine and isoproterenol

Leukocyte adherence was examined in atopic and normal subjects and the influence of histamine and the beta-adrenergic agonist, isoproterenol, evaluated. Atopics included patients with mild to severe atopic dermatitis and patients with asthma and hayfever. No inter-group differences in leukocyte adherence of untreated leukocytes could be demonstrated, but there was a significantly smaller histamine and isoproterenol effect on the adherence of cells from patients with atopic dermatitis and hayfever. The induced inhibition of leukocyte adherence by histamine could be blocked by the H-2 histamine receptor antagonist, metiamide, suggesting that this effect may be mediated via cAMP. Our findings support the hypothesis that atopic dermatitis patients may have a defect or blockade of their cellular response to histamine.     

皮炎湿疹类疾病规范化诊断术语专家共识

【摘要】 针对皮炎湿疹类疾病在概念、分类和诊断术语等方面的混乱现状,中华医学会皮肤性病学分会免疫学组、中国医师协会皮肤科医师分会指南制定与规范委员会组织专家按照德尔菲法原则对皮炎湿疹类疾病的诊断现状及存在问题进行讨论,提出7条规范化诊断建议,主要包括：①“皮炎”和“湿疹” 是疾病的类别名称而非具体诊断术语;②临床遇到湿疹性皮损时,应积极寻找其临床特征和/或实验室特点,按照特应性皮炎、接触性皮炎和其他皮炎进行分类诊断;③建议暂时保留“湿疹”这一术语,并只用作以湿疹性皮损为表现但尚不能给出确定诊断的、暂时性和描述性诊断用词。本共识旨在推动皮炎湿疹类疾病诊断术语的规范化、同质化,为更好地进行疾病管理、流行病学研究和开展个体化治疗和预防奠定基础。