八正散单味中药及7味清热利湿药体外抗沙眼衣原体活性研究

目的:明确八正散中单味中药及黄柏等7种清热利湿中药的体外抗沙眼衣原体活性.方法:应用微量McCoy细胞培养法检测八正散中单味中药及黄柏等7种清热利湿药体外抗沙眼衣原体的最小抑菌浓度(MIC)和最小杀菌浓度(MBC).结果:生大黄、黄柏在体外有较强的抗沙眼衣原体活性,两者MIC与MBC相同,分别为6.25 mg/mL和12.5 mg/mL.其余中药未检测出MIC值与MBC值,但栀子、瞿麦在最大无毒浓度(TD0)时孔内沙眼衣原体包涵体数目明显减少,体积缩小.结论:生大黄、黄柏具有较强的体外抗沙眼衣原体活性,栀子、瞿麦有一定的体外抗沙眼衣原体活性.     

复方茯苓汤及冲剂治疗湿疹的临床疗效观察

我们按中医治则选用显著抑制小鼠变态反应性接触性皮炎的中药 [1]组成复方茯苓汤并制成冲剂，用于治疗湿疹，比较汤剂和冲剂的疗效。 一、方剂及方法 复方茯苓汤：茯苓 15 g、泽泻 9 g、黄柏 9 g、栀子 9 g、赤芍 9 g、浮萍 9 g、当归 9 g、甘草 6 g。每日 1剂，水煎服 2次。复方茯苓冲剂：取 500剂的量（ 40 500 g），以含 0.2％吐温 20的 50％乙醇水溶液 3次重复渗滤，收获提取液 40 500 mL，浓缩成稠膏 8 100 mL,加蔗糖、糊精制成颗粒，干燥，每克冲剂相当于生药 2.5 g。每次服 10 g，每日 2～ 3次。 二、治疗对象及分组 治疗对象为急性…     

复方茯苓汤对小鼠接触性过敏反应的影响

复方茯苓汤是按照中医对湿疹的治疗法则,由动物实验筛试具有抗Ⅳ型变态反应的中药所组成,经临床应用对湿疹具有明显疗效^[1]。为了探讨其作用机制,我们利用小鼠二硝基氟苯(DNFB)变应性接触性皮炎(ACD)为动物模型,观察中药复方茯苓汤抗Ⅳ型变态反应的作用及其对白介素-1、2、6(IL-1、2、6)、粒细胞巨噬细胞集落刺激因子(GM-CSF)的影响,并与氢化可的松比较。     

祛风止痒口服液对豚鼠变应性接触性皮炎的影响及其作用机制研究

目的研究祛风止痒口服液对豚鼠变应性接触性皮炎(ACD)的抑制作用,并探讨其作用机制.方法采用2,4-二硝基氯苯(DNCB)建立豚鼠ACD模型,观察口服不同剂量祛风止痒口服液对豚鼠耳肿胀的抑制作用.以RIA法检测ACD豚鼠产生白细胞介素-1,2,6(IL-1,2,6)和粒细胞-巨噬细胞集落因子(GM-CSF)的水平及祛风止痒口服液对这4种细胞因子的作用.结果口服不同剂量祛风止痒口服液均能明显抑制ACD豚鼠耳肿胀(P＜0.01),降低ACD豚鼠血清IL-2、IL-6及GM-CSF水平(P＜0.01或P＜0.05),但小剂量组ACD豚鼠血清GM-CSF水平无明显变化(P＞0.05);ACD豚鼠血清IL-1水平无明显变化(P＞0.05).结论祛风止痒口服液对豚鼠ACD有抑制作用,其作用机制可能是通过抑制IL-2、IL-6及GM-CSF等细胞因子的释放有关,而与血清IL-1水平无关.     

雷公藤甲素对变应性接触性皮炎小鼠淋巴细胞周期及凋亡的影响

目的研究雷公藤甲素对变应性接触性皮炎小鼠淋巴细胞周期及凋亡的影响。方法以二硝基氯苯制作ACD小鼠模型,体外培养淋巴细胞,分别以0.1、1.0、10μmol/L浓度雷公藤甲素作用后,采用Annexin V-FITC试剂盒,PI染料流式细胞仪分别检测细胞周期及细胞凋亡。结果甲素三个浓度组对G1、S期细胞的影响与对照组比较差异均具有统计学意义(P<0.01),对G2期及亚二倍体细胞的影响只有高、中浓度组与对照组之间的差异具有统计学意义(P<0.01)。同时高浓度组对G1、S、G2和亚二倍体的影响与低浓度组比较差别也具有统计学意义(P<0.01)。三个浓度组凋亡细胞比率与对照组比较差异均有显著性(P<0.01);其中高浓度组凋亡细胞比率高于低浓度组及中浓度组(P<0.01),而中浓度组与低浓度组比较差异无统计学意义(P>0.05)。结论诱导体外培养的ACD小鼠淋巴细胞凋亡,调节淋巴细胞周期,可能是雷公藤甲素治疗ACD的机理之一。     

湿疹反应的免疫学

变应性接触性皮炎(ACD)和异位性皮炎都是湿疹皮炎类的代表性疾病,尤其是其中的ACD,可以作为研究湿疹反应的模式。本文就以ACD为重点,介绍有关湿疹反应及其免疫现象的新观点。一、变应性接触性皮炎(ACD) ACD是第Ⅳ型变态反应引起的免疫性疾病,与结核菌素反应和移植排斥反应同属一种免疫反应,但具有如下特点,即变应原是简单化学物质(分子量小于1,000),在免疫学上称为半抗原;可经皮肤侵入体内,并以皮肤为变态反应的靶器官,在病理组织学上     

新一代抗组胺药对变应性接触性皮炎小鼠3种细胞因子影响的比较研究

目的:研究咪唑斯汀、氯雷他定及西替利嗪对变应性接触性皮炎(allergiccontactdermatitis,ACD)小鼠产生干扰素(IFN)、肿瘤坏死因子(TNF)及白介素(IL)-4的影响,探讨抗组胺药治疗ACD的作用机制。方法:建立小鼠ACD模型,采用ELISA法检测ACD小鼠产生IFN-γ、TNF-α和IL-4的水平及3种药物分别对它们的作用。结果:ACD小鼠血清及脾淋巴细胞IFN-γ水平均明显升高(P<0.01);血清TNF-α水平明显升高(P<0.01),腹腔巨噬细胞产生TNF-α水平无明显变化(P>0.05);血清及脾淋巴细胞产生IL-4水平无明显变化(P>0.05)。咪唑斯汀对血清及细胞培养液中3种细胞因子的水平均有显著或不同程度的抑制作用,而氯雷他定、西替利嗪仅对部分细胞因子产生一定的抑制作用。结论:咪唑斯汀对ACD小鼠产生的3种细胞因子的抑制作用强于氯雷他定和西替利嗪。它们对ACD小鼠3种细胞因子的抑制作用与临床疗效的关系有待进一步研究。     

咪唑斯汀对小鼠接触性变态反应模型的作用研究

目的探讨咪唑斯汀对小鼠变应性接触性皮炎(ACD)的治疗作用及可能机制。方法以2,4-二硝基氟苯(DNFB)诱发的小鼠ACD为模型,设立两个不同阶段用药组观察3种剂量咪唑斯汀对小鼠耳肿胀、真皮内炎性细胞浸润、血清IL-4,IL-12和IFN-γ水平的影响。结果两个不同阶段用药组咪唑斯汀均能显著抑制ACD小鼠的耳肿胀及真皮炎症细胞浸润,并呈剂量依赖性。咪唑斯汀可降低诱发后24h和72h小鼠血清IL-12和诱发后72hIFN-γ水平。结论咪唑斯汀对小鼠ACD具有治疗作用,这种作用可能与下调致炎性细胞因子的水平有关。     

咪唑斯汀抑制小鼠变应性接触性皮炎机制的研究

目的 研究咪唑斯汀对小鼠变应性接触性皮炎(ACD)的抑制作用,探讨其作用机理.方法 建立小鼠ACD模型,观察口服不同剂量咪唑斯汀对小鼠耳肿胀的抑制作用.采用ELISA法检测ACD小鼠产生干扰素γ(IFN-γ)、肿瘤坏死因子α(TNF-α)和白介素4(IL-4)的水平及咪唑斯汀对这3种细胞因子的作用.结果 口服各剂量咪唑斯汀均能明显抑制ACD小鼠耳肿胀(P<0.05);ACD小鼠血清及脾淋巴细胞IFN-γ水平均明显升高(P<0.01).ACD小鼠血清TNF-α水平明显升高(P<0.01),腹腔巨噬细胞产生TNF-α水平无明显变化(P>0.05).ACD小鼠血清及脾淋巴细胞产生IL-4水平无明显变化(P>0.05).不同剂量咪唑斯汀对3种细胞因子均有显著或不同程度的抑制作用.结论 咪唑斯汀对小鼠ACD疗效可能通过其对细胞因子的抑制而发挥作用.     

指甲疾病

20 0 32 857　中药黄柏酊治疗甲沟炎 115例临床疗效观察 /杨坤 (西双版纳州医院中医科 )…∥云南中医中药杂志 .- 2 0 0 3,2 4 ( 3) .- 16黄柏、黄连、大黄、苦参、龙胆草、银花、红花、焦栀子、血竭各 2 0 0 g,儿茶 10 0 g。将上药加 75%酒精 2 0 0 0 m l,浸泡 10天后 ,密封装入 10 0 m l瓶内 ,每天用棉花搽患处 3次 ,7天为 1个疗程。结果治愈 51例 ,显效 4 0例 ,有效 19例 ,无效 5例 ,有效率 95.6 7%。 (刘汉平 )指甲疾病…     

某些炎症介质拮抗剂抗过敏作用的实验研究

目的：为了探讨抗组胺药及抗５ 羟色胺（５ ＨＴ）药对迟发型超敏反应（ＤＨＲ）的作用及其机制。方法：我们观察了扑尔敏、特非那丁、多虑平、利血平、赛庚啶、苯噻啶对小鼠变应性接触性皮炎（ＡＣＤ）及真皮肥大细胞（ＭＣ）、表皮郎格罕细胞（ＬＣＳ）的影响。结果：发现这６种药物对小鼠ＡＣＤ均有不同程度的抑制作用，提示这些药物的抗过敏作用不限于Ⅰ型变态反应疾病，对Ⅳ型变态反应疾病亦可有效。受试药物中扑尔敏、特非那丁、多虑平、利血平、赛庚啶等５种能减少真皮ＭＣ数，扑尔敏、多虑平、利血平等３种能减少表皮ＬＣＳ数。结论：提示这些药物抑制ＤＨＲ的机制至少部分地与减少真皮ＭＣ数及／或减少表皮ＬＣＳ数有关。     

不同类型钙通道阻滞剂对小鼠变应性接触性皮炎及表皮郎格罕细胞的影响

为了探讨钙通道阻滞剂（ＣＣＢｓ）对迟发型超敏反应（ＤＨＲ）的作用及其机制，我们观察了三类８种ＣＣＢｓ对小鼠变应性接触性皮炎（ＡＣＤ）及表皮郎格罕细胞（ＬＣｓ）的影响。结果发现Ⅰ类ＣＣＢｓ异搏定、硫氮酮，Ⅱ类ＣＣＢｓ尼莫地平、尼群地平及Ⅲ类ＣＣＢｓ脑益嗪在抑制ＤＨＲ的同时，亦减少表皮ＬＣｓ数。提示上述药物可通过降低表皮ＬＣｓ数而抑制ＤＨＲ。另外３种Ⅱ类ＣＣＢｓ心痛定、尼卡地平及络活喜亦显著抑制小鼠ＡＣＤ，但并未显示同时减少表皮ＬＣｓ数，提示ＣＣＢｓ对ＡＣＤ抑制作用的机理可能因药而异。     

Eyelid discoid lupus erythematosus and contact dermatitis: a case report

We report a patient with discoid lupus erythematosus (DLE) and associated allergic contact dermatitis (ACD) in the eyelids. In women, ACD caused by nail varnish is frequent and often seen in the eyelids. ACD caused by drugs (e.g. neomycin) is also frequent in this region. However, DLE with periorbital presentation without evidence of systemic or other cutaneous involvement is rare.     

Postelicitation model of allergic contact dermatitis for predicting the efficacy of topical drugs

Abstract:  To evaluate the anti-inflammatory efficacies of topical drugs, models of contact hypersensitivity (CHS) can be used, but the conventional murine models of CHS need revision in this respect. These models utilize sensitized mice to study suppression of sensitization or elicitation by test compounds. To mimick the events occurring in allergic contact dermatitis (ACD), a modification of the murine model of CHS is needed in a way that a chronic postelicitation phase of CHS is maintained for studies of anti-inflammatory effects of topical drugs, typically relevant for ACD therapy, not for ACD prevention. A method for the quantification of the suppression of ACD by a test compound is presented here. Two experimental drugs for topical use, imidazole-4-carboxylate and imidazole-4-acetate, were tested in parallel with the corticosteroid prednisolone. We found that prednisolone showed strong suppressive effects, while imidazole-4-carboxylate and imidazole-4-acetate showed mild suppressive effects during persistent ACD simulation. Multiple elicitations on the mouse ears led to scratching and the formation of abrasions and scabbings with, presumably, worsening of discomfort. Clear reduction of these side-phenomena was achieved by tailoring the topical amount of contact sensitizer, while the ability of the ACD model to test anti-inflammatory compounds, was not affected. By focussing on a prolonged postelicitation phase of CHS, a simulation of ACD has been established. We demonstrated that this model may provide an improved predictability for the clinical efficacies of (experimental) mild or strong anti-inflammatory drugs.     

Incidence rates of occupational allergic contact dermatitis caused by metals.

BACKGROUND: Data on the incidence rates (IR) of occupational dermatoses are scarce. MATERIAL AND METHODS: We calculated the IR of occupational allergic contact dermatitis (ACD) caused by chromium, nickel and cobalt by occupation, during a 7-year period (1991-1997) from the data of the Finnish Register of Occupational Diseases and from the statistics on the working population in different occupations. RESULTS: A total of 2543 cases of occupational ACD were reported during 1991-1997. Cr caused 143 (5.6%) cases of ACD, Ni 176 cases (6.9%) and Co 41 cases (1.6%) of ACD. Women had greater number of occupational ACD from nickel, whereas occupational ACD from chromate and cobalt was more frequent in men. The ranking list of the IR of occupational ACD caused by Cr per 10,000 working years was (incidence rate in parenthesis) (1) tanners, fellmongers, and pelt dressers (12.20); (2) cast concrete product workers (6.94); (3) leather goods workers (4.71), (4) metal plating and coating workers (3.66); (5) bricklayers (3.44); (6) reinforcement concreters (2.79); and (7) building workers (1.32). The corresponding ranking list for Ni was (1) footwear workers (2.55); (2) machine and metal product assemblers (2.40); (3) electrical and teletechnical equipment assemblers (2.03); (4) precision instrument mechanics (1.73); (5) postal officials (1.48); (6) hairdressers, beauticians, and bath attendants (1.24); (7) industrial tailors and seamstresses (1.08); and (8) waiters in cafes and snack bars (1.04). The corresponding ranking list for Co was (1) printers (0.80); (2) turners, machinists, and toolmakers (0.36); and (3) machine and engine mechanics (0.17). CONCLUSION: The Finnish Register of Occupational Diseases forms a good basis for calculating IR. As IR illustrates the risk to become sensitized, preventive measures should be directed at occupations with the highest IR.     

Occupational allergic airbone contact dermatitis and delayed bronchial asthma from epoxy resin revealed by bronchial provocation test

Diglycidyl ether of bisphenol A (DGEBA) epoxy resins belong to the most common causes of occupational allergic contact dermatitis. DGEBA has on rare occasions caused occupational asthma. Here we present a patient who first developed occupational allergic contact dermatitis (ACD) caused by a single accidental exposure to DGEBA. Then, on continued occupational exposure to DGEBA, the patient developed occupational asthma from DGEBA, in addition to ACD. A bronchial provocation test with DGEBA caused a 36% drop in the peak expiratory flow, reflecting a delayed type of occupational asthma. This bronchial provocation test caused a strong dermatitis of the exposed skin of the face, in accordance with airborne ACD from DGEBA.     

Occupational allergic contact dermatitis caused by epoxy diacrylate in ultraviolet-light-cured paint, and bisphenol A in dental composite resin

Allergic contact dermatitis (ACD) caused by epoxy di(meth)acrylates or bisphenol A is rare. Here 2 such cases are reported. A dental assistant had allergic contact dermatitis (ACD) caused by bisphenol A contained in denial composite resin (DCR) products based on epoxy dimethacrylate. The contact allergy was verified by allergic patch lest reactions to bisphenol A and 2 DCRs. The OCRs giving allergic reactions were analyzed, and 0.014–0.015% of bisphenol A was detected. Occupational ACD caused by bisphenol A in dental composite resins has not been described before. The other patient was a male process worker in a paint factory. He was sensitized by an epoxy diacrylate, 2.2-bis[4-(2-hydroxy-3-acryloxypropoxy)pheny]-propane (BIS-GA), and other acrylate compounds contained in raw materials of ultraviolet-light-curable paint. The epoxy diacrylate gave an allergic patch test reaction down to 0.016% in pet. He also had an allergic patch lest reaction to several other acrylate compounds. 2-hydroxypropyl acrylate, 2-hydroxypropyl acrylate, 1,4-butanediol diacrylate, 1,6-hexanediol diacrylate, diethyleneglycol diacrylate, triethylene glycol diacrylate, and tripropylene glycol diacrylate, indicating cross and/or concomitant sensitization.     

The clinical and histopathologic spectrum of "dermal hypersensitivity reactions," a nonspecific histologic diagnosis that is not very useful in clinical practice,and the concept of a "dermal hypersensitivity reaction pattern"

BACKGROUND: "Dermal hypersensitivity reaction" (DHR) is diagnosed by dermatopathologists but is not an accepted clinical disease entity. There are no clear guidelines for its diagnosis, differential diagnosis, or management. OBJECTIVES: The objectives were to define the histologic criteria for cases histologically diagnosed as DHR and identify corresponding clinical disorders. METHODS: Skin biopsy specimens from 130 patients diagnosed as "consistent with DHR" were reviewed. Additional information was obtained from patients, their dermatologists, and medical records. RESULTS: Follow-up in 74 of 110 patients (median, 26.6 mo) revealed, most commonly, diagnoses of urticaria, drug reactions, and spongiotic (eczematous) dermatitis. Among the remaining cases, 37 of 59 reported persistence of disease, some exhibiting a uniform phenotype characterized by excoriated, edematous papules on the trunk. Histopathologic features present in more than 90% of 143 biopsy specimens included superficial and mid-perivascular lymphocytic infiltrates with eosinophils. CONCLUSION: DHR is a perivascular lymphocytic dermatitis with eosinophils involving the papillary and upper reticular dermis and minimal, if any, primary epidermal alteration. The term DHR does not represent any known clinical disorder; rather, it corresponds to many clinical disorders. The use of the phrase "dermal hypersensitivity reaction pattern" may be helpful in conveying the idea that a particular histologic pattern may be seen in a number of clinical disorders.     

Does allergic contact dermatitis from formaldehyde in clothes treated with durable‐press chemical finishes exist in the USA?

Recent US studies have presented case series of patient with allergic contact dermatitis (ACD) allegedly caused by formaldehyde in clothes treated with durable‐press chemical finishes (DPCF), which are known formaldehyde releasers. However, the amounts of formaldehyde released by modern DPCF are thought to be well below the levels previously estimated to be able to elicit ACD. The objectives of this review are (i) to investigate whether clothes sold in the USA may contain enough free formaldehyde to elicit ACD in previously sensitized individuals and (ii) to assess the validity of US reports on ACD from formaldehyde in DPCF treated clothes. Literature was examined using various resources. The threshold level for formaldehyde in clothes that may cause ACD in sensitized individuals is unknown; we present data suggesting that levels < 200 ppm will be safe for most patients and that textiles will rarely contain higher amounts. All US studies presenting patients with ACD from formaldehyde in clothes had some weaknesses and in no report was the diagnosis proven beyond doubt. Currently, there is no definite proof that textile ACD from formaldehyde in DPCF in the USA exists. Future research should be directed at establishing the elicitation threshold and the amounts of formaldehyde present in textiles.     

Amyloidosis cutis dyschromica in two siblings and review of the epidemiology,clinical features and management in 48 cases

Amyloidosis cutis dyschromica (ACD) is a rare form of primary cutaneous amyloidosis (PCA). There is a paucity of information in the dermatology literature to guide its diagnosis, investigation and treatment. We present two siblings with ACD and summarise the epidemiology, clinical features, natural history and treatments in 48 cases of ACD from the literature. Familial cases were more common (37) than sporadic cases. ACD is predominantly reported in those of East and South‐East Asian ethnicity (63%). The mean age of onset was 6 years in familial cases, and 23 years in sporadic cases. The clinical features of familial and sporadic ACD do not differ substantially. Pruritus was the only symptom, and was reported in 19% of all cases. There were no reported ACD cases with systemic amyloidosis. Acitretin was reported to result in improvement in seven of 10 patients treated. Routine investigation for systemic involvement is not necessary. Acitretin may be helpful.