我们想感谢加州大学旧金山分校的牛皮癣和皮肤病治疗中心的工作人员对他们的工作，尤其是我们的Goeckerman协调员萨拉·赫尔斯RN

1。评估和准备<ol><li>执行一个完整的病史和身体开始治疗之前。在过去的牛皮癣治疗方法，任何历史环境阳光或光疗，皮肤瘙痒症的严重程度，以及睡眠质量不良反应的病史和体格检查，文件等重要信息现在/过去的药物，响应。 </li><li>设立了门诊室与所有必要的材料，真皮应用药物和闭塞[查看材料部分和图1]。此外，放置在房间里，如手套，保鲜膜，袜子，磨砂/睡衣袍的其他材料。 </li><li>弥漫性和激烈性红斑开始治疗前评估患者。 </li><li>如果病人具有广泛或有强烈的红斑，进行“降温”的过程（见下文），，直到红斑显著减少。如果没有广泛或有强烈的红斑出现，进行“光疗+焦油”步骤。 </LI&gt; </ol> 2。冷静下来（如果需要） <ol><li>外用皮质类固醇应用到灾区。应用曲安奈德软膏0.1％，躯干和四肢，0.05％地奈德软膏霜/面部/腋下/腹股沟，肤轻松0.01％，油或确炎舒松0.1％洗剂头皮。储备氯倍他索软膏地区最激烈的炎症0.05％。 </li><li>躯干和四肢，防渗手套的手和脚上的袜子内，浴帽浴帽头皮，用保鲜膜闭塞的外用药物。 </li><li>病人降温，直到红斑明显减少（范围从3-14天）。 </li></ol> 3。光疗+焦油<ol><li>病人完成后降温期间，管理彩光每天早上粗煤焦油中的应用[ 图2]前。光疗选项包括窄带UVB（最常用的psori阿齐兹）或宽带UVB（最常用的湿疹）。 Fitzpatrick皮肤类型确定初始光疗剂量[ 见表1和表2]。 </li><li>慢慢滴定随后向上彩光剂量的耐受性。彩光根据病人的反应，需要进行个性化给药方案和时间表。 </li><li>光疗后，局部应用2％粗煤焦油（CCT）AQUAPHOR灾区[ 图3]。如果患者有头皮受累，应用20％：液体carbonis detergens（LCD）头皮在nutraderm。 </li><li>最初，使用2％的CCT（最低强度）。在随后的治疗的天数，从2％至5％，患者的耐受性，然后为10％，以达到更好的效果，提高强​​度的焦油。 </li><li>对于牛皮癣的增厚区域，使用tar复合水杨酸（2％/ 5％/ 10％水杨酸），以帮助减少结垢和硬结斑块。最初使用制剂2％水杨酸10％色温，和滴定的百分比水杨酸耐受的患者在随后的日子。水杨酸，可能是糖尿病或胃溃疡患者的禁忌。 </li><li>闭塞所述相同的方法，在步骤2.2中的冷却过程中的局部焦油。 </li><li>外用药物保持在皮肤上至少4小时。经过4小时的最低限度，去除咬合材料，洗淋浴与矿物油和肥皂[ 图4]中的焦油。 </li><li>给的患者的20％的LCD AQUAPHOR 20％LCD nutraderm的申请对身体和头皮，分别在家里。 </li><li>湿疹患者往往有皮肤敏感。使用2％的CCT最初湿疹患者。时要小心滴定至5％，持续关连交易，湿疹患者往往有皮肤敏感。不要使用10％色温（或任何中建比例高于5％），以及不使用任何水杨酸制剂。 </li></ol> 4。每日评估<ol><li>每一天，进行评估，评估患者的皮肤和对治疗的反应。具体评估，它可以表明病人不能耐受光疗，或瘙痒 ，这可以表明刺激的焦油及/或保鲜膜燃烧的感觉。 </li><li>如果患者表现出的迹象燃烧（燃烧感，显着增加红斑，痒或很少增加预示着即将到来的烧伤，如果进一步增加剂量测定），减少彩光剂量或不给光疗的那一天，因为它可能已造成以前的UV光剂量的光毒性反应。 </li><li>这是不寻常的病人有不同区域的解剖反应和耐受性彩光。为了获得最佳的治疗，调整接触到身体的不同区域的光疗剂量根据病人的反应的量。例如，如果病人出现轻度蒲式耳的树干，rning那么首先把整个身体彩光剂量降低，比覆盖行李箱，并提供额外的光线到四肢。 </li></ol> 5。放电规划和维护<ol><li>继续直到Goeckerman治疗疾病被清除，患者准备出院。 </li><li>将维修方案的患者，其中可以包括门诊光疗，外用药物</li><li>管理门诊彩光每周三次（至少第一个月）。最终的频率是逐渐下降到每周两次，然后每周一次） </li><li>门诊外用药物，包括：曲安西龙霜/软膏身体每日两次，氯倍他索顽抗病变（如需要），每天两次，20％AQUAPHOR的身体LCD和20％以上的液晶nutraderm在头皮上。 </li><li>出院一个月内，安排跟进医师与病人访问，以监测疾病状态。 </li></ol>

<ol>
	<li>Parisi, R., Symmons, D. P., Griffiths, C. E., Ashcroft, D. M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Global+Epidemiology+of+Psoriasis:+A+Systematic+Review+of+Incidence+and+Prevalence.">Global Epidemiology of Psoriasis: A Systematic Review of Incidence and Prevalence.</a> The Journal of Investigative Dermatology. , (2012).</li><li>H, G. W. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=The+treatment+of+psoriasis.">The treatment of psoriasis.</a> Northwest Med. 24, 229-230 (1925).</li><li>Koo, J., Lebwohl, M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Duration+of+remission+of+psoriasis+therapies.">Duration of remission of psoriasis therapies.</a> Journal of the American Academy of Dermatology. 41, 51-59 (1999).</li><li>Menter, A., Cram, D. L. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=The+Goeckerman+regimen+in+two+psoriasis+day+care+centers.">The Goeckerman regimen in two psoriasis day care centers.</a> Journal of the American Academy of Dermatology. 9, 59-65 (1983).</li><li>Lee, E., Koo, J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Modern+modified+'ultra'+Goeckerman+therapy:+a+PASI+assessment+of+a+very+effective+therapy+for+psoriasis+resistant+to+both+prebiologic+and+biologic+therapies.">Modern modified 'ultra' Goeckerman therapy: a PASI assessment of a very effective therapy for psoriasis resistant to both prebiologic and biologic therapies.</a> The Journal of Dermatological Treatment. 16, 102-107 (2005).</li><li>Kim, I. H., West, C. E., Kwatra, S. G., Feldman, S. R., O'Neill, J. L. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Comparative+efficacy+of+biologics+in+psoriasis:+a+review.">Comparative efficacy of biologics in psoriasis: a review.</a> American journal of clinical dermatology. 13, 365-374 (2012).</li><li>Serrao, R., Davis, M. D. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Goeckerman+treatment+for+remission+of+psoriasis+refractory+to+biologic+therapy.">Goeckerman treatment for remission of psoriasis refractory to biologic therapy.</a> Journal of the American Academy of Dermatology. 60, 348-349 (2009).</li><li>Chern, E., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Positive+effect+of+modified+Goeckerman+regimen+on+quality+of+life+and+psychosocial+distress+in+moderate+and+severe+psoriasis.">Positive effect of modified Goeckerman regimen on quality of life and psychosocial distress in moderate and severe psoriasis.</a> Acta Dermato-venereologica. 91, 447-451 (2011).</li><li>Dennis, M., Bhutani, T., Koo, J., Liao, W. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Goeckerman+therapy+for+the+treatment+of+eczema:+a+practical+guide+and+review+of+efficacy.">Goeckerman therapy for the treatment of eczema: a practical guide and review of efficacy.</a> The Journal of Dermatological Treatment. , (2011).</li><li>Papp, K. A., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Biologic+therapy+in+psoriasis:+perspectives+on+associated+risks+and+patient+management.">Biologic therapy in psoriasis: perspectives on associated risks and patient management.</a> Journal of Cutaneous Medicine and Surgery. 16, 153-168 (2012).</li><li>Menter, A., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Guidelines+of+care+for+the+management+of+psoriasis+and+psoriatic+arthritis:+Section+5.+Guidelines+of+care+for+the+treatment+of+psoriasis+with+phototherapy+and+photochemotherapy.">Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 5. Guidelines of care for the treatment of psoriasis with phototherapy and photochemotherapy.</a> Journal of the American Academy of Dermatology. 62, 114-135 (2010).</li><li>de Miguel, R., el-Azhary, R. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Efficacy,+safety,+and+cost+of+Goeckerman+therapy+compared+with+biologics+in+the+treatment+of+moderate+to+severe+psoriasis.">Efficacy, safety, and cost of Goeckerman therapy compared with biologics in the treatment of moderate to severe psoriasis.</a> International Journal of Dermatology. 48, 653-658 (2009).</li><li>Busse, K., Koo, J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Introducing+the+delayed+retinoid+burn:+a+case+report+and+discussion+of+this+potential+risk+of+retinoid-phototherapy+combination+management.">Introducing the delayed retinoid burn: a case report and discussion of this potential risk of retinoid-phototherapy combination management.</a> Journal of the American Academy of Dermatology. 64, 1011-1012 (2011).</li><li>Maughan, W. Z., Muller, S. A., Perry, H. O., Pittelkow, M. R., O'Brien, P. C. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Incidence+of+skin+cancers+in+patients+with+atopic+dermatitis+treated+with+ocal+tar.+A+25-year+follow-up+study.">Incidence of skin cancers in patients with atopic dermatitis treated with ocal tar. A 25-year follow-up study.</a> Journal of the American Academy of Dermatology. 3, 612-615 (1980).</li><li>Pittelkow, M. R., Perry, H. O., Muller, S. A., Maughan, W. Z., O'Brien, P. C. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Skin+cancer+in+patients+with+psoriasis+treated+with+coal+tar.+A+25-year+follow-up+study.">Skin cancer in patients with psoriasis treated with coal tar. A 25-year follow-up study.</a> Archives of Dermatology. 117, 465-468 (1981).</li><li>Roelofzen, J. H., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=No+increased+risk+of+cancer+after+coal+tar+treatment+in+patients+with+psoriasis+or+eczema.">No increased risk of cancer after coal tar treatment in patients with psoriasis or eczema.</a> The Journal of Investigative Dermatology. 130, 953-961 (2010).</li></ol>

顾博士雅培，狮子座，和Stiefel的葛兰素史克是一个扬声器。顾博士进行Amgen公司，西安杨森，诺华，Photomedex，Galderma公司和辉瑞公司的研究。顾博士有任何制药公司没有股票，就业，或董事会成员。没有利益冲突的披露任何其他作者。

上面概述的的养生Goeckerman协议是利用在UCSF，并根据患者对治疗的反应，可以以多种方式变化。由于病人每天看到和检查，该协议可以为每一个病人个性化，以确保最大的功效。仅的传统Goeckerman治疗包括使用持续关连交易及UVB光疗，然而，该方案已经被修改，包括使用外用皮质类固醇（在其他外用药物如卡泊三醇，蒽和他扎罗汀）5预现有可以继续治疗牛皮癣的药物组合与Goeckerman治疗帮助患者达到缓解与治疗的天数少，也可以是有益的。如果患者没有回应的最佳治疗Goeckerman，患者可给予辅助的全身药物如阿维A。前处理前与阿维A（10-25毫克）启动Goeckerman治疗可以帮助清除银屑病皮损与CCT +光疗所需的天量减少。应当指出的是，阿维A能令患者感光性，光疗剂量应减少后开始阿维A 13 谁在弥漫性红斑的患者应冷却下来之前，任何局部的焦油或彩光。当务之急是给不给这些疗法直到红斑已明显减少，病人没有出现激烈的皮肤红斑。此外，当病人的经验对紫外线暴露的二次燃烧或不适，因此重要的是停止进一步暴露于紫外线，直到病人的症状，已经大大降低了任何明显的炎症。 UVB和/或焦油可加剧病情恶化的炎症，如果不采取谨慎评估患者确保炎症不极端。 局部APPLICATI对焦油通常开始于2％色温。但是，如果患者没有任何不良反应的焦油，焦油制剂（5％，然后10％）更强的可局部应用。 CCT复合水杨酸可用于，如果顽固斑有显着的缩放和硬结不单独实现焦油充分反应。最初使用2％水杨酸，用10％的CCT，和然后增加（5％和10％，10％的中建）的耐受性。焦油或水杨酸的严重不良反应是极其罕见的。 ，一般仅限于局部刺激，如果不良反应发生，患者被切换到一个较低强度的焦油或焦油举行。使用局部皮质类固醇，以减少皮肤发炎。如果对皮肤的刺激性是局部的，则外用类固醇可以被应用到局部区域的区域的其余部分都可以应用在建。 安全档案Goeckerman治疗是比较优秀的口腔SYST主位如环孢素，甲氨蝶呤或生物治疗。如前所述，治疗Goeckerman也不会携带相同的内部作为生物制剂，如癌症，严重的感染风险，增加心血管疾病的危险。10，由于治疗Goeckerman的副作用是最小的，尤其是在比较等全身药物治疗，治疗方案可用于每个人，包括老人，儿童，癌症史的患者，免疫抑制的病人，并与其他合并症的患者。在气候比较温和，但更常见的副作用的Goeckerman治疗毛囊炎，光毒性反应。虽然有可能是一个问题煤焦油局部应用的潜在致癌作用，临床研究患者建在相当长的一段时间内未示出皮肤癌的危险性增加。在多个评论和随访研究中，有没有比较外用使用CCT相关的癌症的风险增加牛皮癣或湿疹的患者。14-16类固醇治疗的安全性和有效性的基础上，的Goeckerman方案是一个很好的治疗方式，任何病人有中度至严重 ​​的牛皮癣，湿疹和其他严重的瘙痒和/或皮肤炎症。

牛皮癣是一种慢性，免疫介导的炎症性皮肤疾病，影响约2-3％的人口，三分之一的患者体验广义牛皮癣，使衰弱的身体和心理的影响。广义牛皮癣的治疗，于1925年首次出版的Goeckerman方案，包括暴露于紫外线B（UVB）光，应用粗煤焦油（CCT）。虽然新的内部剂如生物增强了治疗牛皮癣，治疗Goeckerman仍然作为一个非常有效的选项，同时提供缓解持续时间长。3,4在发表的研究报告，在加州大学旧金山分校进行，100％的患者上Goeckerman治疗取得PASI75（75％的改善牛皮癣严重程度指数评估[PASI评分]从基线），由3个月。5比较（虽然不是头对头），最有效的生物制剂的患者实现只有67-68％PASI75 3星期一部份效果。6 Goeckerman的方案有起效快，并已成功地利用光疗或内部药物难治性难治性牛皮癣患者7 Goeckerman方案也有一个非常安全的毒性，基本上内部没有副作用，这是更严重的风险与其它的牛皮癣的治疗方法。此外，该疗法已经被证明与广义牛皮癣患者的生活质量有重大而积极的影响。 Goeckerman方案前身是一天24小时，直到病人在住院设施被清除了他们的牛皮癣。然而，由于报销的变化和托管护理，患者现在被视为一个至少4-8小时/天，每周5天/日托设施，直到他们的疾病清除。最初制定goeckerman治疗牛皮癣的治疗，但修改后的版本最近已用于其他皮肤疾病的治疗，如湿疹成功。以下协议专门用于在加州大学旧金山分校，治疗牛皮癣，湿疹，全身皮肤瘙痒，结节性痒疹，慢性苔藓样糠疹，红皮病，以及其他相关的皮肤疾病，但略有变化的程序可以根据。 虽然这是可用于牛皮癣的最古老的疗法之一，是一种没有任何已发布的视频演示过程。一个视频可以有广泛的吸引力，因为它可以被用来作为一种资源指的医疗从业人员（初级保健医生和皮肤科医生），了解的过程，感觉很舒服，建议治疗。因为只有少数机构继续提供这种类型的我离开的视频演示Goeckerman的过程也将是教育居民和医学生谁不暴露的养生治疗ntensive。为那些有兴趣在接受Goeckerman治疗的潜在患者的视频也将是有益的。

<table><tbody><tr><td>2% Crude Coal Tar in White Petrolatum or Cetaphil</td><td>Compounded at Pharmacy</td><td></td><td></td></tr><tr><td>5% Crude Coal Tar in White Petrolatum or Cetaphil</td><td>Compounded at Pharmacy</td><td></td><td></td></tr><tr><td>10% Crude Coal Tar in White Petrolatum +/- 2/5/10% Salicyclic Acid</td><td>Compounded at Pharmacy</td><td></td><td></td></tr><tr><td>10% Crude Coal Tar in Cetaphil</td><td>Compounded at Pharmacy</td><td></td><td></td></tr><tr><td>20% Liquid Carbonis Detergenis in Nutraderm</td><td>Compounded at Pharmacy</td><td></td><td></td></tr><tr><td>20% Liquid Carbonis Detergenis in Aquaphor or Cetaphil</td><td>Compounded at Pharmacy</td><td></td><td></td></tr><tr><td>Triamcinolone 0.1% ointment/cream/lotion</td><td>Prescription Medication - Generic</td><td></td><td></td></tr><tr><td>Desonide 0.05% cream/ointment</td><td>Prescription Medication - Generic</td><td></td><td></td></tr><tr><td>Fluocinolone 0.01% oil</td><td>Prescription Medication - Generic</td><td></td><td></td></tr><tr><td>Clobetasol 0.05% ointment/cream</td><td>Prescription Medication - Generic</td><td></td><td></td></tr><tr><td>Hydrophillic Ointment</td><td>Over the Counter - Generic</td><td></td><td></td></tr><tr><td>Mineral Oil</td><td>Over the Counter - Generic</td><td></td><td></td></tr><tr><td>Narrow-Band Phototherapy Unit</td><td>National Biologic Corporation</td><td></td><td></td></tr><tr><td>Broad-Band Phototherapy Unit</td><td>National Biologic Corporation</td><td></td><td></td></tr></tbody></table>

the goeckerman regimen for the treatment of moderate to severe psoriasis

牛皮癣是一种慢性，免疫​​介导的炎症性皮肤疾病，影响约2-3％的人口。 Goeckerman方案由暴露在紫外线B（UVB）光粗煤焦油（CCT）和应用。 goeckerman治疗是非常有效和相对安全的用于牛皮癣的治疗和改善患者的生活质量。在下面的文章中，我们提出了我们的协议，特别是利用在美国加州大学旧金山的的Goeckerman治疗。该协议的细节用品，行政编制外用焦油光疗和应用。此协议还介绍了如何评估病人每天，监测不良反应（包括瘙痒和灼热），并根据病人的反应调整治疗。虽然这是可用于牛皮癣的最古老的疗法之一中，有一个展示了详细的过程中没有任何已发布的视频金正日。视频要管理治疗，学员谁想要了解更多的过程，并为有意患者要经过他们的皮肤疾病治疗的医疗服务提供者是有益的。

在我们中心进行的一项研究，在美国加州旧金山大学，PASI75响应牛皮癣评估严重性指数（提高75％），达到了100％的患者接受Goeckerman组（n = 25）超过3个月的时间内5 24/25例患者只需要2个月实现PASI75，而其余的病人在3个月获得一个PASI75响应。 Menter博士等人在另一项研究中，管理Goeckerman的方案为300例，100％的患者达到90％以上的结算基线银屑病皮损。为患者治疗的天数达到90％以上，结算在第二项研究的平均金额只有18天。4 PAS75治疗3个月的反应被认为是标准的工具，以评估疗效，治疗牛皮癣的治疗方式。虽然生物治疗牛皮癣的新发展，其疗效报告是在3 MONT 67-68％的患者实现PASI75HS。 此外 ，生物都与潜在的严重的内部风险，如内部癌症，严重感染（结核，组织胞浆菌病，球孢子菌病等）和心血管疾病的风险。10 Goeckerman疗法避免这些严重的内部风险，同时仍然极为灵验。外用焦油和光疗的使用具有协同作用。的协同作用是焦油的结果，是一个光敏剂，并记录单独比较彩光联合治疗疗效较高的研究支持。 通常进行20-30次的Goeckerman方案，导致在结算或清算牛皮癣。虽然个别结果可能会有所不同，通常10天的治疗后，我们观察到，患者会出现下降的比例和硬结斑块。经过二十次治疗，我们通常观察到完整的扁平斑块只存在残余红斑。 30处理后，我们观察到完全清除牛皮癣病变，包括剩余的红斑，只存在可能的炎症后色素沉着的改变。患者在治疗过程中也经历显着改善其痒。如果病人有顽固的牛皮癣，并没有显示改善他们的斑块，该疗法可以延长。此外，如果病人不响应所有外用CCT和彩光，牛皮癣的诊断应重新评估，并确认通过皮肤活检（尤其是排除蕈样肉芽肿，毛发红糠疹）。 Goeckerman治疗有一个最长的任何牛皮癣治疗病情缓解的时间。后完成Goeckerman治疗，缓解期的平均长度可以在任何地方从9.5个月到一年多。4,12因此患者可以期望保持长达一年的治疗。何WEVER，因为牛皮癣是一种慢性，终身性疾病，本病容易复发的患者，尤其是在那些人停止任何类型的治疗包括外用药物和/或门诊彩光。有严重的，经常性牛皮癣的患者根据需要重复Goeckerman方案，这通常是上每年（或更长）的基础上。反复入院治疗的天数较少，往往需要实现间隙，病人往往会变得更加迅速寻求帮助和患者还没有养成生理性（快速耐受性）的治疗单身的照片前正在接受治疗Goeckerman [ 图5]对病人有严重的银屑病斑块。虽然他的轻度红斑仍然存在，有显着减少的规模和4周的治疗后，他的斑块硬结[ 图5b]。完成全疗程的治疗后，患者可以期待他们的一个完整的间隙ŗ病变[ 图6a和6b。 <table border="1"><tbody><tr><td> 皮肤类型 </td><td> 初始剂量 </td><td> 随后增加 </td><td> 错过了参观配料 </td><td> 所有肤质 </td></tr><tr><td>我</td><td> MJ * 130 </td><td> 15兆焦耳</td><td> 1-7天</td><td>根据皮肤类型增加</td></tr><tr><td>二</td><td> 220 MJ </td><td> 25兆焦耳</td><td> 8-11天</td><td>保持剂量不变</td></tr><tr><td>三</td><td> 260 MJ </td><td> 40兆焦耳</td><td> 12-20天</td><td>减少25％ </td></tr><tr><td>四</td><td> 330 MJ </td><td> 45兆焦耳</td><td> 21-27天</td><td>减少50％ </td></tr><tr><td> V </td><td> 350兆焦耳</td><td> 60兆焦耳</td><td> 28天或多个</td><td>重新开始</td></tr><tr><td>六</td><td> 400兆焦耳</td><td> 65兆焦耳</td><td></td><td> ＆提供; </td></tr></tbody></table> 表1中。牛皮癣的窄波段UVB剂量协议指引初始剂量，剂量增加在以后的访问，错过探访* MJ =毫焦的剂量调整。 <table border="1"><tbody><tr><td> 皮肤类型 </td><td> 开始剂量范围 </td><td> 随后增加 </td><td> 错过了参观配料 </td><td> 所有肤质 </td></tr><tr><td>我</td><td> 10-20 MJ * </td><td> 10-20兆焦耳</td><td> 1-7天</td><td>根据皮肤类型增加</td></tr><tr><td>二</td><td> 20-30兆焦耳</td><td> 20-30兆焦耳</td><td> 8-11天</td><td>保持剂量不变</td></tr><tr><td>三</td><td> 30-50兆焦耳</td><td> 30-50兆焦耳</td><td> 12-20天</td><td>减少25％ </td></tr><tr><td>四</td><td> 40-60兆焦耳</td><td> 40-60兆焦耳</td><td> 21-27天</tD&gt; <td>减少50％ </td></tr><tr><td> V </td><td> 40-60兆焦耳</td><td> 40-60兆焦耳</td><td> 28天或多个</td><td>重新开始</td></tr><tr><td>六</td><td> 50-100兆焦耳</td><td> 50-100兆焦耳</td><td></td><td></td></tr></tbody></table> 表2中。宽带UVB剂量协议牛皮癣。指引初始剂量，剂量增加在随后的访问中，错过探访* MJ =毫焦的剂量调整。 <img alt="图1" src="/files/ftp_upload/50509/50509fig1.jpg" /> 图1。用品治疗Goeckerman。焦油和局部应用皮质类固醇（顺时针）所需的药物和用品。前中东：丙酸氯倍他索0.05％;左前：肤轻松0.01％石油;左：亲水软膏;左上：保湿化妆水;左中：20％理屈罐ID Carbonis Detergens在AQUAPHOR软膏与瓶盖打开，返回中东：保鲜膜闭塞的外用药物中右：粗煤焦油2％，白凡士林软膏与瓶盖打开一罐;软膏;底部中间右：曲安奈德0.01 ％软膏;右上：矿物油洗外用药物前右：20％液晶洗剂。 <img alt="图2" src="/files/ftp_upload/50509/50509fig2.jpg" /> 图2。窄谱UVB站左窄谱中波紫外线灯框患者输入和接收UVB光疗。右边是连接的计算机制图光疗剂量和病人的反应彩光站。 <img alt="图3" src="/files/ftp_upload/50509/50509fig3.jpg" /> 图3。护士正在粗煤焦油应用粗煤焦油。整个车身前用保鲜膜闭塞。 <img alt="图4" src="/files/ftp_upload/50509/50509fig4.jpg" /> 图4。淋浴，淋浴与矿物油和肥皂洗去外用药物。淋浴配备安全地垫，以防止地板滑。安全把手也存在和重要，尤其是对老人。 <img alt="图5（A）" src="/files/ftp_upload/50509/50509fig5.jpg" /> 图5。四个星期后回应Goeckerman治疗（一）治疗前，患者在上背部厚厚的斑块型银屑病。请注意斑块硬结，厚的规模，并显着的红斑（B）的 4周后的Goeckerman治疗，患者规模降低和硬结作为治疗的结果。残差人的红斑依然存在。 <img alt="图6（A）" src="/files/ftp_upload/50509/50509fig6.jpg" /> 图6。六个星期后回应Gockerman治疗。 （A）（B）在治疗之前，患者与重度斑块型银屑病在后面。清除银屑病皮损后完成Goeckerman治疗。

Watch this Scientific Journal Video about The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis at JoVE.com

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis

牛皮癣是一种慢性，免疫​​介导的炎症性皮肤病。 ，配制用于治疗牛皮癣的Goeckerman方案，由暴露在紫外线（UVB）光粗煤焦油（CCT）和应用。以下协议是用于治疗中度至重度牛皮癣的行政的Goeckerman治疗。

Goeckerman方案用于治疗中度至重度牛皮癣

Psoriasis is a  chronic, immune-mediated inflammatory skin disease affecting approximately 2-3%  of the population. The Goeckerman regimen consists of ...

the-goeckerman-regimen-for-treatment-moderate-to-severe

Universidad San Sebastian

Research

JoVE Journal

Medicine

38.8K 次观看.  University of Southern California. 牛皮癣是一种慢性，免疫​​介导的炎症性皮肤病。 ，配制用于治疗牛皮癣的Goeckerman方案，由暴露在紫外线（UVB）光粗煤焦油（CCT）和应用。以下协议是用于治疗中度至重度牛皮癣的行政的Goeckerman治疗。

视频: The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis

Minimal Erythema Dose (MED) Testing

Ultraviolet radiation (UV) therapy is sometimes used as a treatment for various common skin conditions, including psoriasis, acne, and eczema. The dosage of UV light is prescribed according to an individual's skin sensitivity. Thus, to establish the proper dosage of UV light to administer to a patient, the patient is sometimes screened to determine a minimal erythema dose (MED), which is the amount of UV radiation that will produce minimal erythema (sunburn or redness caused by engorgement of capillaries) of an individual's skin within a few hours following exposure. This article describes how to conduct minimal erythema dose (MED) testing. There is currently no easy way to determine an appropriate UV dose for clinical or research purposes without conducting formal MED testing, requiring observation hours after testing, or informal trial and error testing with the risks of under- or over-dosing. However, some alternative methods are discussed.

Minimal Erythema Dose MED Testing

This article describes how to conduct minimal erythema dose (MED) testing in order to determine the lowest dose of ultraviolet radiation that will cause erythema (burning) when administered to an individual.

最小红斑剂量（MED）测试

Ultraviolet radiation (UV) therapy is  sometimes used as a treatment for various common skin conditions, including  psoriasis, acne, and eczema. The ...

科研

医学

Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model

Fairness of skin, UV sensitivity and skin cancer risk all correlate with the physiologic function of the melanocortin 1 receptor, a Gs-coupled signaling protein found on the surface of melanocytes. Mc1r stimulates adenylyl cyclase and cAMP production which, in turn, up-regulates melanocytic production of melanin in the skin. In order to study the mechanisms by which Mc1r signaling protects the skin against UV injury, this study relies on a mouse model with "humanized skin" based on epidermal expression of stem cell factor (Scf). K14-Scf transgenic mice retain melanocytes in the epidermis and therefore have the ability to deposit melanin in the epidermis. In this animal model, wild type Mc1r status results in robust deposition of black eumelanin pigment and a UV-protected phenotype. In contrast, K14-Scf animals with defective Mc1r signaling ability exhibit a red/blonde pigmentation, very little eumelanin in the skin and a UV-sensitive phenotype. Reasoning that eumelanin deposition might be enhanced by topical agents that mimic Mc1r signaling, we found that direct application of forskolin extract to the skin of Mc1r-defective fair-skinned mice resulted in robust eumelanin induction and UV protection 1. Here we describe the method for preparing and applying a forskolin-containing natural root extract to K14-Scf fair-skinned mice and report a method for measuring UV sensitivity by determining minimal erythematous dose (MED). Using this animal model, it is possible to study how epidermal cAMP induction and melanization of the skin affect physiologic responses to UV exposure.

Epidermal melanin is induced by topical application of forskolin in a murine model of the fair-skinned UV-sensitive human. Pharmacologic manipulation of cAMP levels in the skin and epidermal darkening strongly protect against UV-mediated inflammation (sunburn) as measured by the minimum erythematous dose (MED) assay.

表皮黑色素和防止晒斑的人性化小鼠模型的诱导药物

Fairness of skin, UV sensitivity and skin cancer  risk all correlate with the physiologic function of the melanocortin 1  receptor, a Gs-coupled signaling ...

Daily Phototherapy with Red Light to Regulate Candida albicans Biofilm Growth

Here, we present a protocol to assess the outcomes of per diem red light treatment on the growth of Candida albicans biofilm. To increase the planktonic growth of C. albicans SN425, the inoculums grew on Yeast Nitrogen Base media. For biofilm formation, RPMI 1640 media, which have high concentrations of amino acids, were applied to help biofilm growth. Biofilms of 48 h were treated twice a day for a period of 1 min with a non-coherent light device (red light; wavelength = 635 nm; energy density = 87.6 J&#183;cm-2). As a positive control (PC), 0.12% chlorhexidine (CHX) was applied, and as a negative control (NC), 0.89% NaCl was applied to the biofilms. Colony forming units (CFU), dry-weight, soluble and insoluble exopolysaccharides were quantified after treatments. Briefly, the protocol presented here is simple, reproducible and provides answers regarding viability, dry-weight and extracellular polysaccharide amounts after red light treatment.

Daily Phototherapy with Red Light to Regulate Candida albicans Biofilm Growth

Here, we present a protocol to assess the outcome of red light application on the growth of Candida albicans biofilm. A non-coherent red light device with the wavelength of 635 nm and energy density of 87.6 J&#183;cm-2 was applied throughout the growth of Candida albicans biofilms for 48 h.

红光光疗法调节白色念珠菌生物膜生长

Here, we present a protocol to assess the outcomes of per diem red light treatment on the growth of Candida albicans biofilm. To increase the planktonic ...

免疫与感染

Mechanical and Controlled PRP Injections in Patients Affected by Androgenetic Alopecia

23 patients (18 male and 5 female) aged 21-70 years who displayed male pattern hair loss (MPHL) in Stage 1 to Stage 5 as determined by the Norwood-Hamilton classification scale, and female pattern hair loss (FPHL) in Stage 1 to Stage 2 as determined by the Ludwig classification scale, were treated with non-activated autologous platelet-rich plasma (A-PRP). Autologous blood (55 mL) was harvested using sodium citrate as an anticoagulant. A-PRP (23 mL) was produced for all cases using a closed system according to the transfusion service protocol. Following centrifugation (260 x g for 10 min) the A-PRP was inserted in a laser light selector device, and after the centrifugation, 9 mL of A-PRP was collected.
The scalp of the patients affected by androgenetic alopecia (AGA) was divided into four areas (frontal, parietal, vertex, and occipital); local anesthesia was not performed. Interfollicular A-PRP injections (0.2 mL x cm2) were performed by controlled and mechanical injections scheduled at a depth of 5 mm using a medical injector gun. Treatment sessions were performed with a 30-day interval. For each patient, three treatment sessions were performed.
PRP was injected in the androgen-related areas of scalp affected by hair loss. Placebo (normal saline solution) was loaded in another syringe (10 mL) and injected on the adjacent side in a similar fashion.

This paper aims to describe the interfollicular autologous platelet-rich plasma injections (0.20 mL x cm2) in the scalp of 23 patients affected by androgenetic alopecia at a depth of 5 mm using a medical injector gun equipped with a 30 gauge needle, in three sessions.

雄脱发患者的机械和控制 PRP 注射

23 patients (18 male and 5 female) aged 21-70 years who displayed male pattern hair loss (MPHL) in Stage 1 to Stage 5 as determined by the ...

Establishing Transcription Profile of Psoriasiform Cutaneous In Vitro using HaCaT Cells Stimulated with Combination of Cytokines

Psoriasis is a common chronic inflammatory skin disease mediated by innate and adaptive immune systems, characterized by abnormal proliferation and differentiation of epidermal keratinocytes and infiltration of inflammatory cells. Skin-specific keratinocytes are key participants in innate immunity, responding to immune cells and environmental stimulation, thereby serving an important role in the immunopathogenesis of psoriasis. Here, we present a method for inducing psoriasiform keratinocytes inflammation at transcription level with HaCaT cell line using five proinflammatory cytokines combination (M5 combination), including IL-17A, IL-22, IL-1&#945;, TNF-&#945;, and oncostatin M. Results demonstrate that M5 combination induced HaCaT cells showed increased levels of antimicrobial peptides (BD2, S100A7, S100A8, and S100A9), chemokines, and cytokines (CXCL1, CXCL2, CXCL8, CCL20, IL-1&#946;, IL-6 and, IL-18). The mRNA levels of keratinocytes differentiation markers (Keratin1, Keratin10, Filaggrin, and Loricrin) were down regulated, which was consistent with the transcriptome data derived from psoriasis-like keratinocytes. The method described here, therefore, establishes an in vitro psoriasiform cutaneous inflammation at transcription level and contributes to the research for molecular pathogenesis of psoriasis.

<meta charset="utf8"></head><body>使用细胞因子组合刺激的 HaCaT 细胞在体外建立银屑病样皮肤的转录谱

This paper presents a method of establishing an in vitro psoriasiform cutaneous inflammatory model at the transcription level using a combination of five cytokines (IL-17A, IL-22, IL-1&#945;, TNF-&#945;, OSM) on HaCaT cell line.

使用细胞因子组合刺激的 HaCaT 细胞在体外建立银屑病样皮肤的转录谱

Psoriasis is a common chronic inflammatory skin disease mediated by innate and adaptive immune systems, characterized by abnormal proliferation and ...

Precision Implementation of Minimal Erythema Dose (MED) Testing to Assess Individual Variation in Human Inflammatory Response

Minimal erythema dose (MED) testing is frequently used in clinical settings for determining the smallest amount of ultraviolet (UV) irradiation necessary to produce erythema (inflammatory reddening) on the surface of the skin. In this context, the MED is regarded as a key factor in determining starting doses for UV phototherapy for common skin conditions such as psoriasis and eczema. In research settings, MED testing also has potential to be a powerful tool for assessing within- and between-persons variation in inflammatory responses. However, MED testing has not been widely adopted for use in research settings, likely owing to a lack of published guidelines, which is a barrier to obtaining reproducible results from this assay. Also, protocols and equipment for establishing MED vary widely, making it difficult to compare results across laboratories. Here, we describe a precise and reproducible method to induce and measure superficial erythema using newly designed protocols and methods that can easily be adapted to other equipment and laboratory environments. The method described here includes detail on procedures that will allow extrapolation of a standardized dosage schedule to other equipment so that this protocol can be adapted to any UV radiation source.

Precision Implementation of Minimal Erythema Dose MED Testing to Assess Individual Variation in Human Inflammatory Response

Minimal erythema dose (MED) testing is used to establish dosage schedules for ultraviolet radiation phototherapy. It can assess individual variation in inflammatory response but lacks methodology for achieving reproducible results. Here, we present a precision implementation of MED and demonstrate its ability to capture individual variation in inflammatory response.

精确实施最小红斑剂量（MED）测试，以评估人体炎症反应中的个体变异

Minimal erythema dose (MED) testing is frequently used in clinical settings for determining the smallest amount of ultraviolet (UV) irradiation necessary ...

肛门湿疹治疗中 SDG 的网络药理学和 GEO 数据集分析

The Efficacy and Underlying Pathway Mechanisms of ShiDuGao Treatment for Anus Eczema Based on GEO Datasets and Network Pharmacology

Anus eczema is a chronic and recurrent inflammatory skin disease affecting the area around the anus. While the lesions primarily occur in the anal and perianal skin, they can also extend to the perineum or genitalia. ShiDuGao (SDG) has been found to possess significant reparative properties against anal pruritus, exudation control, moisture reduction, and skin repair. However, the genetic targets and pharmacological mechanisms of SDG on anal eczema have yet to be comprehensively elucidated and discussed. Consequently, this study employed a network pharmacological approach and utilized gene expression omnibus (GEO) datasets to investigate gene targets. Additionally, a protein-protein interaction network (PPI) was established, resulting in the identification of 149 targets, of which 59 were deemed hub genes, within the "drug-target-disease" interaction network.
The gene function of SDG in the treatment of perianal eczema was assessed through the utilization of the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analysis. Subsequently, the anti-perianal eczema function and potential pathway of SDG, as identified in network pharmacological analysis, were validated using molecular docking methodology. The biological processes associated with SDG-targeted genes and proteins in the treatment of anus eczema primarily encompass cytokine-mediated responses, inflammatory responses, and responses to lipopolysaccharide, among others. The results of the pathway enrichment and functional annotation analyses suggest that SDG plays a crucial role in preventing and managing anal eczema by regulating the Shigellosis and herpes simplex virus 1 infection pathways. Network pharmacology and GEO database analysis confirms the multi-target nature of SDG in treating anal eczema, specifically by modulating TNF, MAPK14, and CASP3, which are crucial hub targets in the TNF and MAPK signaling pathways. These findings provide a clear direction for further investigation into SDG's therapeutic mechanism for anal eczema while highlighting its potential as an effective treatment approach for this debilitating condition.

作者聚焦:探索 ShiDuGao 在肛门湿疹治疗中的多靶点方法

This investigative effort sought to elucidate the mechanism of topical drug administration using a synergistic integration of network pharmacology and gene expression omnibus (GEO) datasets. This article evaluated the feasibility, target, and mechanism of ShiDuGao (SDG) in treating anus eczema.

基于GEO数据集和网络药理学的石都高治疗肛门湿疹的疗效及潜在通路机制

Anus eczema is a chronic and recurrent inflammatory skin disease affecting the area around the anus. While the lesions primarily occur in the anal and ...

Goeckerman方案用于治疗中度至重度牛皮癣

摘要

探索更多视频

最小红斑剂量（MED）测试

表皮黑色素和防止晒斑的人性化小鼠模型的诱导药物

红光光疗法调节白色念珠菌生物膜生长

雄脱发患者的机械和控制 PRP 注射

使用细胞因子组合刺激的 HaCaT 细胞在体外建立银屑病样皮肤的转录谱

使用细胞因子组合刺激的 HaCaT 细胞在体外建立银屑病样皮肤的转录谱

精确实施最小红斑剂量（MED）测试，以评估人体炎症反应中的个体变异

基于GEO数据集和网络药理学的石都高治疗肛门湿疹的疗效及潜在通路机制

基于GEO数据集和网络药理学的石都高治疗肛门湿疹的疗效及潜在通路机制

基于GEO数据集和网络药理学的石都高治疗肛门湿疹的疗效及潜在通路机制