调胃承气汤加减联合苦参汤药浴治疗斑块型银屑病（风热血燥证）疗效观察

摘要 目的：观察调胃承气汤加减联合苦参汤药浴治疗斑块型银屑病（风热血燥证）临床疗效。方法：选取2020年3月~2021年3月湖南中医药大学第二附属医院收治的斑块型银屑病患者96例,按抛掷硬币法分为对照组（n=48,基础对症治疗）和观察组（n=48,在对照组基础上给予调胃承气汤加减联合苦参汤药浴综合治疗）。比较两组临床疗效、炎症反应[肿瘤坏死因子-α （TNF-α）、白细胞介素-17（IL-17）、白细胞介素-22（IL-22）]、血清血管内皮生长因子（VEGF）和转化生长因子β1（TGF-β1）水平、银屑病皮损面积、严重程度指数（PASI）和瘙痒程度及不良反应。结果：与对照组77.08%比较,观察组总有效率93.75%更高（P<0.05）。两组治疗后IL-17、TNF-α、IL-22水平及PASI、瘙痒程度评分均较治疗前降低,且观察组较对照组低（P<0.05）。两组治疗后VEGF和TGF-β1水平均较治疗前降低,且观察组较对照组低（P<0.05）。观察组不良反应总发生率为10.42%略高于对照组4.17%,经比较两组无统计学差异（P>0.05）。结论：针对斑块型银屑病患者而言,调胃承气汤加减联合苦参汤综合治疗具有较好的临床疗效,可减轻炎症反应,预防纤维化和抑制血管新生,改善PASI评分和瘙痒程度,安全性较好。     

雷公藤多苷片联合NB-UVB对寻常型银屑病炎症水平、血脂指标及卒中风险的影响

摘要 目的：探讨雷公藤多苷片联合NB-UVB对寻常型银屑病炎症水平、血脂指标及卒中风险的影响。方法：选择2020年1月到2021年12月来我院诊治的寻常型银屑病患者72例,根据随机数字表法,将72例患者分为对照组（36例）与观察组（36例）,对照组患者给予NB-UVB的全身照射治疗,观察组在对照组基础上给予雷公藤多苷片治疗,对比两组的治疗效果,对比两组患者治疗前、治疗12周时的PASI评分,对比两组患者治疗前、治疗12周的血清IL-22、IL-17、TNF-α及YKL-40水平,对比两组患者治疗前、治疗12周的血清血脂水平,对比两组患者治疗12周时的卒中风险程度,对比两组患者治疗期间的不良反应发生情况。结果：观察组有效98.33%明显较对照组86.67%高,P<0.05。治疗前,两组的PASI评分对比无差异（P>0.05）;治疗12周时,两组的PASI评分降低明显,且观察组明显较对照组低（P<0.05）。治疗前,两组的血清IL-22、IL-17、TNF-α及YKL-40水平对比无统计学意义,治疗12周时,两组的血清IL-22、IL-17、TNF-α及YKL-40水平明显降低,且观察组明显较对照组低（P<0.05）。治疗前,两组患者的血清血脂水平对比无统计学意义（P>0.05）;治疗12周后,观察组的总胆固醇、甘油三酯、低密度脂蛋白水平明显降低,高密度脂蛋白水平明显升高,且观察组与对照组对比有统计学意义（P<0.05）,对照组与治疗前对比无统计学意义（P>0.05）;治疗12周时,观察组的卒中风险程度明显较对照组低（P<0.05）。治疗期间,两组患者均完成治疗,无明显不良反应。结论：与单独应用NB-UVB相比,雷公藤多苷片联合NB-UVB可降低寻常型银屑病患者的炎症水平,改善血脂指标水平,降低患者的卒中风险。     

寻常型银屑病患者血清肽基脯氨酰顺反异构酶1、摄食抑制因子1、血管生成素2的变化及临床意义

摘要 目的：观察寻常型银屑病患者血清肽基脯氨酰顺反异构酶1（Pin1）、摄食抑制因子1（nesfatin-1）、血管生成素2（ANGPT2）水平的变化,并探讨分析其临床意义。方法：选择我院2019年5月～2021年5月收治的寻常型银屑病患者98例,分别比较不同疾病严重程度和不同疾病分期患者的血清Pin1、nesfatin-1、ANGPT2水平,采用Pearson检验分析血清Pin1、nesfatin-1、ANGPT2水平与皮损面积及严重程度指数（PASI）评分的相关性,采用光疗仪对患者进行治疗,比较治疗前后血清Pin1、nesfatin-1、ANGPT2水平变化。结果：重度组和中度组患者的Pin1、ANGPT2水平均高于轻度组,且重度组高于中度组（P＜0.05）;重度组和中度组患者的nesfatin-1水平均低于轻度组,且重度组低于中度组（P＜0.05）。进行期组患者的Pin1、ANGPT2水平高于静止期组和退行期组患者,而nesfatin-1水平低于静止期组与退行期组患者（P＜0.05）;静止期组与退行期组之间上述各指标比较差异无统计学意义（P＞0.05）。Pearson相关性分析结果显示,寻常型银屑病患者的血清Pin1、ANGPT2水平与PASI评分呈正相关,而nesfatin-1水平与PASI评分呈负相关（P＜0.05）。治疗后,寻常型银屑病患者的血清Pin1、ANGPT2水平明显降低,nesfatin-1水平则明显升高（P＜0.05）。结论：寻常型银屑病患者的病情越重,血清Pin1、ANGPT2水平越高,而nesfatin-1水平越低,且三者对患者疗效有一定评估价值。     

愈创紫草油对头颈部恶性肿瘤患者放疗所致放射性皮肤黏膜损伤的改善作用研究

摘要 目的：探讨愈创紫草油改善头颈部恶性肿瘤放疗患者所致放射性皮肤黏膜损伤的临床疗效,以期为头颈部恶性肿瘤放疗患者所致放射性皮肤黏膜损伤提供新的治疗方法。方法：选取安徽中医药大学附属六安医院2021年3月-2023年3月头颈部恶性肿瘤放疗患者100例作为研究对象,随机数字表随机分为观察组和对照组,各50例。两组均采用适形调强放射治疗,对照组给予常规放疗皮肤管理与宣教,观察组在对照组基础上给予涂抹愈创紫草油治疗。比较两组皮肤黏膜损伤程度、临床疗效、放疗完成率、皮损愈合时间,放疗2、4、6周时数字评分法（NRS）评分、Karnofsky功能状态（KPS）评分、皮肤病生活质量量表（DLQI）评分;放疗前、放疗6周时炎性细胞因子[白介素-6（IL-6）、降钙素原（PCT）、超敏C反应蛋白（hs-CRP）]水平及皮肤不良反应。结果：观察组皮肤黏膜损伤程度分级低于对照组（P＜0.05）;观察组总有效率94.00%较对照组80.00%高（P＜0.05）;放疗4、6周时观察组NRS评分、DLQI评分低于对照组,KPS评分高于对照组（P＜0.05）;两组放疗完成率均为100%,观察组皮损愈合时间较对照组短（P＜0.05）;放疗6周时观察组血清IL-6、PCT、hs-CRP水平低于对照组（P＜0.05）;两组患者均未出现过敏所致皮疹、红肿、瘙痒等皮肤不良反应。结论：愈创紫草油可有效减轻头颈部恶性肿瘤放疗所致放射性皮肤黏膜损伤,降低血清炎性细胞因子水平,促进患者皮损愈合,提高生活质量,疗效显著,且安全性高。     

阿达木单抗治疗重度银屑病的临床疗效及对外周血Th1/Th2平衡和单核细胞p38MAPK/NF-κB信号通路的影响

摘要 目的：观察阿达木单抗治疗重度银屑病的临床疗效及对外周血Th1/Th2平衡和单核细胞p38丝裂原活化蛋白激酶（MAPK）/核转录因子κB（NF-κB）信号通路的影响。方法：选择解放军总医院第五医学中心2019年3月-2022年3月期间收治的118例重度银屑病患者,根据随机数字表法分为对照组（常规治疗,59例）和研究组（对照组的基础上结合阿达木单抗治疗,59例）。观察两组疗效、症状评分变化、外周血Th1/Th2平衡和单核细胞p38MAPK/NF-κB信号通路的变化,记录两组不良反应发生情况。结果：研究组的临床总有效率高于对照组（P<0.05）。研究组治疗后的Th1、白细胞介素-2（IL-2）、γ-干扰素（IFN-γ）低于对照组,白细胞介素-4（IL-4）、白细胞介素-10（IL-10）、Th2高于对照组（P<0.05）。研究组治疗后的p38MAPK、NF-κB蛋白表达水平低于对照组（P<0.05）。研究组治疗后的银屑病皮损面积及严重程度指数（PASI）评分低于对照组（P<0.05）。两组不良反应发生率组间比较,差异不显著（P>0.05）。结论：阿达木单抗治疗重度银屑病的疗效较好,可能与调节外周血Th1/Th2平衡和单核细胞p38MAPK/NF-κB信号通路有关,且不增加不良反应发生率,具有较好的安全性。     

奥洛他定联合金蝉止痒颗粒治疗对湿疹患者皮肤损伤、皮肤屏障功能及炎症因子的影响

摘要 目的：探究金蝉止痒颗粒辅助治疗对湿疹患者皮肤损伤、皮肤屏障功能及炎症因子的影响。方法：选取2020年6月~2022年5月来我院皮肤科就诊治疗的120例慢性湿疹的患者,按照治疗方式的不同分为对照组（n=60）与观察组（n=60）,其中对照组口服奥洛他定治疗,观察组在对照治疗基础之上加服金蝉止痒颗粒。对比两组患者治疗后的临床疗效、湿疹皮肤损伤严重程度评分皮肤屏障功能和炎性因子水平的变化。记录并比较两组患者的不良反应发生情况。结果：观察组总有效率（95.00%）显著高于对照组总有效率（60.00%）,差异有统计学意义（P<0.05）。治疗后与治疗前相比,两组患者瘙痒评分、皮损面积评分及EASI评分均显著下降,且观察组各项指标优于对照组,有统计学意义（P<0.05）。两组患者TEWL指标显著降低,而WCSC和SC指标显著升高,且观察组上述指标显著优于对照组,差异均有统计学意义（P<0.05）。两组患者血清IL-2水平明显升高,而IL-4、TNF-α水平显著降低,且观察组较对照组变化更为明显,差异均有统计学意义（P<0.05）。对照组患者的不良反应发生率为5.00%,治疗组为3.33%,两组比较无统计学意义（P>0.05）。结论：奥洛他定联合金蝉止痒颗粒治疗湿疹能够减少皮肤损伤,修复湿疹患者皮肤屏障损伤,调节血清炎症因子的变化,改善湿疹患者临床症状。     

银屑病患者血清sPD-1、C反应蛋白及LRG1的表达与病情严重程度的关系

摘要 目的：探讨银屑病患者血清sPD-1、C反应蛋白及LRG1的表达与病情严重程度的关系。方法：选取2019年1月至2022年12月我院收治的银屑病患者70例纳入研究组,并选取同期体检健康者70例纳入对照组。按照患者病情将研究组患者进行进一步分组,分为进行期（21例）、静止期（22例）、退行期（27例）。采用ELISA检测sPD-1、CRP、LRG1的表达水平。采用Pearson检验分析sPD-1、CRP、LRG1的表达与银屑病患者病情的关系;采用logistics回归分析分析银屑病患者不同分期的独立危险因素;采用受试者工作曲线（ROC）分析sPD-1、CRP、LRG1对银屑病患者病情发展的预测价值。结果：三组患者年龄和性别比较（P＞0.05）;进行期sPD-1、CRP、LRG1、PASI积分显著高于静止期和退行期（P<0.05）,静止期sPD-1、CRP、LRG1、PASI积分显著高于退行期（P<0.05）;sPD-1、CRP、LRG1的表达与银屑病分期及PASI评分均显著相关(P<0.05),而与年龄和性别无关（P＞0.05）;多因素logistic回归分析结果显示,sPD-1、CRP、LRG1是影响银屑病患者病情分期的独立危险因素;sPD-1、CRP、LRG1拟合诊断预测银屑病患者病情分期的敏感度86.00%,特异度89.00%,AUC值为0.813。结论：sPD-1、CRP、LRG1的表达上调与银屑病患者疾病分期密切相关,临床早期可通过监测sPD-1、CRP、LRG1的表达对银屑病患者病情的发展做出可靠的预测评估。     

解毒化瘀汤联合刺络放血疗法对血瘀热结证寻常型银屑病患者血清炎性因子及CREB信号传导通路相关蛋白表达的影响

摘要 目的：探讨解毒化瘀汤联合刺络放血疗法对血瘀热结证寻常型银屑病患者血清炎性因子及cAMP反应元件结合蛋白（CREB）信号传导通路相关蛋白表达的影响。方法：选取2018年5月到2020年5月武警成都支队卫生队和武警四川总队医院收治的寻常型银屑病患者共80例,随机分成对照组（维A酸哈西奈德乳膏治疗）与观察组（解毒化瘀汤联合刺络放血疗法治疗）,各40例。两组均以4周为1个疗程,共治疗2个疗程。对比两组疗效、中医证候积分、血清炎性因子及CREB信号传导通路相关蛋白表达水平。结果： 观察组的临床总有效率高于对照组（P<0.05）。两组治疗后中医证候主证、次证总评分和血清白介素-17（IL-17）、肿瘤坏死因子-α（TNF-α）、干扰素-γ（IFN-γ）、C反应蛋白（CRP）水平以及CREB微小核糖核酸（mRNA）、PKA mRNA、P38 mRNA相对表达量均较治疗前下降,且观察组较对照组低（P<0.05）。结论：解毒化瘀汤联合刺络放血疗法治疗血瘀热结证寻常型银屑病患者,疗效显著,可有效改善临床症状,减轻机体炎性反应,其主要作用机制可能与调节CREB信号传导通路相关蛋白表达有关。     

医用保湿霜对湿疹患者皮肤屏障、皮损状况及炎症因子的影响

摘要 目的：探究医用护肤品对湿疹患者皮肤屏障损伤、免疫指标和血清因子的影响。方法：选取2020年12月~2021年3月来我院皮肤科就诊治疗的115例慢性湿疹的患者,按照其治疗不同分为单药组（n=66）与联合组（n=49）,其中单药组外涂糠酸莫米松乳膏,联合组外涂糠酸莫米松乳膏加用护肤品（保湿霜）。观察并记录治疗前后两组患者血清白细胞介素（IL）-2、IL-4、IL-5、Th细胞群、IgE水平及嗜酸性粒细胞（EOS）数目变化。对比两组患者湿疹病情严重程度评分差异。分析两组患者皮肤屏障功能[经表皮水分流失（TEWL）、皮肤油脂（SC）和角质层含水量（WCSC）]差异,并对比两组患者的临床疗效。结果：治疗后,联合组总有效率显著高于单药组（P<0.05）。两组患者血清IL-2水平与治疗前相比明显升高,而IL-4、IL-5水平显著降低,且联合组较单药组变化更为明显（P<0.05）。两组患者Th1、Th2与治疗前相比均显著下降,但联合组Th1/Th2比值较单药组显著升高（P<0.05）。两组患者外周血IgE、EOS与治疗前相比明显降低,且联合组更为明显（P<0.05）。两组患者瘙痒、皮损面积评分及EASI评分与治疗前相比下降明显,且联合组优于单药组（P<0.05）。两组患者TEWL指标与治疗前相比明显降低,而WCSC和SC指标显著升高,且联合组较单药组变化更为明显（P<0.05）。治疗后,两组患者皮损处TLR4,MyD88及NF-κB mRNA表达量与治疗前相比明显降低,且联合组更为明显,差异均有统计学意义（P<0.05）。结论：糠酸莫米松乳膏联合医用护肤品能够修复湿疹患者皮肤屏障损伤,调节免疫指标和血清因子的变化,改善湿疹患者临床症状。其机制可能与抑制TLR4/MyD88/NF-κB信号通路有关。     

夹脊电针疗法联合重复经颅磁刺激对不完全性脊髓损伤后神经病理性疼痛患者心理状态、血清炎性因子和疼痛介质的影响

摘要 目的：观察夹脊电针疗法联合重复经颅磁刺激（rTMS）对不完全性脊髓损伤（ISCI）后神经病理性疼痛（NP）患者心理状态、血清炎性因子和疼痛介质的影响。方法：选择ISCI后并发NP患者113例,根据随机数字表法分为对照组（n=56,rTMS治疗）和研究组（n=57,对照组基础上结合夹脊电针疗法）,连续治疗4周后观察两组疼痛改善、心理状态、血清炎性因子和疼痛介质水平的变化。结果：研究组的临床总有效率高于对照组（P<0.05）。研究组治疗4周后的疼痛评级指数（PRI）、现实疼痛指数（PPI）、视觉模拟评分（VAS）评分低于对照组（P<0.05）。研究组治疗4周后的焦虑自评量表（SAS）、抑郁自评量表（SDS）评分低于对照组（P<0.05）。研究组治疗4周后的肿瘤坏死因子-α（TNF-α）、降钙素原（PCT）低于对照组,白细胞介素-10（IL-10）则高于对照组（P<0.05）。研究组治疗4周后的前列腺素E₂（PGE₂）、5-羟色胺（5-HT）低于对照组,β-内啡肽（β-EP）则高于对照组（P<0.05）。结论：夹脊电针疗法联合rTMS治疗ISCI后NP患者,可有效减轻疼痛症状,改善其心理状态、血清炎性因子和疼痛介质水平。     

寻常型银屑病患者血清IL-17、IL-18、VEGF的表达及与病情严重程度的相关性研究

目的:探讨寻常型银屑病患者血清白介素17(IL-17)、白介素18(IL-18)、血管内皮生长因子(VEGF)的表达及与病情严重程度的相关性。方法:选取2015年8月到2017年4月在我院接受治疗的寻常型银屑病患者86例为研究组,另选取同期在我院体检结果为健康的志愿者40例作为健康对照组,并根据临床症状和病情变化对研究组患者进行分组,其中进行期银屑病组32例,静止期银屑病组24例,退行期银屑病组30例。对比研究组和健康对照组血清中IL-17、IL-18、VEGF水平,对比不同严重程度的寻常型银屑病患者血清中IL-17、IL-18、VEGF水平和PASI评分,采用Spearman相关性分析IL-17、IL-18、VEGF的表达与PASI评分的相关性。结果:研究组患者血清中的IL-17、IL-18、VEGF水平显著高于健康对照组(P0.05),进行期银屑病组患者血清中IL-17、IL-18、VEGF水平和PASI评分显著高于静止期银屑病组和退行期银屑病组,静止期银屑病组患者血清中IL-17、IL-18、VEGF水平和PASI评分显著高于退行期银屑病组(P0.05),Spearman相关性分析结果显示,研究组患者血清中IL-17、IL-18、VEGF水平与PASI评分均呈正相关(P0.05)。结论:寻常型银屑病患者血清中IL-17、IL-18、VEGF水平异常升高,且其水平与病情严重程度有关,对上述三种指标进行监测有助于临床治疗寻常型银屑病。     

5%环孢菌素霜对银屑病合并代谢综合征患者血清IL-17 及IL-18 水平的 影响

目的:探讨5%环孢菌素霜对银屑病合并代谢综合征患者外周血IL-17、IL-18水平及PASI评分的影响。方法:选择我院收治的寻常型银屑病合并代谢综合症患者68例,分为实验组和对照组。对照组予以复方甘草酸苷和卡泊三醇治疗,实验组在此基础上加用制备好的5%环孢菌素霜,观察并比较两组患者治疗前后外周血IL-17及IL-18水平的变化情况以及血压、空腹血糖、血脂及PASI评分结果。结果:与治疗前比较,两组患者治疗后IL-17及IL-18水平、血压、FPG、TG及PASI评分均显著降低,而HDL-C明显升高,差异均具有统计学意义(P0.05);与对照组比较,实验组治疗后IL-17及IL-18水平、血压、FPG、TG及PASI评分较低,而HDL-C较高,差异均具有统计学意义(P0.05)。结论:5%环孢菌素霜辅助治疗可调节银屑病合并代谢综合征患者外周血IL-17、IL-18水平,降低其PASI评分,改善患者机体代谢紊乱状态,对银屑病合并代谢综合症有显著临床疗效。     

FTIR spectroscopic studies of lipid dynamics in phytosphingosine ceramide models of the stratum corneum lipid matrix

IR spectroscopic studies are reported for N-stearyl-d-erythro-phytosphingosine (Cer NP) and N-stearyl-2-hydroxy-d-erythro-phytosphingosine (Cer AP) in a hydrated model of the skin lipid barrier comprised of equimolar mixtures of each ceramide with cholesterol and d₃₅-stearic acid. Examination of the methylene stretching, rocking and bending modes reveal some rotational freedom and hexagonal packing in both the ceramide and stearic acid chains. Analysis of the acid carbonyl stretch and the ceramide Amide I modes show both shift to higher frequencies, indicating weaker hydrogen bonding, in the mixed systems compared to the pure materials. For both systems, the fatty acid chain disordering temperatures are significantly increased from those of the pure acids. The observed behaviors of these phytosphingosine ceramide systems are fundamentally different from the previously reported analogous sphingosine ceramide systems. The implications of these observations for lipid organization in the stratum corneum are briefly discussed.     

Optimization of submerged keratinocyte cultures for the synthesis of barrier ceramides

Epidermal differentiation results in the formation of the extracellular lipid barrier in the stratum corneum, which mainly consists of ceramides, free fatty acids, and cholesterol. Differentiating keratinocytes of the stratum granulosum synthesize a series of complex long-chain ceramides and glucosylceramides with different chain lengths and hydroxylation patterns at intracellular membranes of the secretory pathway. Formation of complex extracellular ceramides parallels the transition of keratinocytes from the stratum granulosum to the stratum corneum, where their precursors, complex glucosylceramides and sphingomyelin, are secreted and exposed to extracellular lysosomal lipid hydrolases. Submerged cultures used so far showed a reduced ceramide content compared to the native epidermis or the air-exposed, organotypic culture system. In order to investigate the sphingolipid metabolism during keratinocyte differentiation, we optimized a simple cell culture system to generate the major barrier sphingolipids. This optimized model is based on the chemically well-defined serum-free MCDB medium. At low calcium ion concentrations (0.1mM), keratinocytes proliferate and synthesize mainly Cer(NS) and a small amount of Cer(NP). Supplementation of the MCDB cell culture medium with calcium ions (1.1mM) and 10 microM linoleic acid triggered differentiation of keratinocytes and synthesis of a complex pattern of free and covalently bound ceramides as found in native epidermis or air-exposed organotypic cultures, though at a reduced level. The mRNA levels of the differentiation markers keratin 10 and profilaggrin increased, as well as those of ceramide glucosyltransferase and glucosylceramide-beta-glucosidase. The described culture system was thus suitable for biochemical studies of the sphingolipid metabolism during keratinocyte differentiation. The addition of serum or vitamin A to the medium resulted in a decrease in ceramide and glucosylceramide content. Lowering the medium pH to 6, while maintained cell viability, led to an increase in the processing of probarrier lipids glucosylceramide and sphingomyelin to free ceramides and protein-bound ceramide Cer(OS).     

Impaired Epidermal Permeability Barrier in Mice Lacking Elovl1, the Gene Responsible for Very-Long-Chain Fatty Acid Production

The sphingolipid backbone ceramide (Cer) is a major component of lipid lamellae in the stratum corneum of epidermis and has a pivotal role in epidermal barrier formation. Unlike Cers in other tissues, Cers in epidermis contain extremely long fatty acids (FAs). Decreases in epidermal Cer levels, as well as changes in their FA chain lengths, cause several cutaneous disorders. However, the molecular mechanisms that produce such extremely long Cers and determine their chain lengths are poorly understood. We generated mice deficient in the Elovl1 gene, which encodes the FA elongase responsible for producing C₂₀ to C₂₈ FAs. Elovl1 knockout mice died shortly after birth due to epidermal barrier defects. The lipid lamellae in the stratum corneum were largely diminished in these mice. In the epidermis of the Elovl1-null mice, the levels of Cers with ≥C₂₆ FAs were decreased, while those of Cers with ≤C₂₄ FAs were increased. In contrast, the levels of C₂₄ sphingomyelin were reduced, accompanied by an increase in C₂₀ sphingomyelin levels. Two ceramide synthases, CerS2 and CerS3, expressed in an epidermal layer-specific manner, regulate Elovl1 to produce acyl coenzyme As with different chain lengths. Elovl1 is a key determinant of epidermal Cer chain length and is essential for permeability barrier formation.     

Effect of sphingosine and phytosphingosine ceramide ratio on lipid arrangement and barrier function in skin lipid models

The lipids in the uppermost layer of the skin, the stratum corneum (SC), play an important role in the skin barrier function. The three main subclasses in the SC lipid matrix are ceramides (CER), cholesterol, and free fatty acids. In inflammatory skin diseases, such as atopic dermatitis and psoriasis, the SC lipid composition is modulated compared to the composition in healthy SC. One of the main alterations is the molar ratio between the concentration of CER N-(tetracosanoyl)-sphingosine (CER NS) and CER N-(tetracosanoyl)-phytosphingosine (CER NP), which correlated with an impaired skin barrier function. In the present study, we investigated the impact of varying the CER NS:CER NP ratios on the lipid organization, lipid arrangement, and barrier functionality in SC lipid model systems. The results indicate that a higher CER NS:CER NP ratio as observed in diseased skin did not alter the lipid organization or lipid arrangement in the long periodicity phase encountered in SC. The trans-epidermal water loss, an indication of the barrier functionality, was significantly higher for the CER NS:CER NP 2:1 model (mimicking the ratio in inflammatory skin diseases) compared to the CER NS:CER NP 1:2 ratio (in healthy skin). These findings provide a more detailed insight into the lipid organization in both healthy and diseased skin and suggest that in vivo the molar ratio between CER NS:CER NP contributes to barrier impairment as well but might not be the main factor.     

Correlation of IL-12, IL-22, and IL-23 in patients with psoriasis and metabolic syndrome. Preliminary report

BackgroundPsoriasis is an autoimmune skin disease characterised by proliferation of keratinocytes, primarily due to cytokines Th1 and Th17. This profile is involved in pathogenesis of metabolic syndrome, a frequently found comorbidity in patients with psoriasis.ObjectiveIn this study we determine the correlation of levels of pro-inflammatory cytokines TNF-α, IL-23, IL-12, and IL-22 in patients with psoriasis with and without metabolic syndrome and clinically healthy controls.MethodsWe included 55 patients with plaque psoriasis: 30 with metabolic syndrome (PPMS), 25 without metabolic syndrome (PP), 15 healthy subjects (HS) and 15 with metabolic syndrome (MS). Quantification of serum levels of IL-12, TNF-α, IL-22, and IL-23 was done by ELISA.ResultsWe observed that serum levels of IL-12 were more elevated in PP group, while the lowest levels of TNF-α were seen in HS group. IL-22 was found to be higher in PP than in PPMS (p < 0.05). PP patients with PASI scores rating as severe showed higher levels of IL-12. TNF-α level analysis showed significant differences in HS group compared with the others; levels of this cytokine were lower in patients with PP and moderate PASI scores than in MS group (p < 0.05). We found no correlation between cytokine levels and psoriasis or between cytokines and PASI scores. In PP group, a positive correlation was observed between IL-23 and fasting glucose (r = 0.432, p < 0.05), as well as a negative correlation between IL-23, IL-22, and IL-12 versus waist circumference (r = −0.504, r = −0.556 and r = −0.511, respectively; p < 0.05).ConclusionsPsoriasis is not just a skin disorder, but rather a condition with systemic implications, with intervention of pro-inflammatory cytokines that contribute to metabolic syndrome and other comorbidities, which in turn increases the risk of developing cardiovascular disease.     

Junctions and Inflammation in the Skin

Abstract

The skin forms a life-sustaining barrier between the organism and physical environment. The physical barrier of skin is mainly localized in the stratum corneum (SC); however, nucleated epidermis also contributes to the barrier through tight, gap, and adherens junctions (AJs), as well as through desmosomes and cytoskeletal elements. Many inflammatory diseases, such as atopic dermatitis (AD) and psoriasis, are associated with barrier dysfunction. It is becoming increasingly clear that the skin barrier function is not only affected by inflammatory signals but that defects in structural components of the barrier may be the initiating event for inflammatory diseases. This view is supported by findings that mutations in filaggrin, a key structural epidermal barrier protein, cause the inflammatory skin disease AD, and that a loss of AJ components, namely epidermal p120 catenin or α-catenin results in skin inflammation.