内皮素-1和降钙素基因相关肽与白癜风的相关性研究-内科学;内分泌专业论文 word格式.docxVIP

内皮素-1 和降钙素基因相关肽与白癜风的相关性研究硕士研究生：屈铭一导师：刘志军副教授中文摘要目的：通过检测白癜风患者血浆中内皮素-1和降钙素基因相关肽的水平变化，探讨二者与白癜风发病及病情活动的相关性，为白癜风的发病机制研究及治疗提供新的理论依据。方法：选择湖南省衡阳地区汉族人群白癜风患者60名和40名健康志愿者为研究对象，采肘静脉血5毫升，取血浆，应用ELISA法检测血浆中ET-1 及CGRP 的浓度。结果：1白癜风患者血浆中ET-1的浓度低于健康对照组（P0.05），进展期白癜风患者血浆中ET-1 的浓度低于稳定期与健康对照组（P0.01），泛发型白癜风患者血浆中ET-1 的浓度明显低于局限型与健康对照组（P0.01）。而稳定期与局限型白癜风患者血浆中ET-1的浓度与健康对照组无明显差异（P＞0.05）。2白癜风患者血浆中CGRP的浓度明显高于健康对照组（P0.01），进展期白癜风患者血浆中CGRP的浓度，明显高于稳定期和健康对照组（P0.01），而泛发型白癜风患者血浆中CGRP的浓度明显高于局限型与健康对照组（P0.01）。而稳定期与局限型型白癜风患者血浆中CGRP 的浓度与健康对照组无明显差异（P＞0.05）。3白癜风患者组血浆中的ET-1与CGRP的浓度相关系数为-0.72(r=-0.72 p=0.002)，呈负相关。进展期白癜风患者血浆中ET-1与CGRP的浓度相关系数为-0.45(r=-0.538p=0.002），呈负相关。泛发型白癜风患者血浆中ET-1 与CGRP 的浓度相关系数为-0.52(r=-0.376 p=0.04)，呈负相关。结论：1 ET-1和CGRP与白癜风发病有关。2白癜风病情活动时，ET-1和CGRP呈负相关。关键词：白癜风；内皮素-1；降钙素基因相关肽InvestigationontherelationshipofEndotheli-1andCalcitonin generelated peptied withvitiligoAbstractObjectives: To explorethe relationship betweenEndotheli-1 and Calcitoningene related peptiedamongHanpeople in Hengyangof Hunan province with vitiligo, and to providethe new theoryandclinical evidence forvitiligo treatmentmethods.Methods:Aenzyme-linkedimmunosorbentassaywasusedtodetectthelevelsof ET-1andCGRPinplasmabycollectingcubitalveinbloodof60vitiligopatientsand 40normal controls amongHanpeople in HengyangofHunan province.Results:1Thelevel ofET-1 in theplasma ofpatients with vitiligo isobviouslylower thanthehealthycontrols（P0.01）.ThelevelofET-1intheplasmaofpatientswith progressiveanddiffusevitiligowasobviouslylowerthanthestableandlocalized vitiligo（P0.01）.NoobviouslydifferencewasobseventinseraET-1levelbetweenpatients with stable and localized vitiligo and thehealthycontrol(P0. 05) .TheplasmalevelofCGRPinvitiligowashigherthanHealthycontrols（P0.01）. ThelevelofCGRPintheplasmaofpatientswithprogressiveanddiffusevitiligowas significantiyhigherthanthestableandlocalizedvitiligo（P0.01）.NoobviouslydifferencewasobseventinseraCGRPlevelbetweenpatientswithstableand localized vitiligo and thehealthycontrol(P0. 05).Negativecorrelationbetwe