阻塞性睡眠呼吸暫停綜合征致缺血性腦卒中炎性機制的相關研究
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本文關鍵詞:阻塞性睡眠呼吸暫停綜合征致缺血性腦卒中炎性機制的相關研究 出處:《昆明醫(yī)科大學》2013年碩士論文 論文類型:學位論文
更多相關文章: 阻塞性睡眠呼吸暫停綜合征 缺血性腦卒中 相關性 炎癥因子 炎癥機制
【摘要】:目的:通過檢測血漿炎癥因子可溶性血管內(nèi)皮蛋白C受體(soluble endothelial protein C receptor, SEPCR)、急性時相血清淀粉樣蛋白A (acute phase serum amyloid A, SAA)、可溶性CD40配體(soluble CD40ligand, SCD40L)水平,分析其與阻塞性睡眠呼吸暫停綜合征(obstructive sleep apnea syndrome, OSAS)、.缺血性腦卒中的相關性,以探討OSAS導致缺血性腦卒中可能的炎癥反應機制。 方法:收集昆明醫(yī)科大學第二附屬醫(yī)院神經(jīng)內(nèi)科于2011年11月至2012年11月期間住院病人120例,其中無缺血性腦卒中的OSAS組病人30例(A組),無OSAS的缺血性腦卒中組病人30例(B組),合并OSAS的缺血性腦卒中組病人30例(C組),共90例作為觀察組;并選取同期無OSAS及缺血性腦卒中的病人30例作為對照組(D組)。記錄患者的一般情況,包括性別、年齡、身高、體重、吸煙史及高血壓病、糖尿病等既往病史,對有缺血性腦卒中的患者進行神經(jīng)功能缺損量表(National Institutes of Health Stroke Scale, NIHSS)評分,并記錄分值。所有入選病例均于入院次日采集空腹靜脈血3ml,測定血漿SEPCR、 SAA、 SCD40L及血超敏C-反應蛋白(high sensitive C reactive protein, HS-CRP)、同型半胱氨酸(Homocysteine, HCY)、纖維蛋白原(Fgrinogen, Fg)。對所有入選病例均進行頸部血管超聲,多導睡眠呼吸監(jiān)測檢查,并分別記錄頸動脈內(nèi)-中膜厚度(intima-media thickness, IMT)、呼吸暫停指數(shù)(apnea hypopnea index, AHI)、最低動脈血氧飽和度(minimal arterial oxygen saturation, SaO2min)。應用SPSS17.0統(tǒng)計學軟件對相關因素進行相關性分析。 結果:A、 B、 C、D四組整體在性別、AHI、 SaO2min、體重指數(shù)(BMI)、 IMT、 Fg、 HCY、 SEPCR、SAA、 SCD40L、 NIHSS評分存在統(tǒng)計學差異。組間比較結果顯示,AHI、SaO2min、 BMI、 IMT、 Fg、 HCY、 SEPCR、 SAA、 SCD40L、NIHSS在A-C、 B-C、 A-D、 C-D組間存在統(tǒng)計學差異,而在A-B組間無明顯統(tǒng)計學差異;AHI在B-D組間、NIHSS評分在A-D組間無明顯統(tǒng)計學差異。AHI與NIHSS評分密切相關,呈線性正相關。SEPCR、 SAA、 SCD40L與AHI、 NIHSS評分、IMT、 HCY、 Fg正相關,與SaO2min負相關。 結論:OSAS是缺血性腦卒中的獨立危險因素;OSAS患者系統(tǒng)性炎癥,直接或間接刺激血SEPCR、SAA、 SCD40L水平升高,誘發(fā)炎癥機制,促進動脈內(nèi)膜增厚,參與動脈粥樣硬化過程,揭示了OSAS可能通過炎癥反應機制獨立導致缺血性腦卒中的發(fā)生發(fā)展。
[Abstract]:Objective: to detect the plasma inflammatory factors of soluble endothelial protein C receptor (soluble endothelial protein C receptor, SEPCR), acute phase serum amyloid A (acute phase serum amyloid A, SAA), soluble CD40 ligand (soluble CD40ligand, SCD40L) level, and the analysis of obstructive sleep apnea syndrome (obstructive sleep apnea, syndrome, OSAS). The correlation of ischemic stroke, to explore the mechanism of the OSAS induced inflammatory response in ischemic stroke may.
Methods: collect the neurology department of the Second Affiliated Hospital of Kunming Medical University from November 2011 to November 2012 120 cases of hospitalized patients, 30 cases of group OSAS patients without ischemic stroke (A group), 30 patients with non OSAS ischemic stroke patients (B group), 30 patients with OSAS in ischemic stroke patients (C group), a total of 90 cases were selected as the observation group; and OSAS and ischemic stroke in 30 patients as control group (group D). Record the general condition of patients, including gender, age, height, weight, smoking history, hypertension, diabetes and other medical history, the neurological deficit scale for ischemic stroke patients (National Institutes of Health Stroke Scale, NIHSS) score, and record the score. All the cases were in the hospital the next day fasting venous blood 3ml, plasma SEPCR, SAA, SCD40L and serum high-sensitivity C- reactive protein (hig H sensitive C reactive protein, HS-CRP), homocysteine (Homocysteine, HCY), fibrinogen (Fgrinogen, Fg). All selected cases were performed neck vascular ultrasound, polysomnography examination and recording of carotid artery intima-media thickness (intima-media, thickness, IMT), apnea index (apnea hypopnea index, AHI), the lowest arterial oxygen saturation (minimal arterial oxygen saturation, SaO2min). SPSS17.0 was used to analysis the correlation of related factors.
Results: A, B, C, D four groups in the overall gender, AHI, SaO2min, body mass index (BMI), IMT, Fg, HCY, SEPCR, SAA, SCD40L, NIHSS, there were significant differences between the groups score. The comparison results show that AHI, SaO2min, BMI, IMT, Fg, HCY, SEPCR, SAA SCD40L, NIHSS, B-C, A-D, in A-C, there was significant difference between the C-D group, but no statistically significant difference in A-B between group AHI; in group B-D, NIHSS score in group A-D between.AHI and NIHSS had no statistically significant difference was closely related to a linear positive correlation between.SEPCR, SAA, SCD40L and AHI, NIHSS IMT, HCY, Fg score, positive correlation, negative correlation with SaO2min.
Conclusion: OSAS is an independent risk factor for ischemic stroke; OSAS patients with systemic inflammation, directly or indirectly stimulate the blood SEPCR, SAA, SCD40L levels increased, induced inflammation, promote intimal thickening, participate in the process of atherosclerosis, revealed by OSAS might lead to inflammatory reaction mechanism independent of occurrence and development of ischemic stroke.
【學位授予單位】:昆明醫(yī)科大學
【學位級別】:碩士
【學位授予年份】:2013
【分類號】:R743.3;R766
【參考文獻】
相關期刊論文 前8條
1 陳紹森;陳飛鵬;陳曉軍;;阻塞性睡眠呼吸暫�;颊哐宓矸蹣拥鞍譇水平研究[J];南方醫(yī)科大學學報;2009年08期
2 李連;曹非;;阻塞性睡眠呼吸暫停綜合征與腦血管病相關性臨床研究[J];神經(jīng)疾病與精神衛(wèi)生;2008年04期
3 包海榮,余勤,劉曉菊;阻塞性睡眠呼吸暫停綜合征患者血清白細胞介素8和單核細胞趨化蛋白1水平的變化及意義[J];臨床薈萃;2004年20期
4 曹惠芳;張萍;馮瑩;徐晶;張梓楠;李維浩;;腦梗塞合并阻塞性睡眠呼吸暫停綜合征患者血栓形成相關因素分析[J];臨床肺科雜志;2011年12期
5 陳梅f^;田小梅;;間歇性低氧對大鼠白細胞介素-1水平的影響[J];臨床肺科雜志;2012年07期
6 劉領;趙淑敏;盧青;薛兵;李秀業(yè);吳文杰;楊霽;趙曉靜;;阻塞性睡眠呼吸暫停綜合征患者血漿超敏C反應蛋白和IL-6水平的觀察[J];臨床內(nèi)科雜志;2006年12期
7 張群;李,
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