CAJ | 학술논문

目的研究未经高效抗逆转录病毒治疗(HAART)的HIV感染者血管内皮损伤、血浆脂肪细胞因子及血栓形成因子的水平,以探讨单纯HIV感染者体内是否存在心血管病高危因素.方法收集2009年2-10月在我中心就诊的HIV感染者43例和17例同期院内正常体检者的一般资料并采集外周静脉血,ELISA法检测血浆瘦素、脂联素、可溶性细胞间黏附分子1(sICAM-1)、D-二聚体水平,在两组人群中比较这4项指标及TC、TG、空腹血糖等指标.流式细胞仪检测病例组CD4+T淋巴细胞计数、CD8+CD38+/CD8+、CD8+HLA-DR+/CD8+,用病毒定量检测仪和分支DNA技术检测HIV病毒载量,两组人群中有统计学差异的指标与CD4+T淋巴细胞计数、CD8+CD38+/CD8+、CD8+HLA-DR+/CD8+、HIV病毒载量进行Spearman相关性分析.结果 43例HIV感染者CD4+T淋巴细胞为(133±82)个/μl,HIV RNA为(4.42±0.66)lg拷贝/ml,瘦素[11.41(7.91,14.53)μg/L]、脂联素[1.79(1.40,4.00)mg/L]水平显著低于对照组[55.31(16.49,229.65)μg/L,3.36(2.92,4.18)mg/L,P值均＜0.005],sICAM-1[1.71(1.11,2.40)mg/L]显著高于对照组[0.69(0.57,0.80)mg/L,P=0.0000],并且sICAM-1与HIV病毒载量及免疫激活指标CD8+ CD38+/CD8+显著正相关(r=0.3378,P=0.0267和r=0.3904,P=0.0096).结论未经HAART治疗的HIV感染者体内存在某些心血管病高危因素的显著变化,应进一步研究其内在机制,寻求预防和处理方法.
목적 연구미경고효항역전록병독치료(HAART)적HIV감염자혈관내피손상、혈장지방세포인자급혈전형성인자적수평,이탐토단순HIV감염자체내시부존재심혈관병고위인소.방법 수집2009년2-10월재아중심취진적HIV감염자43례화17례동기원내정상체검자적일반자료병채집외주정맥혈,ELISA법검측혈장수소、지련소、가용성세포간점부분자1(sICAM-1)、D-이취체수평,재량조인군중비교저4항지표급TC、TG、공복혈당등지표.류식세포의검측병례조CD4+T림파세포계수、CD8+CD38+/CD8+、CD8+HLA-DR+/CD8+,용병독정량검측의화분지DNA기술검측HIV병독재량,량조인군중유통계학차이적지표여CD4+T림파세포계수、CD8+CD38+/CD8+、CD8+HLA-DR+/CD8+、HIV병독재량진행Spearman상관성분석.결과 43례HIV감염자CD4+T림파세포위(133±82)개/μl,HIV RNA위(4.42±0.66)lg고패/ml,수소[11.41(7.91,14.53)μg/L]、지련소[1.79(1.40,4.00)mg/L]수평현저저우대조조[55.31(16.49,229.65)μg/L,3.36(2.92,4.18)mg/L,P치균＜0.005],sICAM-1[1.71(1.11,2.40)mg/L]현저고우대조조[0.69(0.57,0.80)mg/L,P=0.0000],병차sICAM-1여HIV병독재량급면역격활지표CD8+ CD38+/CD8+현저정상관(r=0.3378,P=0.0267화r=0.3904,P=0.0096).결론 미경HAART치료적HIV감염자체내존재모사심혈관병고위인소적현저변화,응진일보연구기내재궤제,심구예방화처리방법.
Objectives To investigate the markers of endothelial injury, adipocytokine and thrombotic activity and explore whether there are cardiovascular disease risk factors in antiretroviral-naive HIV patients. Methods Clinical data and venous blood samples were collected from 43 anti-retroviral naive HIV-infected patients during February -October 2009 in our center, and compared with 17 healthy subjects.Plasma leptin, adiponectin, soluble intercellular adhesion molecule-1 ( sICAM-1 ), D-dimer were measured by ELISA. Four markers and cholesterol, triglyceride, fasting plasma glucose were compared between the two groups. The CD4+ T cells and percentages of CD38, HLA-DR on CD8+ T were determined by flow cytometry and plasma HIV copies were detected with bDNA analyzer among HIV-infected participants.Spearman correlations between the significant markers and CD4+ T cells, CD8+ CD38+/CD8+, CD8+ HLA-DR +/CD8+, HIV viral load were examined among HIV-infected participants. Analyses were conducted by using Stata version 7. Results Thirty-eight of the 43 patients were sexually infected by HIV and the median absolute CD4+ T cell count was ( 133 ± 82 ) cells/μl, HIV RNA was (4. 42 ± 0. 66 ) lg copies/ml. HIV-infected patients, compared with healthy subjects, had lower leptin [11.41 (7.91,14. 53 )μg/L vs 55.31( 16. 49,229.65 ) μg/L, P= 0. 0005], adiponectin [1.79 ( 1.40,4. 00 ) mg/L vs 3.36 ( 2. 92,4. 18 ) mg/L,P =0. 003] and higher sICAM-1 [1.71 (1.11,2.40) mg/L vs 0. 69 ( 0. 57, 0. 80 ) mg/L, P = 0. 0000].No significant differences exist in cholesterol, triglyceride, fasting plasma glucose. For HIV-infected participants, sICAM-1 tended to correlate with CD8+ CD38+/CD8+ and HIV viral load ( r= 0.3378, P= 0.0267;r = 0.3904,P = 0.0096). Conclusion Patients with untreated HIV infection have lower leptin, adiponectin and higher sICAM-1 levels and the relationship of these markers to HIV-mediated atherosclerotic risk requires further study.