228例AIDS患者高效抗反转录病毒治疗效果分析

目的了解南宁国家免费高效抗反转录病毒治疗（highly active antiretroviral therapy,HAART）对AIDS患者的疗效。方法228例AIDS患者应用HAART3～18个月后,进行病毒载量（viral load,VL）和CD4^＋T淋巴细胞计数的检测及分析。结果调查临床及实验室检查资料较完整的病例共228例。100例在应用HAART6-18个月时进行VL检测,治疗6、12、18个月时与治疗前比较,VvL明显下降,下降发生在6个月以前,6个月以后VL比较稳定。151例在HAART3-18个月时进行了CD4^＋T淋巴细胞计数检测,治疗3、6、12、18个月时CD4＋T淋巴细胞绝对值明显增加,分别为195、228、255、277／μl;CD4^＋T淋巴细胞累计增值随时间变化呈上升趋势,分别为115、148、175、197／μl。结论HAART对AIDS患者有确切疗效。VL下降主要发生在6个月以前,6个月以后VL比较稳定;CD4^＋T淋巴细胞绝对值随时间变化呈逐渐上升趋势。     

300例艾滋病患者高效抗逆转录病毒治疗后免疫重建规律探讨

目的探讨高效抗逆转录病毒治疗（HAART）对中国南部地区艾滋病患者的免疫重建规律。方法收集近3年来300例患者的完整资料,按基线CD4^＋T细胞数分为A、B、C三组,观察基线及治疗1、3、6、12月末CD4^＋T淋巴细胞数、12月末血浆病毒载量（VL）、临床症状和毒副作用。结果抗病毒治疗12月末300例患者CD4^＋T淋巴细胞计数平均上升127个／1,以治疗3月后增长明显,3、12月末与基线CD4^＋T淋巴细胞计数比较差异有显著性（P〈0．05）;12月末273例（91％）患者血浆病毒载量（VL）〈5copies/ml,27例（9％）患者病毒载量（VL）〉50copies/ml,高病毒载量A组16例,C组4例;A组与C组比较差异有显著性（P〈0．05）;药物不良反应主要是外周神经炎（35．4％）、骨髓抑制（18．2％）、皮疹（15．2％）、肝功能损害（12．1％）、乳酸酸中毒（12．1％）和肾结石（6．1％）。结论HAART治疗对中国南部地区的艾滋病患者有效,能够实现免疫重建,但存在较多毒副作用。     

抗病毒治疗对HIV/AIDS患者自然杀伤细胞和γδT细胞的重建作用研究

目的 研究高效联合抗逆转录病毒治疗(HAART)对HIV/AIDS患者NK细胞和γδT细胞的重建作用,比较HAART对获得性免疫和固有免疫重建规律的异同.方法 对59例接受规律HAART的HIV/AIDS患者于治疗前、治疗后1、3、6、9、12个月末进行随访,采用分支DNA(bDNA)法检测血浆病毒载量,经流式细胞仪检测患者外周血淋巴细胞亚群.以56例健康献血员作为正常对照.结果 基线时HIV/AIDS患者CD4+T细胞中位数为45(164,13)个/μl,NK细胞和γδT细胞中位数分别为96(135,56)个/μl和30(45,19)个/μl,与正常对照组相比均显著减低(P<0.001).HAART开始后1个月,血浆病毒载量降低了2.33 lg拷贝/ml(P<0.001),CD4+T细胞数增长了111个/μl(P<0.001),主要以记忆CD4+T细胞的快速增长为主,而NK细胞和γδT细胞与基线相比无显著变化.在HAART后3个月NK细胞和.γδT细胞数量出现增长,分别较基线增加26个/μl(P=0.007)和15个/μl(P<0.001).治疗12个月,CD4+T细胞、NK细胞及γδT细胞计数分别达到271(365,134)个/μl、166(281,108)个/μl和46(66,34)个/μl,但仍低于正常对照.结论 HAART可以重建HIV/AIDS患者固有免疫,但NK细胞和γδT细胞数量的增加晚于CD4+ T细胞,HAART对固有免疫的重建作用机制有待进一步研究.     

14例艾滋病病人高效抗逆转录病毒治疗的临床研究

目的探讨艾滋病（AIDS）高效抗逆转录病毒治疗（HAART）的疗效及副作用。方法对14例应用HAART（拉米夫定、司他夫定、奈伟拉平）的AIDS病人进行回顾性分析,并评价药物的不良反应。结果CD4＋T细胞〈50个/μl的7例AIDS病人中,1例疗效较好,6例短期内死亡;而CD4^＋T细胞〉50个/μl的7例AIDS病人中,6例较好,1例在短期内死亡。7例持续治疗的病人,CD4^＋T细胞治疗前与治疗后比较差异有统计学意义（P〈0.05）。结论HAART对多数AIDS病人效果显著,然病情较重者,多难以见到疗效,因此需严格掌握HAART时机。另外,本组免费药物显示出良好的耐受性,是多数病人的一个重要选择。     

中药复方对艾滋病病人CD4^＋T淋巴细胞计数的影响

目的探讨中药复方对艾滋病（AIDS）病人CD4^＋T淋巴细胞计数的影响。方法40例AIDS期病人随机分成治疗组和对照组。观察基线和治疗3、6、9、12个月末的CD4^＋T淋巴细胞计数和肝功能。结果采用重复测量检验,显示两组病人观察时间点与基线CD4^＋T淋巴细胞计数升高程度,差异有统计学意义（P〈0．001）。丙氨酸转氨酶（ALT）下降程度的差异有统计学意义（P〈0．001）。治疗组病人CD4^＋T淋巴细胞计数升高程度,较对照组差异有统计学意义（P=0．035〈0．05）;治疗组病人ALT下降程度较对照组差异也有统计学意义（P=0．027〈0．05）。结论中药复方能够提高AIDS期病人CD4^＋T淋巴细胞计数,减轻病人高效抗反转录病毒治疗（HAART）的不良反应。     

96例服刑AIDS患者高效抗逆转录病毒治疗临床观察

目的探索在监管场所应用高效抗逆转录病毒治疗（highly active antiretroviral therapy,HAART）服刑人员AIDS的临床疗效、安全性及管理特点。方法对2007年2月-2009年3月收治的应用HAART疗程满6个月以上的96例服刑AIDS患者资料进行分析,评价疗效及安全性。结果所有患者临床症状有不同程度的改善,无严重不良事件发生,服药依从性为100％。治疗6个月时93．0％的患者病毒载量（viral load,VL）〈50copies／ml,CD4＋T淋巴细胞计数较治疗前平均增加108．8／mm^3;治疗12个月时95．8％的患者VL〈50copies／ml,CD4＋T淋巴细胞计数较治疗前平均增加119．9／mm^3。结论在监管场所对服刑AIDS患者施行HAART治疗,可使患者血中CD4＋T淋巴细胞计数显著升高,VL显著下降。对服刑AIDS患者严格管理、规范治疗、严密监测及100％服药依从性是治疗成功的关键。     

CD+8 T细胞激活分子CD38、HLA-DR与HIV-1载量的相关性研究

目的研究HIV/AIDS患者CD8^＋ T细胞表达激活分子CD38、HLA-DR水平与血浆病毒载量（VL）的相关性,以及用CD8CD38、CD8HLA-DR比例替代VL检测的可行性.方法用流式细胞术分析103例接受12个月高效抗逆转录病毒治疗（HAART）患者的CD＋8 T细胞表达CD38和HLA-DR水平;用分支DNA扩增技术检测血浆VL.用敏感性、特异性、准确性等参数分析能有效预测VL＜50拷贝/ml、VL＜500拷贝/ml、VL＞1000拷贝/ml和VL＞10 000拷贝/ml时CD8CD38和CD8HLA-DR的检测范围.结果103例艾滋病患者CD38、HLA-DR和VL在12个月治疗中均呈下降趋势;CD38和VL在HAART治疗前及治疗第1、3、6、9、12个月6个检测点的总相关系数为0.483（P＜0.001）、HLA-DR和VL的总相关系数为0.477（P＜0.001）.用CD8CD38和CD8HLA-DR的水平预测VL值有显著诊断价值：当CD38＜68.5%和＜72.5%时预测VL＜50拷贝/ml和＜500拷贝/ml有较高的灵敏度和特异性;当HLA-DR在＞39.5%和＞46.5%时预测VL＞1000拷贝/ml和＞10 000拷贝/ml有较高的灵敏度和特异性.结论在条件匮乏的艾滋病高发区,可以用CD8CD38和CD8HLA-DR激活亚群的结果来预测血浆VL,作为监测HIV疾病进展和评价抗病毒疗效的参考.     

天津市高效抗逆转录病毒治疗艾滋病临床观察

目的评价天津市艾滋病（AIDS）初治患者,应用高效抗逆转录病毒治疗（HAART）的疗效、安全性和预后。方法将在天津市传染病医院就诊的62例AIDS患者,随机分成治疗组（45例）及对照组（17例）;治疗组应用一线HAART方案：AZT／D4T＋3TC＋NVP／EFV。观察两组患者的临床表现、免疫功能变化及预后。结果（1）HAART治疗组与对照组患者基线CD4 T细胞计数差异无统计学意义（P〉0．5）;治疗组的45例患者,HAART前CD4 T细胞计数均值为73／μl;HAART后3、6、12个月时分别为120／μl（39例）、139．5／μl（30例）和200／μl（22例）。（2）治疗组患者应用HAART后,机会性感染、肿瘤的发生率和病死率分别为40％和4．44％,均显著低于对照组的88．24％和47．06％（P〈0．01）。（3）初治患者一线HAART治疗的有效率为95．55%（43／45）,有17．78％（8／45）的患者因药物不良反应而调整HAART方案。结论天津市AIDS患者对一线HAART有较好的疗效,随着HAART疗程的延长,免疫功能得到恢复并改善了预后,存在药物不良反应和资源有限等问题。     

成人HIV/AIDS病人HAART前血小板减少的发生率及相关因素分析北大核心

目的描述成人艾滋病病毒（HIV）感染者/艾滋病（AIDS）病人（简称HIV/AIDS病人）在高效抗病毒治疗（HAART）前,发生血小板减少的基本特征,探讨HIV合并血小板减少的发生率及相关因素。方法以2003年6月至2015年12月,在北京地坛医院门诊就诊的3452例HIV/AIDS病人为研究对象,比较HAART前不同基本情况[人口学资料、身体质量指数（BMI）、CD4^＋T淋巴细胞（简称CD4细胞）计数、病毒载量、是否合并机会性感染及症状体征、其他混合性感染的合并情况及是否服用复方新诺明（SMZ-TMP）情况]的血小板减少的发生率,通过Logistic回归分析HIV/AIDS病人合并血小板减少症的相关因素。结果 HAART前合并血小板减少的有137例（3.97%）,其中轻度104例（3.01%）,中度19例（0.55%）,重度14例（0.41%）。血小板减少的发生率随CD4细胞计数的增加而降低（P〈0.001）。HAART前HIV RNA≥105拷贝/mL[调整OR值（AOR）=1.903,95%CI：1.125-3.218,P=0.016],CD4细胞计数≤50个/μL（AOR=8.828,95%CI：2.939-26.519,P〈0.001）及CD4细胞计数51-199个/μL（AOR=3.714,95%CI：1.317-10.479,P=0.013）,HBsAg＋（AOR=4.949,95%CI：2.372-10.323,P〈0.001）是发生血小板减少的危险因素。结论成人HIV/AIDS病人HAART前血小板减少发生率较低。低基线CD4细胞计数、高基线病毒载量及合并乙型肝炎是HAART前发生血小板减少的相关因素,因此对存在这些危险因素的病人及早的诊断和治疗是必须的。     

艾滋病免疫重建炎性综合征与基线CD4^＋T淋巴细胞计数的相关性及治疗分析

目的探讨艾滋病（AIDS）免疫重建炎性综合征（IRIS）与基线CD4^＋T淋巴细胞（简称CD4细胞）计数的相关性及治疗方法。方法将选取的艾滋病病毒（HIV）感染者／艾滋病（AIDS）病人（HIV／AIDS病人）,根据不同基线CD4细胞水平分为两组,观察这两组在高效抗反转录病毒治疗（HAART）后,发生IRIS的情况,以及糖皮质激素在治疗IRIS中的作用。结果共选取HIV／AIDS病人312例,A组157例,CD4细胞计数≤100个／μL：B组155例,CD4淋巴细胞计数〉100个／μL。A组IRIS发生率为40．1％（63／157）,死亡率为6．3％（4／63）;B组IRIS发生率为3．9％（6／155）,无死亡病例;两组IRIS发生率差异有统计学意义（P〈0．01）,死亡率虽有差异,但无统计学意义（P〉0．05）。两组IRIS最常见并发结核病,分别为71．4％（45／63）和33．3％（2／6）。糖皮质激素治疗重症病人症状的有效率为90．2％。结论基线CD4细胞低下是IRIS发生的重要因素,CD4细胞计数≤100个／μL的病人发生IRIS合并结核的较多见,糖皮质激素治疗有效。     

Higher risk of AIDS or death in patients with lower CD4 cell counts after virally suppressive HAART

Background The clinical implications of a failure to achieve high CD4 cell counts while receiving virally suppressive highly active antiretroviral therapy (HAART) are uncertain.
Methods We analysed data from HIV-infected men participating in the Multicenter AIDS Cohort Study (MACS) to elucidate associations between CD4 cell counts achieved during virally suppressive HAART and risks of AIDS or death. Inclusion criteria were: CD4 cell count <200 cells/μL before HAART initiation; ≥2 viral load (VL) determinations after HAART initiation; and sustained viral suppression, defined as all VL <50 HIV-1 RNA copies/mL, but allowing a single VL of 50–1000 copies/mL.
Results One hundred and twenty-one men were included; median age was 42 years. After first VL <50 copies/mL, six participants had a new AIDS diagnosis and seven died. The median CD4 cell count change/year (cells/μL) after first VL <50 copies/mL was zero among patients who either developed AIDS or died vs . 39 among those who did not meet either endpoint ( P =0.119). After controlling for time from HAART initiation to first VL <50 copies/mL, age at first VL <50 copies/mL, history of AIDS and antiretroviral therapy (ART) experience before HAART, the hazard ratio for AIDS or death at CD4 cell count of ≤200 vs . >350 cells/μL was 10.7 ( P =0.013), and at CD4 cell count of 201–350 vs . >350 cells/μL was 8.54 ( P =0.014).
Conclusion In this cohort, lower CD4 cell count at the time of viral suppression was associated with increased risk of AIDS or death.     

Impact of baseline viral load and adherence on survival of HIV-infected adults with baseline CD4 cell counts > or = 200 cells/microl

BACKGROUND: Baseline plasma HIV RNA levels > 100 000 copies/ml have been associated with elevated mortality rates after the initiation of HAART. There is uncertainty regarding the optimal strategy for patients with high plasma HIV RNA but CD4 cell count > or = 200 cells/microl. OBJECTIVE: To evaluate the impact of baseline plasma HIV RNA on survival among patients with CD4 cell counts > or = 200 cells/microl. METHODS: Patients were stratified by plasma HIV RNA, CD4 cell count and adherence level. Mortality rates were evaluated using Kaplan-Meier methods and Cox regression. RESULTS: Among 1166 patients initiating HAART with a CD4 cell count > or = 200 cells/microl, a baseline HIV RNA > or = 100 000 copies/ml was statistically associated with elevated mortality among non-adherent patients (log-rank P = 0.032), but not for adherent patients (log-rank P = 0.690). In a multivariate Cox model comparing patients with a baseline CD4 cell count > or = 200 cells/microl and a baseline plasma HIV RNA < 100 000 copies/ml, the mortality rate was statistically similar among patients with a baseline CD4 cell count > or = 200 cells/microl and a baseline plasma HIV RNA > or = 100 000 copies/ml (relative hazard, 1.21; 95% confidence interval, 0.89-1.65; P = 0.232). CONCLUSION: HIV RNA > or = 100 000 copies/ml was only associated with mortality among HIV-infected patients initiating HAART with CD4 cell counts > or= 200 cells/microl if the patients were non-adherent.     

Immunologic and virologic consequences of temporary antiretroviral treatment interruption in clinical practice

To determine the long-term immunologic and virologic effects of antiretroviral treatment interruptions, a retrospective analysis of an ongoing observational database was performed at a university HIV clinic. All patients who began highly active antiretroviral therapy (HAART) after January 1, 1996 and (1) were HAART experienced for >/=90 days, (2) had a treatment interruption (TI) for >/=30 days, (3) resumed HAART for >/=30 days, and (4) had CD4(+) cell counts performed pre- and post-TI were included. Main outcome measures included the following: Immunologic success was defined as a post-TI CD4(+) cell count >90% of the pre-TI CD4(+) cell count (post-TI/pre-TI, >90%). Virologic success was defined as a post-TI viral load (VL) less or equal to twice the pre-TI VL (post-TI/pre-TI, 相似文献   

The impact of highly active antiretroviral therapy (HAART) on visceral leishmaniasis in Spanish patients who are co-infected with HIV

Clinicians in Madrid have been observing and treating HIV-positive patients with visceral leishmaniasis (VL) for over a decade. As their records cover some of the co-infection cases that occurred before and after highly active antiretroviral therapy (HAART) was introduced into Spain, retrospective analysis of the records has allowed some of the effects of HAART on local VL to be determined. Encouragingly, HAART appears to have decreased the annual incidence of VL among local AIDS cases, from 4.81 cases/100 to just 0.8 case/100 (P <0.0005), a first episode of VL now appearing only when there is obvious HAART failure. Unfortunately, it does not seem to be very good at preventing VL relapses; within 24 months of antileishmanial treatment, 70% of patients who were receiving HAART had such relapses. The mean time between antileishmanial treatment and VL relapse was, however, longer when HAART was used than when it was not (20 v. 13 months). In those receiving HAART, relapses of the VL often occurred despite increasing CD4+ cell counts and undetectable HIV loads, indicating that successful treatment of the viral infection is insufficient to prevent the relapse of the leishmaniasis. These results are in general agreement with other observations made in Spain. VL relapses are possible and even frequent in HIV-positives who have no more than 200 CD4+ cells/microl, but secondary prophylaxis to prevent VL relapses may be safely suspended if a CD4+ count of >200 cells/microl can be maintained using HAART. VL also seems to hamper the immunological recovery of the HIV-positive, although HAART appears to have little effect on the clinical manifestations of VL.     

Polymorphisms of Cx(3)CR1 and CXCR6 receptors in relation to HAART therapy of HIV type 1 patients

The chemokine polymorphisms CXCR6-3E/K, In1.1T/C, H7 haplotype, CX(3)CR1-V249I, and CX(3)CR1-T280M have been shown to affect the course of HIV infection. We studied their influence on immunologic and virologic response to HAART in a group of 143 HIV-1 patients. We performed Kaplan-Meier analysis using the following end-point criteria: (1) time from HAART initiation to undetectable viral load (VL < 50 copies/ml), (2) maximum duration of viral suppression, (3) time from HAART administration until CD4 elevation above 200 cells/microl for patients with baseline CD4 below 200 cells/microl and above 500 cells/microl for patients with baseline CD4 between 200 and 500 cells/microl, respectively, and (4) time from HAART initiation until CD4 reduction below baseline values. Our results revealed an improved immunologic response to HAART in patients with the CX(3)CR1-249I or CX(3)CR1-280M allele. On the contrary, patients with initial VL suppression due to HAART showed a faster virologic failure in the presence of the CXCR6-3K allele. The In1.1T/C polymorphism and H7 haplotype did not reveal any specific effect on HAART response.     

Disease progression in patients with virological suppression in response to HAART is associated with the degree of immunological response

OBJECTIVE: To determine if immunological response is associated with disease progression in patients with virological suppression after initiating HAART. DESIGN: A cohort study of 1084 treatment-naive participants in the British Columbia HIV/AIDS Drug Treatment Program who had achieved viral loads < 500 copies/ml at 3-9 months after initiating triple-drug therapy. METHODS: Cox proportional hazards was used to model the association with disease progression of baseline variables, change in CD4 cell counts and CD4 cell count strata at 6 months. Logistic regression analysis was used to examine associations with two definitions of poor immunological response. RESULTS: Patients were followed for a median of 51.4 months. In univariate analyses, increases in CD4 cell counts of < 25 cells/microl and absolute CD4 cell counts of < 200 cells/microl were associated with an increased risk of death or new AIDS events. Two mulitivariate models, one including baseline CD4 cell count and change in CD4 cell count from baseline and the other including only absolute CD4 cell counts at 6 months, were found to predict disease progression in this setting. Increases in CD4 cell count of < 25 cells/microl were associated with increasing age and inversely associated with low baseline CD4 cell counts, high baseline viral loads and good adherence to therapy. CD4 cell counts of < 200 cells/microl at 6 months were associated with low baseline CD4 cell counts and having AIDS at baseline. CONCLUSION: Patients with virological suppression are still at risk for HIV disease progression if adequate immunological responses are not achieved.     

湖南省6558例HIV/AIDS病人HAART疗效及不良反应分析

目的了解湖南省开展艾滋病病毒（HIV）感染者/艾滋病（AIDS）病人（简称HIV/AIDS病人）高效抗反转录病毒治疗（HAART）的疗效、不良反应及耐药等情况。方法采用回顾性研究,对湖南省2003年9月至2012年12月间接受HAART的病例进行分析。结果共有6558例HIV/AIDS病人接受了HAART：1）CD＋4T淋巴细胞（简称CD4细胞）计数随治疗时间的延长明显升高,按照基线CD4细胞水平划分为≤99个/μL、100~199个/μL、200~350个/μL三组,然后做两两比较,差异有统计学意义（P〈0.01）。2）在治疗后7-12个月,64%的病人体内病毒复制得到了完全抑制,病毒载量检测值〈50拷贝/mL;在治疗后7-12个月,病毒载量〈50拷贝/mL的比例及病毒载量常用对数值lgVL变化幅度最大,12个月以后下降趋势减缓,约3年后进入平台期。3）服药后较常见的不良反应是胃口改变、恶心呕吐、皮疹及疲倦等,因不良反应更换治疗方案的病例占总换药病例的70.1%（1719/2451）,因不良反应停药占总停药病例的33.6%（178/529）。4）最近一次病毒载量检测〈50拷贝/mL的2739例病人中,连续2次CD4细胞计数较基线水平增幅〈20%,或治疗一年以上未达200个/μL的共375例,免疫无应答比例13.7%。5）2011及2012连续两年耐药监测显示,总耐药率为2.6%,处于较低水平。结论湖南省艾滋病HAART在免疫学和病毒学方面均取得了较好的疗效,需进一步加强不良反应、免疫无应答及耐药情况的监测和处理。     

Diagnostic accuracy of CD4 cell count increase for virologic response after initiating highly active antiretroviral therapy

OBJECTIVE: To derive and internally validate a clinical prediction rule for virologic response based on CD4 cell count increase after initiation of HAART in a resource-limited setting. DESIGN AND METHODS: A retrospective cohort study at two HIV care clinics in Gaborone, Botswana. The participants were previously treatment-naive HIV-1-infected individuals initiating HAART. The main outcome measure was a plasma HIV-1 RNA level (viral load) < or = 400 copies/ml (i.e. undetectable) 6 months after initiating HAART. RESULTS: The ability of CD4 cell count increase to predict an undetectable viral load was significantly better in those with baseline CD4 cell counts < or = 100 cells/microl [area under the ROC curve (AUC), 0.78; 95% confidence interval (CI), 0.67-0.89; versus AUC, 0.60; 95% CI, 0.48-0.71; P = 0.018]. The sensitivity, specificity, and positive and negative predictive values of a CD4 cell count increase of > or = 50 cells/microl for an undetectable viral load in those with baseline CD4 cell counts < or = 100 cells/microl were 93.1, 61.3, 92.5 and 63.3%, respectively. Alternatively, these values were 47.8, 87.1, 95.0 and 24.5%, respectively, if a increase in CD4 cell count of > or = 150 cells/microl was used. CONCLUSIONS: CD4 cell count increase after initiating HAART has only moderate discriminative ability in identifying patients with an undetectable viral load, and the predictive ability is higher [corrected] in patients with lower baseline CD4 cell counts. Although HIV treatment programs in resource-constrained settings could consider the use of CD4 cell count increases to triage viral load testing, more accurate approaches to monitoring virologic failure are urgently needed.     

艾滋病合并肺结核的影像学特征及其与CD4+T淋巴细胞的相关性

目的探讨艾滋病合并肺结核病的影像学特征及其与CD+4 T淋巴细胞的相关性.方法回顾性对照分析26例艾滋病晚期合并肺结核患者与60例单纯性肺结核患者的胸部X线表现、CD+4 T淋巴细胞的检测结果.结果 (1) 胸片结果显示艾滋病合并肺结核患者较单纯性肺结核患者出现较多淡片状模糊阴影(53.8%与8.3%;P<0.01)、粟粒结节影(23.1%与5.0%;P< 0.05)、胸内淋巴结肿大(34.6%与8.3%;P< 0.01)及肺外结核(23.1%与3.3%;P< 0.05),较少表现为上肺野或肺尖部病变(23.1%与76.7%;P<0.01)、实变或密度不均匀增高影(11.5%与71.7%;P< 0.01)、合并空洞影(7.7%与30.0%;P< 0.05);二者胸腔积液差异无统计学意义(11.5%与20.0%;P>0.05).(2)CD+4T淋巴细胞检测结果显示26例艾滋病合并肺结核患者与31例单纯性肺结核患者的CD+4 T淋巴细胞相对数分别为(5.0±6.4)%与(65.3±1.5)%,两者比较差异有统计学意义(P<0.01);26例艾滋病合并肺结核患者中,CD+4 T淋巴细胞计数<50个/μl的15例患者均为不典型肺结核,CD+4 T淋巴细胞计数为50～100个/μl的4例中,有3例为不典型肺结核,而4例CD+4T淋巴细胞计数为>100～200个/μl与2例>200个/μl的病例中,不典型肺结核分别为2与0例.结论艾滋病晚期患者影像表现多不典型,这与CD+4T淋巴细胞计数明显减低有关.因此了解艾滋病合并肺结核的影像特征与CD+4T淋巴细胞的相关性,对于艾滋病患者的早诊断、早治疗、早隔离具有重要的意义.     

Prognostic value of plasma HIV RNA among highly active antiretroviral therapy users

BACKGROUND: The study objective was to compare the prognostic value of plasma HIV RNA and CD4 cell count at baseline and as time-updated variables in highly active antiretroviral therapy (HAART) users for two outcomes: development of AIDS and change in CD4 cell count. METHODS: The study population comprised 387 men enrolled in the Multicenter AIDS Cohort Study who were AIDS-free and initiated HAART between 1996 and 2001. Follow-up until AIDS diagnosis (n=36, 9%) or the last AIDS-free visit was included. To determine the predictive value of combining HIV RNA and CD4 cell count, regression tree methods using recursive partitioning at pre-specified cut points for both variables were used. RESULTS: Low CD4 cell count was a strong predictor of AIDS among HAART users. However, HIV RNA showed strong prognostic value for AIDS development among those with CD4 cell counts > 250 x 10(6) cells/l, in whom an HIV RNA level > 1000 copies/ml carried a 4.6-fold greater risk of developing AIDS. HIV RNA < 5000 copies/ml was also predictive of subsequent increase in CD4 cell count with significantly higher increases among those with initial CD4 counts > 300 x 10(6) cells/l. CONCLUSION: Although, in HAART users, CD4 cell count was the primordial prognostic marker, an HIV RNA > 1000 copies/ml attained after HAART initiation was a strong predictor of the rate of subsequent CD4 cell count increase and of developing AIDS in patients whose CD4 cell counts were > 250 x 10(6) cells/l.