Burack J H, Barrett D C, Stall R D, Chesney M A, Ekstrand M L, Coates T J
AIDS Program, San Francisco General Hospital, CA.
JAMA. 1993 Dec 1;270(21):2568-73.
To investigate whether high levels of depressive symptomatology at baseline predict more rapid decline of CD4 lymphocyte counts and progression of clinical disease in persons infected with the human immunodeficiency virus (HIV).
Prospective cohort study with semiannual data collection waves and up to 66 months of follow-up.
Population-based probability sample of single men in areas of San Francisco with high case rates of the acquired immunodeficiency syndrome (AIDS).
All 330 homosexual or bisexual men who by January 1985 had serological evidence of HIV infection but had not had an AIDS diagnosis. Analysis of CD4 lymphocyte change was performed for 277 subjects (83.9%) who had three or more CD4 lymphocyte counts recorded during the study period January 1985 through July 1990.
Depressive symptoms were assessed using the Center for Epidemiologic Studies-Depression scale (CES-D). All subjects were classified according to two indicators of depression: (1) as overall depressed using a cut point of 16 or higher on the complete CES-D, and (2) as affectively depressed using a cut point of more than 1 SD above the mean on a subscale of the CES-D measuring affective depression. Laboratory and symptom measures, antiretroviral use, demographics, and behavioral measures were also used. The primary outcome measure was the rate of change of the CD4 lymphocyte count. Secondary outcomes were AIDS-free survival and mortality.
At baseline 65 subjects (19.7%) were classified as depressed on the overall scale and 53 (16.1%) were classified as depressed on the affective scale. The unadjusted mean rate of CD4 change was 38% greater for overall depressed subjects than for the overall nondepressed (-0.0812 vs -0.0588 x 10(9)/L [-81.2 vs -58.8/microL per year; P = .07) and 34% greater for affectively depressed subjects than for the affectively nondepressed (-0.0804 vs -0.0598 x 10(9)/L per year; P = .06). In hierarchical multivariate analysis controlling for antiretroviral use, symptoms, and other predictors, baseline overall depression was associated with an excess decline in CD4 count of -0.0285 x 10(9)/L per year (95% confidence interval, -0.0496 to -0.0073), and baseline affective depression was associated with an excess decline in CD4 count of -0.0236 x 10(9)/L per year (95% confidence interval, -0.0464 to -0.0008). Neither overall depression nor affective depression was significantly associated with earlier AIDS diagnosis or earlier mortality.
Overall depression and affective depression predicted a more rapid decline in CD4 lymphocyte counts; this association was not attributable to baseline physiological differences. While the mechanism of the association remains unknown and cannot be addressed directly by this study, the data suggest that it can be explained neither as simply a reflection of perceived somatic symptoms nor as the result of differences in recreational drug and alcohol use. Further study is necessary to determine whether treating depression can alter the course of HIV infection.
研究基线时高水平的抑郁症状是否能预测感染人类免疫缺陷病毒(HIV)者的CD4淋巴细胞计数更快下降以及临床疾病进展。
前瞻性队列研究,每半年收集一次数据,随访长达66个月。
在旧金山获得性免疫缺陷综合征(AIDS)发病率高的地区,基于人群的单身男性概率样本。
截至1985年1月,所有330名有HIV感染血清学证据但未被诊断为AIDS的同性恋或双性恋男性。对1985年1月至1990年7月研究期间有三次或更多次CD4淋巴细胞计数记录的277名受试者(83.9%)进行了CD4淋巴细胞变化分析。
使用流行病学研究中心抑郁量表(CES-D)评估抑郁症状。所有受试者根据两个抑郁指标进行分类:(1)使用完整CES-D量表上16分或更高的切点判定为总体抑郁;(2)使用CES-D量表中测量情感抑郁的子量表上高于均值1个标准差以上的切点判定为情感抑郁。还使用了实验室和症状指标、抗逆转录病毒药物使用情况、人口统计学和行为指标。主要观察指标是CD4淋巴细胞计数的变化率。次要观察指标是无AIDS生存期和死亡率。
在基线时,65名受试者(19.7%)在总体量表上被判定为抑郁,53名(16.1%)在情感量表上被判定为抑郁。总体抑郁受试者的未调整CD4变化平均率比总体非抑郁受试者高38%(-0.0812 vs -0.0588×10⁹/L [-81.2 vs -58.8/μL每年;P = 0.07]),情感抑郁受试者的未调整CD4变化平均率比情感非抑郁受试者高34%(-0.0804 vs -0.0598×每年10⁹/L;P = 0.06)。在控制抗逆转录病毒药物使用、症状和其他预测因素的分层多变量分析中,基线总体抑郁与CD4计数每年额外下降-0.0285×10⁹/L相关(95%置信区间,-0.0496至-0.0073),基线情感抑郁与CD4计数每年额外下降-0.0236×10⁹/L相关(95%置信区间,-0.0464至-0.0008)。总体抑郁和情感抑郁均与更早的AIDS诊断或更早的死亡率无显著关联。
总体抑郁和情感抑郁预示着CD4淋巴细胞计数下降更快;这种关联并非归因于基线生理差异。虽然这种关联的机制尚不清楚,本研究也无法直接解决,但数据表明,它既不能简单地解释为对躯体症状的感知反映,也不能解释为娱乐性药物和酒精使用差异的结果。需要进一步研究以确定治疗抑郁是否能改变HIV感染的病程。