*Department of Medicine, University of Washington, Seattle, WA; †Department of Medicine, University of Pittsburgh, Pittsburgh, PA; ‡Department of Medicine, University of California, Los Angeles, Los Angeles, CA; §Department of Medicine, Atlanta Veterans Affairs Medical Center (VAMC) and Emory University, Atlanta, GA; ‖Department of Medicine, West Los Angeles VAMC and David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA; ¶Department of Medicine, James J. Peters Bronx VAMC, Bronx, NY; #Department of Medicine, Michael E. DeBakey Houston VAMC and Baylor College of Medicine, Houston, TX; **Department of Medicine, University of California, San Francisco, San Francisco, CA; ††Department of Medicine, Clinical Trials and Survey Corporation, Owings Mills, MD; ‡‡Department of Medicine, Ohio State University Medical Center, Columbus, OH; §§Department of Medicine, Johns Hopkins University, Baltimore, MD; ‖‖Department of Medicine, New York University School of Medicine, New York, NY; ¶¶Departments of Infectious Diseases and Microbiology; and Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA; and ##Departments of Medicine and Immunology, University of Pittsburgh, Pittsburgh, PA.
J Acquir Immune Defic Syndr. 2013 Nov 1;64(3):271-8. doi: 10.1097/QAI.0b013e3182a9215a.
Prior studies comparing abnormalities in pulmonary function between HIV-infected and HIV-uninfected persons in the current era are limited.
To determine the pattern and severity of impairment in pulmonary function in HIV-infected compared with HIV-uninfected individuals.
Cross-sectional analysis of 300 HIV-infected men and 289 HIV-uninfected men enrolled from 2009 to 2011 in 2 clinical centers of the Lung HIV Study. Participants completed pre- and postbronchodilator spirometry, diffusing capacity of the lung for carbon monoxide (DLCO) measurement, and standardized questionnaires.
Most participants had normal airflow; 18% of HIV-infected and 16% of HIV-uninfected men had airflow obstruction. The mean percent predicted DLCO was 69% in HIV-infected vs. 76% in HIV-uninfected men (P < 0.001). A moderately to severely reduced DLCO of ≤60% was observed in 30% of HIV-infected compared with 18% of HIV-uninfected men (P < 0.001), despite the fact that 89% of those with HIV were on antiretroviral therapy. A reduced DLCO was significantly associated with HIV and CD4 cell count in linear regression adjusting for smoking and other confounders. The DLCO was lowest in HIV-infected men with CD4 cell counts <200 cells per microliter compared with those with CD4 cell counts ≥200 cells per microliter and to HIV-uninfected men. Respiratory symptoms of cough, phlegm and dyspnea were more prevalent in HIV-infected patients particularly those with abnormal pulmonary function compared with HIV-uninfected patients.
HIV infection is an independent risk factor for reduced DLCO, particularly in individuals with a CD4 cell count below 200 cells per microliter. Abnormalities in pulmonary function among HIV-infected patients manifest clinically with increased respiratory symptoms. Mechanisms accounting for the reduced DLCO require further evaluation.
当前时代,比较 HIV 感染者和 HIV 未感染者肺部功能异常的研究有限。
确定 HIV 感染者与 HIV 未感染者相比肺部功能受损的模式和严重程度。
对 2009 年至 2011 年间在 2 个肺部 HIV 研究临床中心入组的 300 名 HIV 感染者和 289 名 HIV 未感染者进行横断面分析。参与者完成了支气管扩张剂后肺量计检查、一氧化碳弥散量(DLCO)测定和标准化问卷。
大多数参与者气流正常;18%的 HIV 感染者和 16%的 HIV 未感染者存在气流阻塞。HIV 感染者的平均预测 DLCO 为 69%,而 HIV 未感染者为 76%(P<0.001)。尽管 89%的 HIV 感染者正在接受抗逆转录病毒治疗,但仍有 30%的 HIV 感染者出现了中度至重度 DLCO 降低(≤60%),而 HIV 未感染者为 18%(P<0.001)。在校正了吸烟和其他混杂因素后,DLCO 降低与 HIV 和 CD4 细胞计数呈线性相关。在 CD4 细胞计数<200 个/微升的 HIV 感染者中,DLCO 最低,与 CD4 细胞计数≥200 个/微升的 HIV 感染者和 HIV 未感染者相比均显著降低。与 HIV 未感染者相比,HIV 感染者的咳嗽、咳痰和呼吸困难等呼吸症状更为常见,特别是那些存在肺部功能异常的患者。
HIV 感染是 DLCO 降低的独立危险因素,特别是在 CD4 细胞计数<200 个/微升的个体中。HIV 感染者的肺部功能异常在临床上表现为呼吸症状增加。需要进一步评估导致 DLCO 降低的机制。