Wall Kristin M, Rida Wasima, Haddad Lisa B, Kamali Anatoli, Karita Etienne, Lakhi Shabir, Kilembe William, Allen Susan, Inambao Mubiana, Yang Annie H, Latka Mary H, Anzala Omu, Sanders Eduard J, Bekker Linda-Gail, Edward Vinodh A, Price Matt A
From the aDepartment of Epidemiology, Rollins School of Public Health, Laney Graduate School, Emory University, Atlanta, GA; bRwanda Zambia HIV Research Group, Department of Pathology & Laboratory Medicine, School of Medicine and Hubert Department of Global Health and the Department of Epidemiology, Rollins School of Public Health, Laney Graduate School, Emory University, Atlanta, GA; cBiostatistics Consultant, Arlington, VA; dDepartment of Gynecology and Obstetrics, Emory University, School of Medicine, Atlanta, GA; eMedical Research Council/Uganda Virus Research Unit, Research Unit on AIDS, Entebbe, Uganda; fRwanda Zambia HIV Research Group, Department of Pathology & Laboratory Medicine, School of Medicine and Hubert Department of Global Health and the Department of Epidemiology, Rollins School of Public Health, Laney Graduate School, Emory University, Kigali, Rwanda; gRwanda Zambia HIV Research Group, Department of Pathology & Laboratory Medicine, School of Medicine and Hubert Department of Global Health and the Department of Epidemiology, Rollins School of Public Health, Laney Graduate School, Emory University, Lusaka, Zambia; hRwanda Zambia HIV Research Group, Department of Pathology & Laboratory Medicine, School of Medicine and Hubert Department of Global Health and the Department of Epidemiology, Rollins School of Public Health, Laney Graduate School, Emory University, Ndola, Zambia; iDepartment of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY; jThe Aurum Institute, Johannesburg and Rustenburg, South Africa; kKenya AIDS Vaccine Initiative Institute of Clinical Research, University of Nairobi, Nairobi, Kenya; lCentre for Geographic Medicine-Coast/Kenya Medical Research Institute, Kilifi, Kenya; mUniversity of Oxford, Oxford, United Kingdom; nDesmond Tutu HIV Centre, University of Cape Town, Cape Town, Republic of South Africa; oSchool of Pathology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa; pInternational AIDS Vaccine Initiative, New York, NY; and qDepartment of Epidemiology and Biostatistics, University of California at San Francisco, San Francisco, CA.
Epidemiology. 2017 Mar;28(2):224-232. doi: 10.1097/EDE.0000000000000590.
Understanding associations between pregnancy and HIV disease progression is critical to provide appropriate counseling and care to HIV-positive women.
From 2006 to 2011, women less than age 40 with incident HIV infection were enrolled in an early HIV infection cohort in Kenya, Rwanda, South Africa, Uganda, and Zambia. Time-dependent Cox models evaluated associations between pregnancy and HIV disease progression. Clinical progression was defined as a single CD4 measurement <200 cells/μl, percent CD4 <14%, or category C event, with censoring at antiretroviral (ART) initiation for reasons other than prevention of mother-to-child transmission (PMTCT). Immunologic progression was defined as two consecutive CD4s ≤350 cells/μl or a single CD4 ≤350 cells/μl followed by non-PMTCT ART initiation. Generalized estimating equations assessed changes in CD4 before and after pregnancy.
Among 222 women, 63 experienced clinical progression during 783.5 person-years at risk (8.0/100). Among 205 women, 87 experienced immunologic progression during 680.1 person-years at risk (12.8/100). The association between pregnancy and clinical progression was adjusted hazard ratio [aHR] = 0.7; 95% confidence interval (CI): 0.2, 1.8. The association between pregnancy and immunologic progression was aHR = 1.7; 95% CI: 0.9, 3.3. Models controlled for age; human leukocyte antigen alleles A03:01, B45, B*57; CD4 set point; and HIV-1 subtype. CD4 measurements before versus after pregnancies were not different.
In this cohort, pregnancy was not associated with increased clinical or immunologic HIV progression. Similarly, we did not observe meaningful deleterious associations of pregnancy with CD4s. Our findings suggest that HIV-positive women may become pregnant without harmful health effects occurring during the pregnancy. Evaluation of longer-term impact of pregnancy on progression is warranted.
了解妊娠与艾滋病毒疾病进展之间的关联对于为艾滋病毒阳性女性提供适当的咨询和护理至关重要。
2006年至2011年,年龄小于40岁的新发艾滋病毒感染女性被纳入肯尼亚、卢旺达、南非、乌干达和赞比亚的早期艾滋病毒感染队列。时间依赖性Cox模型评估妊娠与艾滋病毒疾病进展之间的关联。临床进展定义为单次CD4测量值<200个细胞/微升、CD4百分比<14%或C类事件,因预防母婴传播(PMTCT)以外的原因开始抗逆转录病毒治疗(ART)时进行删失。免疫进展定义为连续两次CD4≤350个细胞/微升或单次CD4≤350个细胞/微升,随后因非PMTCT开始ART。广义估计方程评估妊娠前后CD4的变化。
在222名女性中,63名在783.5人年的风险期内经历了临床进展(8.0/100)。在205名女性中,87名在680.1人年的风险期内经历了免疫进展(12.8/100)。妊娠与临床进展之间的关联调整后风险比[aHR]=0.7;95%置信区间(CI):0.2, 1.8。妊娠与免疫进展之间의关联为aHR = 1.7;95%CI:0.9, 3.3の模型控制了年龄、人类白细胞抗原等位基因A03:01、B45、B*57、CD4设定点和艾滋病毒-1亚型づ。妊娠前后的CD4测量值没有差异。
在这个队列中,妊娠与艾滋病毒临床或免疫进展增加无关。同样,我们没有观察到妊娠与CD4之间有意义的有害关联です。我们的研究结果表明,艾滋病毒阳性女性在孕期可能怀孕而不会对健康产生有害影响。有必要评估妊娠对疾病进展的长期影响。