改进HIV感染儿童免疫状态动态的预测

V. B. Denisenko, E. M. Simovanyan
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摘要

目标是在考虑到临床和实验室检查结果的情况下,改善对艾滋病毒感染儿童免疫状态动态的预测。材料和方法。对81例中位年龄22个月(IQI四分位数间隔13 ~ 42个月)的HIV感染患儿进行临床、免疫学和分子遗传学检查。患者观察时间为Me 10个月(IQI 4-12个月)。根据世卫组织分级确定发生严重免疫抑制前的时间间隔。严重免疫抑制的标准是cd4淋巴细胞的绝对数量下降小于0.5 × 109/l,其相对数量-小于20%。为了确定影响严重免疫抑制发生率的因素,使用事件发生时间(生存期)和Cox比例强度的数学模型进行分析。结果。92.5%的32月龄儿童(IQI 17-54月龄)出现严重免疫抑制。在数学模型中对研究开始时的临床和实验室参数进行测试表明,多因子模型中的“HIV血液病毒载量为10万cop”指标证明了统计学意义(P = 0.011)。/ml或更多»(优势比或3.1;95%置信区间95% CI 1.9-10.2;P = 0.012),“巨细胞病毒感染的活动性形式”(OR 2.3;95% ci 1.2-7.8;P = 0.026),“活动性eb病毒感染”(OR 2.0;95% ci 1.1-4.6;P = 0.040)。结论。绝大多数艾滋病毒感染儿童(92.5%)在32个月(IQI 17-54个月)时出现严重的免疫抑制。影响严重免疫抑制发生时间的独立因素是HIV的高复制率以及巨细胞病毒感染和eb病毒感染的活动性形式。为了防止感染艾滋病毒的儿童免疫功能障碍的进展,不仅有必要尽早开抗逆转录病毒治疗,而且有必要及时诊断和治疗活动性疱疹病毒感染。
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Improving the prediction of the immune status state dynamics in children with HIV infection
The goal is to improve the prediction of the immune status state dynamics in children with HIV infection, taking into account the results of clinical and laboratory examination. Materials and methods. Clinical, immunological and molecular genetic examination was carried in 81 children with HIV infection at the age of median Me 22 months (interquartile interval of IQI 13—42 months). The duration of observation of patients was Me 10 months ( IQI 4—12 months). The time interval before the development of severe immunosuppression according to the WHO classification was determined. The criterion for severe immunosuppression was a decrease in the absolute number of CD4-lymphocytes less than 0.5 x 109/l, their relative number — less than 20%. To determine the factors influencing the rate of development of severe immunosuppression, mathematical models of the analysis of the time to the onset of the event (survival) and Cox proportional intensities were used. Results. Severe immunosuppression developed in 92.5% of children aged Me 32 months (IQI 17—54 months). Testing of clinical and laboratory parameters at the beginning of the study in mathematical models showed that statistical significance in the multifactorial model (P = 0.011) was demonstrated by the indicators «HIV blood viral load of 100 000 cop./ml or more» (odds ratio OR 3.1; 95% confidence interval 95% CI 1.9—10.2; P = 0.012), «Active form of cytomegalovirus infection» (OR 2.3; 95% CI 1.2—7.8; P = 0.026), «Active form of Epstein-Barr virus infection» (OR 2.0; 95% CI 1.1—4.6; P = 0.040). Conclusion. The vast majority of children with HIV infection (92.5%) at the age of Me 32 months ( IQI 17—54 months) developed severe immunosuppression. Independent factors that influenced the timing of severe immunosuppression development were the high rate of HIV replication and the presence of active forms of cytomegalovirus infection and Epstein-Barr virus infection. To prevent the progression of immunological disorders in children with HIV infection, it is necessary not only to prescribe antiretroviral therapy earlier, but also timely diagnosis and treatment of active forms of herpesvirus infections.
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