University Department of Infectious and Tropical Diseases, University of Brescia and Spedali Civili General Hospital, Brescia, Italy.
University Department of Infectious and Tropical Diseases, Spedali Civili General Hospital, Brescia, Italy.
J Transl Med. 2017 Dec 19;15(1):256. doi: 10.1186/s12967-017-1358-6.
Anemia is frequent during HIV infection and is predictive of mortality. Although cART has demonstrated to reduce its prevalence, several patients still experience unresolved anemia. We aimed to characterize iron homeostasis and inflammation in HIV-infected individuals with mild anemia in relation to cART.
In this retrospective cohort study, HIV-infected patients with mild anemia, CD4 cells > 200/mm at baseline, maintaining virological response for 12 months after cART starting were selected within the Standardized Management of Antiretroviral Therapy Cohort (MASTER) cohort. Several inflammation and immune activation markers and iron homeostasis indexes were measured in stored samples, obtained at cART initiation (T0) and 12 months later (T1). Patients were grouped on the basis of hemoglobin values at T1: group A (> 13 g/dl) and B (< 13 g/dl). Wilcoxon rank sum test was used to compare biomarker values. Pearson correlation coefficients were calculated for all variables.
cART improved CD4 and CD8 cell counts and their ratio, but this effect was significant only in group A. Only these patients had mild iron deficiency at T0 and showed higher transferrin and lower percentage of transferrin saturation than patients of group B, but differences disappeared with cART. cART decreased inflammation in all patients, but group B had higher levels of all markers than group A, reaching statistical significance only for IL-8 values at T1 (16 vs 2.9 pg/ml; p = 0.017). Hepcidin and IL-6 levels did not show significant differences between groups. Hemoglobin levels both at T0 and T1 did not correlate with any marker.
Baseline mild anemia in HIV-infected patients cannot always be resolved with durable efficient cART, possibly due to residual inflammation or immune activation rather than unbalanced iron homeostasis. Further research is needed on cytokine profiling to understand the mechanisms that induce anemia in HIV with suppressive cART.
艾滋病病毒（HIV）感染期间常发生贫血，且贫血是死亡的预测因素。尽管高效抗逆转录病毒疗法（cART）已被证明可降低其发病率，但仍有部分患者存在未解决的贫血问题。我们旨在描述轻度贫血的 HIV 感染者的铁稳态和炎症特征，并与 cART 相关联。
在这项回顾性队列研究中，选择了标准管理抗逆转录病毒治疗队列（MASTER）中具有轻度贫血、基线时 CD4 细胞>200/mm、cART 开始后 12 个月保持病毒学反应的 HIV 感染患者。在 cART 开始时（T0）和 12 个月后（T1）收集储存样本，检测多种炎症和免疫激活标志物以及铁稳态指标。根据 T1 时的血红蛋白值将患者分为两组：A 组（>13g/dl）和 B 组（<13g/dl）。使用 Wilcoxon 秩和检验比较生物标志物值。计算所有变量的 Pearson 相关系数。
cART 改善了 CD4 和 CD8 细胞计数及其比值，但这种效果仅在 A 组中显著。仅这些患者在 T0 时存在轻度缺铁，并表现出比 B 组更高的转铁蛋白和更低的转铁蛋白饱和度百分比，但随着 cART 的应用，这些差异消失了。cART 降低了所有患者的炎症水平，但 B 组的所有标志物水平均高于 A 组，仅在 T1 时的白细胞介素-8（IL-8）值上达到统计学意义（16 比 2.9pg/ml；p=0.017）。Hepcidin 和 IL-6 水平在两组之间无显著差异。T0 和 T1 时的血红蛋白水平与任何标志物均无相关性。
HIV 感染者的基线轻度贫血在持续有效的 cART 治疗下并非总能得到解决，这可能是由于残留的炎症或免疫激活而不是不平衡的铁稳态所致。需要进一步进行细胞因子谱分析研究，以了解抑制性 cART 引起 HIV 贫血的机制。
