Schistosoma japonicum reinfection after praziquantel treatment causes anemia associated with inflammation
Schistosoma japonicum reinfection after praziquantel treatment causes anemia associated with inflammation
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DOI：
10.1128/iai.00757-06
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发表时间：
2006-11-01
影响因子：
3.1
通讯作者：
Friedman, Jennifer F.
中科院分区：
文献类型：
--
作者：
Leenstra, Tjalling;Coutinho, Hannah M.;Friedman, Jennifer F.
血吸虫病和贫血之间存在联系，尽管其程度和确切机制尚不清楚。在一项来自菲律宾Leyte的580名7- 30岁日本血吸虫感染患者的队列研究中，我们评估了吡喹酮治疗后日本血吸虫再感染对平均血红蛋白水平、缺铁性贫血（IDA）和非缺铁性贫血（NIDA）以及炎症标志物的影响。所有参与者在基线时接受治疗，每3个月随访一次，共18个月。在每次随访中，参与者提供粪便以量化再感染，并提供静脉血样本用于血象和铁状态和炎症的测量。18个月后，日本血吸虫再感染患者的平均血红蛋白水平较低（-0.39 g/dl； 95%可信区间[95% CI]， -0.63至-0.16），全因贫血的发生率是未再感染患者的1.70倍（95% CI， 1.10至2.61）。再感染仅在高再感染强度时与IDA相关。相反，在所有感染强度下，再感染均与NIDA相关。再感染与血清白细胞介素-6反应相关（P < 0.01），且与NIDA相关（P = 0.019），与IDA无关（P = 0.29）。本研究结果为日本血吸虫感染与贫血之间的因果关系提供了强有力的证据。快速再感染个体对血红蛋白的治疗效果与非再感染个体不同。日本血吸虫相关贫血的主要机制是促炎细胞因子介导的贫血，铁缺乏在高强度感染中起作用。基于提出的机制，贫血不太可能仅通过铁治疗得到改善。
There is a relationship between schistosomiasis and anemia, although the magnitude and exact mechanisms involved are unclear. In a cohort of 580 Schistosoma japonicum-infected 7- to 30-year-old patients from Leyte, The Philippines, we evaluated the impact of reinfection with S.japonicum after treatment with praziquantel on the mean hemoglobin level, iron-deficiency (IDA) and non-iron-deficiency anemia (NIDA), and inflammatory markers. All participants were treated at baseline and followed up every 3 months for a total of 18 months. At each follow-up, participants provided stools to quantify reinfection and venous blood samples for hemograms and measures of iron status and inflammation. After 18 months, reinfection with S.japonicum was associated with a lower mean hemoglobin level (-0.39 g/dl; 95% confidence interval [95% CI], -0.63 to -0.16) and 1.70 (95% CI, 1.10 to 2.61) times higher odds of all-cause anemia than those without reinfection. Reinfection was associated with IDA for high reinfection intensities only. Conversely, reinfection was associated with NIDA for all infection intensities. Reinfection was associated with serum interieukin-6 responses (P < 0.01), and these responses were associated with NIDA (P = 0.019) but not with IDA (P = 0.29). Our results provide strong evidence for the causal relationship between S.japonicurn infection and anemia. Rapidly reinfected individuals did not have the positive treatment effect on hemoglobin seen in nonreinfected individuals. The principle mechanism involved in S.japonicum-associated anemia is that of proinflammatory cytokine-mediated anemia, with iron deficiency playing a role in high-intensity infections. Based on the proposed mechanism, anemia is unlikely to be ameliorated by iron therapy alone.