Leenstra Tjalling, Acosta Luz P, Langdon Gretchen C, Manalo Daria L, Su Li, Olveda Remigio M, McGarvey Stephen T, Kurtis Jonathan D, Friedman Jennifer F
International Health Institute, Brown University, Providence, RI 02903, USA.
Am J Clin Nutr. 2006 Feb;83(2):371-9. doi: 10.1093/ajcn/83.2.371.
Observational and interventional evidence supports a relation between human schistosomiasis and anemia; however, the exact causal mechanisms remain unclear. Eggs translocating across the intestinal or bladder wall may result in extracorporeal blood loss with subsequent iron deficiency. Alternatively, anemia may result from cytokine-mediated dyserythropoiesis, as seen in anemia of inflammation.
By evaluating the cross-sectional relation between the intensity of Schistosoma japonicum infection, hemoglobin concentration, and iron status in 7-30-y-old persons from S. japonicum-endemic rice-farming villages in the province of Leyte, Philippines, we assessed the relative contribution of iron deficiency and anemia of inflammation to schistosomiasis-associated anemia.
We enrolled 627 S. japonicum-infected and 111 S. japonicum-uninfected persons. We obtained stool samples to quantify S. japonicum infection and venous blood samples for hemograms and measures of iron status and inflammation.
Intensity of S. japonicum infection was independently associated with hemoglobin (beta = -0.24; 95% CI: -0.31, -0.17). Persons with high-intensity infection had a greater risk of iron deficiency anemia (adjusted prevalence odds ratio: 6.6; 95% CI: 2.9, 14.7), but there was no evidence of this relation in low-intensity infections. In contrast, anemia without iron deficiency was prevalent across all intensities (adjusted prevalence odds ratio: 3.8; 95% CI: 1.5, 9.5).
Storage iron deficiency is a major contributor to anemia in high-intensity S. japonicum infection. A high prevalence of anemia without iron deficiency, exclusion of other mechanisms of anemia, and the evidence of low bioavailable iron suggest that anemia of inflammation contributes to S. japonicum-associated anemia at all infection intensities.
观察性和干预性证据支持人类血吸虫病与贫血之间存在关联；然而，确切的因果机制仍不清楚。虫卵穿过肠壁或膀胱壁可能导致体外失血，继而引起缺铁。另外，贫血可能是由细胞因子介导的红细胞生成异常所致，如炎症性贫血。
通过评估菲律宾莱特省日本血吸虫病流行的水稻种植村7至30岁人群中日本血吸虫感染强度、血红蛋白浓度和铁状态之间的横断面关系，我们评估了缺铁和炎症性贫血对血吸虫病相关贫血症的相对影响。
我们招募了627名感染日本血吸虫的人和111名未感染日本血吸虫的人。我们采集粪便样本以量化日本血吸虫感染情况，并采集静脉血样本进行血常规检查以及检测铁状态和炎症指标。
日本血吸虫感染强度与血红蛋白独立相关（β=-0.24；95%置信区间：-0.31，-0.17）。高强度感染人群患缺铁性贫血的风险更高（调整后的患病率比值比：6.6；95%置信区间：2.9，14.7），但在低强度感染中未发现这种关联的证据。相比之下，无缺铁的贫血在所有感染强度中都很普遍（调整后的患病率比值比：3.8；95%置信区间：1.5，9.5）。
储存铁缺乏是高强度日本血吸虫感染中贫血的主要原因。无缺铁的贫血患病率高、排除其他贫血机制以及低生物利用度铁的证据表明，炎症性贫血在所有感染强度下都对日本血吸虫病相关贫血有影响。
