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缺铁性贫血婴儿的眨眼频率比非贫血缺铁或铁充足婴儿慢。

Eye-blinking rates are slower in infants with iron-deficiency anemia than in nonanemic iron-deficient or iron-sufficient infants.

机构信息

Center for Human Growth and Development and; 4Department of Pediatrics and Communicable Diseases, University of Michigan, Ann Arbor, MI 48109, USA.

出版信息

J Nutr. 2010 May;140(5):1057-61. doi: 10.3945/jn.110.120964. Epub 2010 Mar 24.

Abstract

Iron deficiency has been shown to impair dopamine functioning in rodent models, but it is challenging to obtain evidence of such effects in human infants. Because spontaneous eye-blink rate may provide a noninvasive assessment of dopamine functioning, we hypothesized that eye-blink rate would be lower in infants with iron-deficiency anemia and would increase with iron therapy. A 4-min eye-blink assessment was conducted for quiet, alert infants sitting on their mother's lap. Data were available for 61 9- to 10-mo-old infants from inner-city Detroit (19 iron-deficient anemic, 23 nonanemic iron-deficient, and 19 nonanemic iron-sufficient). Iron-deficient and iron-sufficient nonanemic groups had similar eye-blink rates (P = 0.90) and were therefore combined. We used Poisson regression based on generalized estimation equation methodology to test for differences between iron-deficient anemic and nonanemic infants in blinks/min and change after 3 mo of iron therapy. Iron-deficient anemic infants had a lower initial eye-blink rate than nonanemic infants (mean +/- SD) (4.0 +/- 1.9 vs. 5.3 +/- 2.8 blinks/min; P = 0.02; effect size = 0.6 SD). At 12 mo, eye-blink rate increased by 2.1 blinks/min in the iron-deficient anemic group (P = 0.008); there was no change in the nonanemic group (P = 0.96). These results are consistent with reduced dopamine function in iron-deficient anemic infants. The clinical importance of a lower eye-blink rate is unclear, but impaired dopamine functioning is likely to have broader impact, given the role dopamine plays in regulating movement, motivation, cognition, and hormone release.

摘要

铁缺乏已被证明会损害啮齿动物模型中的多巴胺功能,但很难在人类婴儿中获得这种影响的证据。由于自发眨眼率可能提供多巴胺功能的非侵入性评估,我们假设铁缺乏性贫血婴儿的眨眼率会更低,并且随着铁治疗会增加。对于安静、警觉地坐在母亲腿上的 9-10 个月大的婴儿进行了 4 分钟的眨眼评估。数据可用于底特律市中心的 61 名 9-10 个月大的婴儿(19 名缺铁性贫血,23 名非贫血性缺铁,19 名非贫血性铁充足)。缺铁性贫血和铁充足的非贫血组的眨眼率相似(P=0.90),因此合并。我们使用基于广义估计方程方法的泊松回归来检验缺铁性贫血和非贫血婴儿在眨眼/分钟和 3 个月铁治疗后的变化之间的差异。与非贫血婴儿相比,缺铁性贫血婴儿的初始眨眼率较低(平均值 +/- 标准差)(4.0 +/- 1.9 vs. 5.3 +/- 2.8 眨眼/分钟;P=0.02;效应大小=0.6 SD)。在 12 个月时,缺铁性贫血组的眨眼率增加了 2.1 次/分钟(P=0.008);非贫血组没有变化(P=0.96)。这些结果与缺铁性贫血婴儿多巴胺功能降低一致。较低的眨眼率的临床重要性尚不清楚,但多巴胺功能受损可能会产生更广泛的影响,因为多巴胺在调节运动、动机、认知和激素释放方面发挥着作用。

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