Development of a Plasma Zinc Concentration Cutoff to Identify Individuals with Severe Zinc Deficiency Based on Results from Adults Undergoing Experimental Severe Dietary Zinc Restriction and Individuals with Acrodermatitis Enteropathica
Development of a Plasma Zinc Concentration Cutoff to Identify Individuals with Severe Zinc Deficiency Based on Results from Adults Undergoing Experimental Severe Dietary Zinc Restriction and Individuals with Acrodermatitis Enteropathica
复制标题
DOI：
10.3945/jn.114.191585
复制
发表时间：
2014-08-01
影响因子：
4.2
通讯作者：
Brown, Kenneth H.
中科院分区：
文献类型：
--
作者：
Wessells, K. Ryan;King, Janet C.;Brown, Kenneth H.
血浆锌浓度（PZC）是一个推荐的生物标志物，以评估锌状态和锌缺乏的风险在人群中。然而，PZC和缺锌的临床症状之间的关系仍然不确定。进行这些分析以评估PZC与缺锌临床体征之间的关系，并确定PZC的截止值，低于该截止值的个体具有与缺锌相关的临床体征的可能性增加。对PubMed、Embase、CINAHL Plus和EBSCO中索引的文献进行了电子书目检索，并与成人实验性锌耗竭研究以及儿童和成人（年龄< 1个月-43岁）肠病性肢端皮炎（AE）病例报告相关。提取的数据包括人口统计学特征，PZCs，以及是否存在可能与锌缺乏相关的临床体征（例如，例如，在一个实施例中，皮炎、腹泻）。与无症状者相比，出现临床症状的严重限锌饮食（< 1 mg Zn/d）成人的平均PZC显著较低（36.0 +/- 16.8 vs. 67.9 +/- 13.3 μ g/dL，P < 0.034）。同样，AE患者有症状时的平均PZC低于无症状时的治疗后PZC（38.2 +/- 20.7 vs. 102 +/- 34.7 mg/dL，P < 0.01）。在限制饮食锌摄入的个体中，当使用50 μ g/dL的临界值时，PZC预测临床体征的灵敏度为82%，特异性为92%。在AE患者中，当应用50 mg/dL的临界值时，PZC预测临床体征的灵敏度为80%，特异性为89%。这些分析表明，在经历饮食锌限制期的假定健康个体中，以及在患有AE的个体中，PZC与存在与锌缺乏相关的临床体征之间存在明确的关系，进一步验证了PZC作为严重锌缺乏的生物标志物的有用性。
Plasma zinc concentration (PZC) is a recommended biomarker to assess zinc status and the risk of zinc deficiency in populations. However, the relation between PZC and clinical signs of zinc deficiency remains uncertain. These analyses were conducted to evaluate the relation between PZC and clinical signs of zinc deficiency and to determine a cutoff for PZC below which individuals would have an increased likelihood of having clinical signs associated with zinc deficiency. Electronic bibliographic searches were conducted of literature indexed in PubMed, Embase, CINAHL Plus, and EBSCO and related to experimental zinc depletion studies in adults and case reports in children and adults (ages < 1 mo-43 y) with acrodermatitis enteropathica (AE). Data extracted included demographic characteristics, PZCs, and the presence or absence of clinical signs likely associated with zinc deficiency (e. g., dermatitis, diarrhea). Mean PZC was significantly lower among adults consuming severely zinc-restricted diets (< 1 mg Zn/d) who developed clinical signs compared with those who remained asymptomatic (36.0 +/- 16.8 vs. 67.9 +/- 13.3 mu g/dL, P < 0.034). Likewise, patients with AE had a lower mean PZC when symptomatic compared with post-treatment PZC when they were asymptomatic (38.2 +/- 20.7 vs. 102 +/- 34.7 mg/dL, P < 0.01). Among individuals with restricted dietary zinc intake, PZC predicted clinical signs with 82% sensitivity and 92% specificity when using a cutoff of 50 mu g/dL. Among individuals with AE, PZC predicted clinical signs with 80% sensitivity and 89% specificity when applying a cutoff of 50 mg/dL. These analyses demonstrate a clear relation between PZC and the presence of clinical signs associated with zinc deficiency among presumably healthy individuals undergoing periods of dietary zinc restriction, as well as in individuals with AE, further validating the usefulness of PZC as a biomarker of severe zinc deficiency.