PubMed · 8157439
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P J Aggett, A Favier. 1993. Zinc.. https://pubmed.ncbi.nlm.nih.gov/8157439/
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BACKGROUND: A minority of blood donors are Rh(D)-negative, and Rh(D)-negative red blood cell (RBC) products are often overutilized. As such, Rh(D)-negative RBCs may be difficult to maintain in blood bank inventory. STUDY DESIGN AND METHODS: We changed our blood bank laboratory policy to approve non-alloimmunized Rh(D)-negative patients to receive Rh(D)-positive RBCs for routine transfusion under defined criteria. Those criteria included Rh(D)-negative males (all ages) and females (aged >50 years) who were designated as do not resuscitate (DNR), either with or without intubation, in the electronic medical record. RESULTS: From August 15, 2024 through August 15, 2025, a total of 204 Rh(D)-negative patients met the above criteria and were approved to receive routine Rh(D)-positive RBC transfusions. Within that group, 23 patients received Rh(D)-positive RBCs. The remaining patients either did not require transfusion or were issued Rh(D)-negative RBC units. Since implementing this practice, a total of 68 Rh(D)-negative units were conserved during this time frame. Notably, 28 of the 68 units (41%) were type O, Rh(D)-negative. DISCUSSION: Rh(D)-positive RBCs can be routinely given to non-alloimmunized Rh(D)-negative patients who are not at risk for developing hemolytic disease of the fetus and newborn (HDFN). By creating clear guidelines for the routine administration of Rh(D)-positive RBCs to patients who are not at risk for HDFN, the inventory of Rh(D)-negative RBC units can be directed to those patients who would most benefit from this limited resource.
In iron deficiency and lead poisoning, the enzyme ferrochelatase catalyzes the incorporation of zinc, instead of iron, into protoporphyrin IX, resulting in the formation of zinc protoporphyrin (ZPP). In healthy blood donors, there is a good inverse correlation between serum ferritin and ZPP levels. In renal failure patients and in patients with anemia caused by a variety of chronic disorders, two different types of iron deficiency are found: (a) absolute iron deficiency and (b) relative, or functional, iron deficiency. The latter occurs when iron, despite adequate stores, is not delivered rapidly enough to the erythroblasts. ZPP is not only indicative of absolute iron deficiency, but it is also, for now, the best indicator of iron-deficient erythropoiesis, along with the percentage of hypochromic red blood cells. By contrast, serum ferritin and transferrin saturation may not adequately assess functional iron deficiency. Elevated ZPP levels in renal failure patients can be caused by different pathogenetic mechanisms, such as chronic inflammatory disease, lead poisoning, and the presence of uremic factors, all of which could potentially inhibit heme biosynthesis. However, ZPP levels do not consistently predict an erythropoietic response to iron supplementation in maintenance hemodialysis patients, and thus, iron overload during i.v. iron supplementation cannot be detected by measuring ZPP.
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