Pathophysiology of intensive care unit-acquired anemia 英文参考文献.docVIP

Available online /content/8/S2/S9 Review Pathophysiology of intensive care unit-acquired anemia Mitchell P Fink Watson Professor of Surgery, Anesthesiology and Critical Care Medicine, University of Pittsburgh Medical School, Pittsburgh, Pennsylvania, USA Correspondence: Mitchell P Fink, finkmp@ Published online: 14 June 2004 Critical Care 2004, 8(Suppl 2):S9-S10 (DOI 10.1186/cc2410) This article is online at /content/8/S2/S9 ? 2004 BioMed Central Ltd Abstract The formation of red blood cells (RBCs) in the bone marrow is regulated by erythropoietin in response to a cascade of events. Anemia in the intensive care unit can be caused by a host of factors. Patients in the intensive care unit may have decreased RBC production and a blunted response to erythropoietin. Administration of recombinant human erythropoietin may stimulate erythropoiesis, increase hematocrit levels and hemoglobin concentration, and reduce the need for RBC transfusions. Keywords anemia, erythropoietin, intensive care unit, recombinant erythropoietin Anemia is a common problem in intensive care unit (ICU) patients. Included among the numerous factors that may con- tribute to the development of anemia in critically ill patients are the following. called hypoxia-inducible factor (HIF)-1 [7]. First identified by Semenza and Wang [8], HIF-1 is a heterodimeric transcrip- tion factor composed of a hypoxia-inducible HIF-1α chain and a constitutively expressed HIF-1β chain. Although mRNA for HIF-1α is expressed at relatively high levels in normoxic cells, HIF-1α protein is present at extremely low levels under these conditions. In normoxic cells, newly synthesized HIF-1α is subjected to polyubiquitination and targeted for degradation in proteosomes. Thus, the half-life for this protein is very short, and its concentration under normoxic conditions is low. However, when cells become hypoxic, polyubiquitinization of nascent HIF-1