Hypotensive Transfusion Reactions Research Articles

Acute Hypotensive Transfusion Reactions

Acute Hypotensive Transfusion Reactions

Bradykinin metabolism and hypotensive transfusion reactions.

TransfusionVolume 41, Issue 1 p. 136-150 Bradykinin metabolism and hypotensive transfusion reactions Melanie Cyr, Melanie Cyr From the Faculty of Pharmacy, University of Montréal, Montréal, Québec, Canada.Search for more papers by this authorTed Eastlund, Ted Eastlund From the Faculty of Pharmacy, University of Montréal, Montréal, Québec, Canada.Search for more papers by this authorCharles Blais Jr., Charles Blais Jr. From the Faculty of Pharmacy, University of Montréal, Montréal, Québec, Canada.Search for more papers by this authorJean Lucien Rouleau, Jean Lucien Rouleau From the Faculty of Pharmacy, University of Montréal, Montréal, Québec, Canada.Search for more papers by this authorAlbert Adam, Albert Adam From the Faculty of Pharmacy, University of Montréal, Montréal, Québec, Canada.Search for more papers by this author Melanie Cyr, Melanie Cyr From the Faculty of Pharmacy, University of Montréal, Montréal, Québec, Canada.Search for more papers by this authorTed Eastlund, Ted Eastlund From the Faculty of Pharmacy, University of Montréal, Montréal, Québec, Canada.Search for more papers by this authorCharles Blais Jr., Charles Blais Jr. From the Faculty of Pharmacy, University of Montréal, Montréal, Québec, Canada.Search for more papers by this authorJean Lucien Rouleau, Jean Lucien Rouleau From the Faculty of Pharmacy, University of Montréal, Montréal, Québec, Canada.Search for more papers by this authorAlbert Adam, Albert Adam From the Faculty of Pharmacy, University of Montréal, Montréal, Québec, Canada.Search for more papers by this author First published: 21 April 2002 https://doi.org/10.1046/j.1537-2995.2001.41010136.xCitations: 65 Address for reprint requests: Albert Adam, PhD, Faculté de pharmacie, Université de Montréal, 2900, Boul. Édouard-Montpetit, C.P. 6128, Succursale Centre-Ville, Montréal, H3C 3J7, Canada; e-mail: adama@pharm.umontreal.ca. Supported in part by the Fonds de la recherche en santé du Québec (CBJr). Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume41, Issue1January 2001Pages 136-150 RelatedInformation

Hypotensive Reactions Associated with Platelet Transfusion Through Leukocyte Reduction Filters

This article reports a case of hypotensive reaction following platelet transfusion (PT) and presents a possible etiologic mechanism implicating negatively charged leukocyte reduction filters (LRFs) and angiotensin converting enzyme (ACE) inhibitors. A 14-year-old boy with acute lymphoblastic leukemia was admitted to the pediatric intensive care unit (PICU) for respiratory failure following bone marrow transplantation. He was being treated with ACE inhibitors and was hemodynamically stable. He received a PT with a negatively charged bedside LRF the day his ACE inhibitor dose was doubled. His blood pressure (BP) dropped from 106/65 to 75/45. The PT was stopped and his BP was stabilized with a bolus of cristalloid. The same PT was restarted using a macroaggregate filter and his BP remained stable. This reaction was characterized by severe and isolated hypotension. It occurred while using a negatively charged bedside LRF in a patient who had a recent increase in ACE inhibitor therapy. The reaction did not recur when the LRF was replaced by a macroaggregate filter. This case provides further evidence to support the hypothesis that the use of negatively charged LRF may lead to hypotensive transfusion reactions in some patients. Bradykinin, which is generated when plasma is exposed to a negatively charged surface, and whose metabolism is decreased by ACE inhibitors, may play a role in these reactions.

Anomaly of the des-Arg9-bradykinin metabolism associated with severe hypotensive reactions during blood transfusions: a preliminary study.

Severe hypotensive reactions have been described after the transfusion of platelets or red cells through negatively-charged bedside white cell-reduction filters. The possibility of a role for bradykinin (BK) in the genesis of these reactions has been raised. To understand if an anomaly of BK metabolism is associated with these reactions, the metabolism of BK and des-Arg9-BK was studied in the sera of four patients who presented with a severe hypotensive transfusion reaction. Tests were performed in the absence and the presence of complete in vitro inhibition of angiotensin-converting enzyme (ACE) activity by enalaprilat. In the presence of ACE inhibition (enalaprilat), the half-life (t1/2) of BK measured in the sera of patients who presented with a severe hypotensive transfusion reaction (361 +/- 90 sec) was not significantly different from that measured in the sera of normal controls (249 +/- 16 sec). In the presence of ACE inhibition (enalaprilat), the t1/2 of des-Arg9-BK was significantly greater in patients who presented with a severe hypotensive transfusion reaction (1549 +/- 319 sec) than in normal controls (661 +/- 38 sec) (p < 0.001). A metabolic anomaly mainly affecting the degradation of des-Arg9-BK could be responsible for its accumulation in vivo. Des-Arg9-BK could be responsible, at least in part, for severe hypotensive transfusion reactions.

Activation of the contact system by filtration of platelet concentrates with a negatively charged white cell-removal filter and measurement of venous blood bradykinin level in patients who received filtered platelets.

Several recent reports have described hypotensive transfusion reactions in patients receiving platelet concentrates (PCs) filtered through white cell-reduction filters. It is well known that a negatively charged surface activates the contact system, consisting of factor XII, prekallikrein, and high-molecular-weight kininogen. To clarify the mechanisms of these hypotensive reactions, the possibility that white cell-reduction filtration activates the contact system was examined. Venous blood plasma bradykinin levels were also measured in patients receiving PC transfusions through filters. None of the measured values were changed by filtration through a positively charged filter. However, filtration through a negatively charged filter resulted in a decrease in the amounts of prekallikrein and an increase in the amount of bradykinin generated, which indicated the activation of the contact system. The bradykinin level was inversely related to the activity of angiotensin-converting enzyme (ACE) in the PCs and was elevated by addition of an ACE inhibitor. Although the venous blood plasma bradykinin level did not change in two patients with a normal ACE activity during PC transfusion through the negatively charged filter, two patients who had decreased ACE activity, showed a significant increase in bradykinin during the transfusion. These results suggest that the generation of a large amount of bradykinin by filtration of PCs through a negatively charged filter might cause hypotensive reactions in patients with decreased ACE activity. The clinical significance of bradykinin generation requires further study.