A severe anaphylactoid reaction during Cascade Filtration in a patient receiving ACE inhibitors

Mazzi, Giorgio; Govoni, Maurizio; Raineri, Antonino; Santarossa, Liliana; Roia, Dina De; Orazi, B M

doi:10.1016/0955-3886(94)90060-4

Cited by 9 publications

(6 citation statements)

References 13 publications

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“…Patients taking ACE inhibitors have been reported to have anaphylactoid reactions-characterized by flushing, hypotension, bradycardia, and dyspnea-during on-line extracorporeal manipulation of blood or separated plasma (hemodialysis, plasma exchange, Staphylococcal protein A affinity absorption, and low density lipoprotein apheresis [23,24]. These reactions appear to be mediated by bradykinin.…”

Section: Angiotensin-converting Enzyme Inhibitorsmentioning

confidence: 94%

Mechanisms of adverse effects during hemapheresis

Strauss

1996

J. Clin. Apheresis

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Section: Angiotensin-converting Enzyme Inhibitorsmentioning

confidence: 94%

Mechanisms of adverse effects during hemapheresis

Strauss

1996

J. Clin. Apheresis

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“…These protein increments in response to anaphylaxis suggest that the endothelium present a dual role not only a prothrombotic state in the anaphylactic reactions but also as an anticoagulant active surface. The activation of PLMN, the main molecule involved in fibrinolysis, has been previously correlated with hypotension during anaphylaxis (60)(61)(62). Accordingly, PLMN and two of its activator proteins were identified in EC-anaphylaxis: CXCL7 and HABP2.…”

Section: Discussionmentioning

confidence: 91%

Proteomic and Biological Analysis of an In Vitro Human Endothelial System in Response to Drug Anaphylaxis

et al. 2021

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Anaphylaxis is a life-threatening systemic hypersensitivity reaction. During anaphylaxis, mediator release by effector cells causes endothelial barrier breakdown, increasing vascular permeability and leakage of fluids, which may lead to tissue edema. Although endothelial cells (ECs) are key players in this context, scant attention has been paid to the molecular analysis of the vascular system, and further analyses of this cell type are necessary, especially in humans. The protein expression pattern of human microvascular ECs was analyzed in response to sera from anaphylactic patients (EC-anaphylaxis) and sera from non-allergic subjects (EC-control) after 2 hours of contact. Firstly, a differential quantitative proteomic analysis of the protein extracts was performed by mass spectrometry using an isobaric labeling method. Second, the coordinated behavior of the identified proteins was analyzed using systems biology analysis (SBA). The proteome of the EC-anaphylaxis system showed 7,707 proteins, of which 1,069 were found to be significantly altered between the EC-control and EC-anaphylaxis groups (p-value < 0.05). Among them, a subproteome of 47 proteins presented a high rate of change (|ΔZq| ≥ 3). This panel offers an endothelial snapshot of the anaphylactic reaction. Those proteins with the highest individual changes in abundance were hemoglobin subunits and structural support proteins. The interacting network analysis of this altered subproteome revealed that the coagulation and complement systems are the main biological processes altered in the EC-anaphylactic system. The comprehensive SBA resulted in 5,512 functional subcategories (biological processes), 57 of which were significantly altered between EC-control and EC-anaphylaxis. The complement system, once again, was observed as the main process altered in the EC system created with serum from anaphylactic patients. Findings of the current study further our understanding of the underlying pathophysiological mechanisms operating in anaphylactic reactions. New target proteins and relevant signaling pathways operating in the in vitro endothelial-serum system have been identified. Interestingly, our results offer a protein overview of the micro-EC-anaphylaxis environment. The relevance of the coagulation, fibrinolytic, contact and complement systems in human anaphylaxis is described. Additionally, the untargeted high-throughput analysis used here is a novel approach that reveals new pathways in the study of the endothelial niche in anaphylaxis.

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“…It was recently demonstrated that negatively (and sometimes positively) charged materials may induce activation of the prekallikrein‐BK cascade through activation of coagulation Factor XII (Hageman) during blood component transfusion or apheresis procedures [9,11]. This results in severe and sometimes life‐threatening situations, mainly in patients given ACE inhibitors as hypertension treatment, owing to blockade of the physiological activity of ACE as a kininase II [4–7]. We therefore investigated possible BK production during donor plasmapheresis procedures performed in a small group of volunteer donors, some of whom were taking ACE inhibitors.…”

Section: Discussionmentioning

confidence: 99%

“…Blood contact with artificial materials used in extracorporeal circuits for the removal of metabolites or toxins, collection of blood components or intraoperative blood salvage, may induce blood cell and humoral activation [1–3]. The issue of biocompatibility of artificial substances has therefore been questioned in recent years by several reports dealing with the onset of severe and sometimes life‐threatening side‐effects in patients undergoing extracorporeal plasma treatment [4–6], intraoperative blood salvage [7], therapeutic apheresis procedures [8,9] or even receiving bedside‐filtered platelet units [10]. With regard to this latter point, it has been demonstrated that materials made of polyvinyl chloride (PVC) coated with a negatively charged surface, may trigger activation of coagulation Factor XII (Hageman factor), with the subsequent production of kallikrein and further cleavage of high‐molecular‐weight kininogen (HMWK), resulting in the generation of bradykinin (BK) [11].…”

Section: Introductionmentioning

confidence: 99%

Bradykinin production during donor plasmapheresis procedures

et al. 2001

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Donors taking ACE inhibitors and undergoing plasmapheresis showed higher levels of BK compared to the control group. Furthermore, the detection of BK in plasma units after a freeze-thaw procedure might explain the sudden hypotensive reaction occurring during therapeutic plasma exchange when plasmapheresis units are adopted as substitution fluids. Further investigations are needed to assess the real clinical importance of the presence of BK in plasma units.

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A severe anaphylactoid reaction during Cascade Filtration in a patient receiving ACE inhibitors

Cited by 9 publications

References 13 publications

Mechanisms of adverse effects during hemapheresis

Mechanisms of adverse effects during hemapheresis

Proteomic and Biological Analysis of an In Vitro Human Endothelial System in Response to Drug Anaphylaxis

Bradykinin production during donor plasmapheresis procedures

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