enalapril and Anaphylaxis

enalapril has been researched along with Anaphylaxis* in 10 studies

Reviews

2 review(s) available for enalapril and Anaphylaxis

ArticleYear
[Diagnostics in recurrent angioedema].
    Praxis, 2012, Feb-29, Volume: 101, Issue:5

    Topics: Algorithms; Anaphylaxis; Angioedema; Angiotensin-Converting Enzyme Inhibitors; Diagnosis, Differential; Enalapril; Humans; Hypertension; Lip Diseases; Male; Middle Aged; Recurrence; Tongue Diseases

2012
Life-threatening angio-oedema and death associated with the ACE inhibitor enalapril.
    South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde, 2007, Volume: 97, Issue:4

    Topics: Anaphylaxis; Angioedema; Angiotensin-Converting Enzyme Inhibitors; Enalapril; Humans; Hypertension; Male; Middle Aged; South Africa

2007

Other Studies

8 other study(ies) available for enalapril and Anaphylaxis

ArticleYear
[Anaphylactoid reactions with the use of ST-AN69 dialysers in patients taking ACE inhibitors].
    Nephrologie & therapeutique, 2008, Volume: 4, Issue:5

    Anaphylactoid reactions from blood contact with AN69 hemodialysis membrane in patients taking ACE inhibitors are well-known. Modified AN69 dialyzers (ST-AN69) were invented to create a membrane combining low thrombogenic properties with safety with ACE inhibitors. We report four patients taking ACE inhibitors that presented anaphylactoid reactions with ST-AN69.

    Topics: Aged; Anaphylaxis; Angiotensin-Converting Enzyme Inhibitors; Captopril; Enalapril; Equipment Design; Female; Hemofiltration; Humans; Hypertension; Kidney Failure, Chronic; Male; Membranes, Artificial; Middle Aged; Renal Dialysis

2008
Extracorporal therapy with AN69 membranes in combination with ACE inhibition causing severe anaphylactoid reactions: still a current problem?
    Clinical nephrology, 2000, Volume: 53, Issue:6

    The negatively charged membrane AN69 is known to evoke anaphylactoid reactions both without and with concomitant ACE inhibition. Underlying reasons are mainly the induction of bradykinin release due to the negatively charged membrane and the reduced degradation of bradykinin due to ACE inhibition. This complication has been reported repeatedly, but anaphylactoid reactions still occur in clinical practice. We recently had to treat two patients who suffered anaphylactoid reactions during extracorporal therapy with an AN69 membrane and simultaneous ACE inhibition. The first incident occurred in a patient on hemodialysis, the second was in a patient on continuous venovenous hemofiltration. An anaphylactoid reaction induced by an AN69 membrane during continuous, extracorporal treatment in combination with ACE inhibition has not been reported so far. Our report intends to serve as a reminder that the potentially lethal combination of AN69 membranes with ACE inhibitor treatment should be avoided.

    Topics: Acrylic Resins; Acrylonitrile; Adolescent; Anaphylaxis; Angiotensin-Converting Enzyme Inhibitors; Captopril; Enalapril; Female; Hemofiltration; Humans; Membranes, Artificial; Middle Aged; Renal Dialysis

2000
[Activation of bradykinin formation cascade on receiving autologous blood transfusion through a white cell-reduction filter in a patient treated with an ACE inhibitor].
    Masui. The Japanese journal of anesthesiology, 1998, Volume: 47, Issue:3

    We have experienced a case of anaphylactoid reaction on receiving autologous blood transfusion through a WBC filter for packed red blood cell (PRBC). The patient was a 71-year-old man with a history of hypertension treated with oral antihypertensive drug; enalapril, an angiotensin converting enzyme (ACE) inhibitor, who received anesthesia for Y-graft replacement. Autologous blood was obtained after the induction of general anesthesia in the operating room. Upon starting to return the stored blood with an unintentional use of a WBC filter, arterial blood pressure (ABP) fell within the first minute of the transfusion. We obtained three blood samples; pre-filtered blood (PRE), postfiltered blood (POST) and arterial blood (CIRC) after the event, and analyzed concentrations of bradykinin (BK), high molecular weight kininogen (HMWK) and high molecular weight kininogen-light chain (HMWK-LC). BK was higher in POST than in PRE. HMWK was lower in POST than in PRE, while HMWK-LC was higher in POST than in PRE. HMWK in CIRC was lower than in PRE, and HMWK-LC was higher in CIRC than in PRE. HMWK and HMWK-LC changes after the event suggest that BK formation cascade in the patient was activated on receiving the transfusion. ACE inhibitors were reported to augment such activation. The WBC filter has the negatively charged surface on filteration material and may activate the cascade. While WBC filters can avoid transfusion related reactions, hemodynamic responses should be watched closely in patients treated with ACE inhibitors.

    Topics: Aged; Anaphylaxis; Anesthesia, General; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Arteriosclerosis; Blood Transfusion, Autologous; Bradykinin; Enalapril; Humans; Kininogens; Leukapheresis; Male

1998
Allopurinol and enalapril. Drug induced anaphylactic coronary spasm and acute myocardial infarction.
    Chest, 1995, Volume: 108, Issue:2

    Topics: Allopurinol; Anaphylaxis; Coronary Vasospasm; Drug Interactions; Emergencies; Enalapril; Humans; Male; Middle Aged; Myocardial Infarction

1995
ACE inhibitors and anaphylactoid reactions during venom immunotherapy.
    Lancet (London, England), 1992, Oct-10, Volume: 340, Issue:8824

    Topics: Adult; Anaphylaxis; Animals; Bites and Stings; Contraindications; Desensitization, Immunologic; Enalapril; Humans; Immunotherapy; Male; Middle Aged; Venoms; Wasps

1992
Anaphylactoid reactions, LDL apheresis with dextran sulphate, and ACE inhibitors.
    Lancet (London, England), 1992, Oct-10, Volume: 340, Issue:8824

    Topics: Adsorption; Anaphylaxis; Blood Component Removal; Blood Pressure; Contraindications; Dextran Sulfate; Enalapril; Heart Rate; Humans; Hypercholesterolemia; Lipoproteins, LDL

1992
Anaphylactoid reactions during hemodialysis and hemofiltration: role of associating AN69 membrane and angiotensin I-converting enzyme inhibitors.
    American journal of kidney diseases : the official journal of the National Kidney Foundation, 1992, Volume: 19, Issue:5

    Over a 20-month period, we observed 15 anaphylactoid reactions in six patients undergoing hemodialysis and three others on hemofiltration with AN69 capillary dialyzers who were receiving angiotensin-converting enzyme (ACE) inhibitors. These reactions were severe in 11 cases. In eight patients, anaphylactoid reactions stopped when AN69 membrane was replaced by polysulfone membrane and ACE inhibitors were continued. In one case, reducing the dose of ACE inhibitors was sufficient to prevent new reactions. Anaphylactoid reactions did not occur in patients undergoing dialysis with another membrane (cellulosic or synthetic), nor in those on AN69 membrane without ACE inhibitor treatment. We conclude that back-filtration of endotoxin-contaminated dialysate does not play the main role in the origin of such reactions, since they occurred in patients on hemofiltration with sterile and pyrogen-free substitution liquids.

    Topics: Acrylic Resins; Acrylonitrile; Adult; Anaphylaxis; Captopril; Enalapril; Hemofiltration; Humans; Male; Membranes, Artificial; Middle Aged; Renal Dialysis

1992
Aggregate anaphylaxis and carboxypeptidase N.
    Advances in experimental medicine and biology, 1986, Volume: 198 Pt A

    Bradykinin (BK) is widely believed to play a role in the pathogenesis of anaphylaxis. To help clarify any such roles, we examined for effects of inhibitors of kininase II (angiotensin converting enzyme, ACE) and "kininase I" (carboxypeptidase N, CPN), on the early course of egg albumin-induced aggregate anaphylaxis in anesthetized guinea pigs. In this model, pulmonary and systemic arterial blood pressure (BP) rise (unless pulmonary fibrillation occurs), lung wgt increases by approximately 60% and pulmonary microvessels are occluded by cell-rich thrombi, all within 5 min of i.v. antigen. The 30 min mortality rate is approximately 2%. ACE inhibitors (BPP9a, Captopril and MK 422; doses up to 140 mumol/kg) do not make anaphylaxis more nor less severe in terms discernible by changes in BP, lung wgt, EKG or intravascular coagulation. In marked contrast, an inhibitor of CPN (2-mercaptomethyl-3-guanidinoethylthiopropionic acid, 2-MGP; 8-16 mumol/kg) increases the 30 min mortality rate to 94% and lung wgt to 180% of control. The animals die in ventricular fibrillation. Given the enormous BK potentiating effects of BPP9a, Captopril and MK 422, it seems likely that little if any BK is formed in the early min of anaphylaxis. 2-MGP does not potentiate BP effects of BK but markedly potentiates effects of C3a anaphylatoxin. Thus, our data support the views that BK is neither a primary nor secondary mediator of aggregate anaphylaxis, and the adverse effects of 2-MGP are best explained in terms of preservation of anaphylatoxins and not in terms of preservation of kinins.

    Topics: 3-Mercaptopropionic Acid; Anaphylaxis; Angiotensin-Converting Enzyme Inhibitors; Animals; Blood Pressure; Captopril; Carboxypeptidases; Enalapril; Enalaprilat; Guinea Pigs; Lung; Lysine Carboxypeptidase; Ovalbumin; Sulfhydryl Compounds

1986