Anaphylactoid reactions with the use of ST-AN69 dialysers in patients taking ACE inhibitors

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.     

A prospective study on intradialytic symptoms associated with reuse of hemodialyzers.

The benefits and disadvantages of hemodialyzer reuse is controversial. While biochemical data have suggested potential benefits from reuse, there is dispute over the clinical impact on the patient. Limited data show that reuse is associated with less intradialytic symptoms compared to first use. We conducted a prospective study of acute symptoms during clinical dialysis using new and reused cellulose acetate membrane hollow-fiber dialyzers. A total of 106 sessions using new dialyzers and 871 sessions employing reused dialyzers were monitored. Dialyzers were processed with an automated machine using hydrogen peroxide and peroxyacetic acid as sterilants. We found that, compared to new ones, reused dialyzers were associated with a similar frequency of overall and specific symptoms. In addition, there was no difference in the magnitude of changes in blood pressure during and after the treatments between the two groups. We conclude that maintenance hemodialysis with reused cellulose acetate membrane dialyzers processed with hydrogen peroxide and peroxyacetic acid was not associated with more or fewer subjective symptoms than dialysis with new dialyzers.     

Anaphylactoid reactions during hemodialysis on AN69 membranes in patients receiving ACE inhibitors

We report five life-threatening anaphylactoid reactions occurring within the very first minutes of hemodialysis on polyacrylonitrile (AN69) capillary dialyzers in three patients receiving ACE inhibitors. Such reactions were not observed either in patients treated with ACE inhibitors but dialyzed on other membranes (N = 9), nor in patients on AN69 who did not receive ACE inhibitors (N = 19). These anaphylactoid reactions could be due to bradykinin accumulation, as a result of both increased synthesis--by interaction of blood with the AN69 polymer--and catabolism blockade by ACE inhibitors.     

Anaphylactoid reactions during haemodialysis in sheep are associated with bradykinin release

Anaphylactoid reactions have been observed in patients treatedwith AN69 dialysers and ACE inhibitors. Recently, it has beenshown in vitro that AN69 membranes induce the release of highamounts of bradykinin in plasma. To verify the possible roleof bradykinin in these shock-like reactions, six sheep weredialysed in a random fashion using AN69 or the new SPAN membranewith and without pretreatment with captopril. All animals weredialysed for 60 min via double-lumen Shaldon catheters. Bloodsamples were drawn at 0, 5, 10, 15, 30, and 60 min from thevenous line. A total of 24 haemodialysis procedures was carriedout: group A (n=6), AN69 without captopril; group B (n=6), SPANwithout captopril; group C (n=6), AN69 with captopril; groupD (n=6), SPAN with captopril. A significant bradykinin release was observed only in groupsA and C, reaching peak values already after 5 min. Animals ingroup C showed the highest bradykinin values. In four of sixanimals in group C anaphylactoid reactions with severe hypotensionwere noted. From this animal model we conclude that dialysis with the AN69membrane is associated with bradykinin release. Pretreatmentwith ACE inhibitors results in further increasing bradykininlevels, which lead to anaphylactoid reactions. In contrast,the new SPAN membrane was well tolerated without detectablechanges in bradykinin concentrations.     

Anaphylactoid reactions due to hydroxyethyl starch infusion.

Incompatibility reactions due to hydroxyethyl starch (HES) were observed during 8 out of 10,273 infusions of 500 ml 6% HES (Plasmasteril). The clinical symptoms ranged from skin reactions to tachycardia, hypotension and shock. In 3 of the 8 patients with incompatibility serum immunoglobulin concentrations were reduced after the anaphylactoid reaction. Specific antibodies against HES were, however, not detected. Serum IgE levels stayed within their normal limits. Positive reactions of the immediate type to intradermal skin tests with different dilutions of Plasmasteril were obtained in five patients.     

Anaphylactoid reactions during hemodialysis and hemofiltration: role of associating AN69 membrane and angiotensin I-converting enzyme inhibitors.

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.     

Anaphylactoid reactions in hemodialysis patients treated with the AN69 dialyzer.

During an 11 week period (May to July, 1990), we observed six anaphylactoid reactions (AR) in six different hemodialysis patients occurring at the onset of treatment with a new AN69 hollow-fiber dialyzer. Four patients required cardiopulmonary resuscitation and one of these expired. Four patients were also receiving an angiotensin converting enzyme (ACE) inhibitor while the other two were not on medication known to affect the renin-angiotensin system. Only patients treated with AN69 dialyzers were affected. A review of the literature indicated that out of 1087 patients reported, 72 patients were on the combination of an AN69 dialyzer and ACE inhibitor therapy and 41 (57%) demonstrated AR. Only two patients (0.4%; both from our series) treated with an AN69 dialyzer without ACE inhibitor therapy developed AR. AR did not occur in patients treated with a variety of other dialyzers during this 11 week period, with or without ACE inhibition. Possible causes for AR are discussed and include: (1.) blood-AN69 membrane interaction leading to the production of bradykinin and other vasodilators, the breakdown of which may be delayed by the presence of ACE inhibitors; (2.) hypersensitivity to ethylene oxide; (3.) passage of bacterial products from dialysate to blood; (4.) changes in membrane manufacturing specifications. Recommendations are proposed for the prevention and treatment of AR.     

Anaphylactoid reactions after cisatracurium administration in six patients.

IMPLICATIONS: We report six cases of anaphylactoid reaction after the administration of the muscle relaxant cisatracurium. They include two first-time documented anaphylactoid reactions after a precurarising dose. These incidents challenge existing views of a substantially reduced anaphylactoid potential of cisatracurium relative to other muscle relaxants.     

Anaphylactoid reaction associated with blood transfusion during anesthesia

Key words  anaphylactoid reaction - blood transfusion - hemodynamics     

Tolerance to ACE inhibitors after cardiac surgery.

OBJECTIVES: Several studies have shown angiotensin-converting enzyme (ACE) inhibitors to confer significant mortality and morbidity benefits in heart failure. First-dose hypotension may necessitate interruption of such therapy. This is more likely to occur if the ACE inhibitor is administered early after coronary artery bypass grafting (CABG). The purpose of this study was to analyse the haemodynamic tolerance to early post-operative treatment with perindopril and enalapril in patients with impaired renal and ventricular function. METHODS: Eighty one consecutive CABG patients with a previous myocardial infarction, impaired pre-operative left ventricular ejection fraction (LVEF) on ventriculography and moderately impaired renal function (serum creatinine of 115-150 micromol/l) were randomised into three groups to receive oral placebo, perindopril (4 mg) or enalapril (5 mg) once daily. Groups were subdivided into those with mild ventricular dysfunction (LVEF = 35-65%, n = 20) and significant ventricular dysfunction (LVEF < 35%, n = 7). Exclusion criteria included oliguria (<0.5 ml/kg per h) or inotrope dependance at the point of entry on the first post-operative day. Intolerance to ACE inhibitor was defined as hypotension (<95 mmHg systolic blood pressure or a decrease exceeding 25 mmHg in systolic blood pressure) leading to oliguria (<0.5 ml/kg per h) which was unresponsive to intravenous furosemide (20 mg). In such cases ACE inhibitor treatment was discontinued and patients commenced on dopamine. RESULTS: In the groups with mild ventricular dysfunction (LVEF = 35-65%) perindopril was discontinued in 1/20 and enalapril in 4/20 patients (P = n.s). However, in the groups with significant ventricular dysfunction (LVEF < 35%) perindopril was discontinued in 2/7 and enalapril in 7/7 patients (P = 0.02). CONCLUSION: Our results suggest that after CABG, patients with moderately impaired renal function and significant ventricular dysfunction do not tolerate ACE inhibitors well when these were commenced on the first post-operative day. However, perindopril was associated with less haemodynamic deterioration than enalapril and consequently may be advantageous in this setting. rights reserved.     

Urolithiasis associated with protease inhibitors.

OBJECTIVE: We evaluated the radiographic characteristics as well as the clinical management of urolithiasis induced by systemic therapy with indinavir sulfate, a protease inhibitor utilized in the treatment of HIV infection. PATIENTS AND METHODS: Fifteen consecutive HIV-positive male patients (average age 41.3 years) who presented with urolithiasis while being treated with indinavir sulfate (average time 11.1 months) were studied. RESULTS: All patients presented with flank pain, and eight had gross hematuria. All but one patient had microscopic hematuria. The location of the stones was the kidney in three, the proximal ureter in four, and the distal ureter in nine. One patient had both a renal and a proximal ureteral stone. The stones were radiolucent on CT imaging in five patients and could not be seen in five. In the five cases in which a stone was not definitely identified, a diagnosis of urolithiasis was established on the basis of ureteral obstruction and periureteral/renal streaking noted on CT. Treatment included observation with hydration in eight patients, ureteral stent placement in two patients, ureteroscopy in three patients, and extracorporeal shockwave lithotripsy in two patients. Stones were analyzed in five patients and proved to be 100% indinavir in three and a mixture of indinavir, calcium oxalate monohydrate, and calcium oxalate dihydrate in two. CONCLUSIONS: Urolithiasis is a recognized complication of treatment with indinavir sulfate. Pure indinavir stones cannot be seen on CT unless intravenous contrast medium is utilized. Mixed calcium and indinavir stones can occur and may be radiopaque. The majority of HIV-positive patients with symptomatic urolithiasis can be treated conservatively with hydration. Metabolic evaluation of these patients with identification and correction of factors predisposing to stone formation may minimize future recurrences. Administration of this effective medication thus can continue uninterrupted.     

Anaphylactoid reactions to vascular graft material presenting with vasodilation and subsequent disseminated intravascular coagulation

This report describes five patients who had immediate adverse reactions following placement of a vascular graft. All had unusually persistent decreases in systemic vascular resistance, and four of these patients had bleeding as an early manifestation of this reaction. In two of three patients in whom the graft was replaced, uneventful recovery followed. Both patients in whom the graft was not replaced died. Blood samples from two of the patients demonstrated activation of complement and of the kinin system, whereas control patients did not demonstrate increased levels of activation products from these cascade systems. Recognition of this syndrome is important to patient survival, which appears to depend on rapid replacement of the graft.