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At least 19 recordsLinked to original sources
PubMed2001

Angioedema associated with angiotensin II receptor antagonists: challenging our knowledge of angioedema and its etiology.

INTRODUCTION: Use of angiotensin converting enzyme inhibitors has long been associated with angioedema. Increased levels of bradykinin caused by the inhibition of angiotensin converting enzyme have been thought to be responsible for this side effect. Angiotensin II receptor antagonists (AT2 blockers), such as losartan potassium (Cozaar; Merck & Co., West Point, PA), are a new class of antihypertensives developed in part to eliminate cough and angioedema associated with ACE inhibitors. These agents act by selectively binding to angiotensin II receptor sites, thereby eliminating the hypertensive effects of angiotensin without affecting local and systemic bradykinin levels. We present three cases of AT2 receptor antagonist-induced angioedema, and examine its significance in the treatment of angioedema and its proposed etiology. METHODS: A retrospective chart review and review of the literature. RESULTS: Three patients taking the AT2 blocker losartan presented with mucosal swelling in the head and neck clinically consistent with angioedema. All three patients had prior episodes of angioedema while on losartan. Two patients presented with involvement of the anterior tongue and face that resolved within 12 hours of discontinuation of the losartan and a course of intravenous steroids. The third patient experienced recurring episodes of angioedema that eventually required a tracheotomy for airway compromise. After discontinuing the losartan and receiving a course of intravenous steroids, the angioedema resolved in 5 days. The patient was decannulated 10 days after onset of symptoms. CONCLUSION: Angioedema is a potentially life-threatening condition commonly associated with ACE inhibitor use. AT2 blockers bind to angiotensin II receptor sites and have no demonstrable effect on local or systemic bradykinin levels. We present three cases that demonstrate AT2 blocker-induced angioedema. They were all complicated by the fact that the inciting agent, losartan, was not discontinued after the initial episode and resulted in recurrent episodes of angioedema, one of which required surgical airway intervention. The incidence of AT2 blocker-induced angioedema brings into question prior theories on the etiology of angioedema and bradykinin's role in its pathogenesis.

Aged↗
PubMed2002

Angiotensin II receptor blocker-associated angioedema: on the heels of ACE inhibitor angioedema.

Angioedema and cough are known side effects of angiotensin-converting enzyme (ACE) inhibitors. Angiotensin-converting enzyme is a potent inhibitor of kinase II, which facilitates the breakdown of bradykinin. An increase in bradykinin levels results in continued prostaglandin E2 synthesis, vasodilation, increased vascular permeability, and increased interstitial fluid. In contrast, the angiotensin II receptor blockers (ARBs) do not increase bradykinin levels. Angioedema as a complication of ACE inhibitor therapy is not widely recognized; this complication is even less recognized with second-line ARBs. We report angioedema associated with losartan (an ARB) in a patient who had experienced angioedema secondary to enalapril (an ACE inhibitor). Almost half of patients with ARB-associated angioedema also had developed angioedema while receiving ACE inhibitor therapy. Clinicians should exercise caution when using ARBs in patients with a history of angioedema secondary to ACE inhibitors.

Adult↗
PubMed1990

Severe angioedema related to ACE inhibitors in patients with a history of idiopathic angioedema.

Angiotensin converting enzyme (ACE) inhibitors have been associated with the onset of angioedema in a small subset of treated patients. The angioedema commonly involves the face and oropharyngeal tissues and may result in life-threatening airway compromise. The mechanism by which ACE inhibitors precipitate angioedema has not been well-defined, and retrospective analysis of reported cases has failed to identify a group of patients at high risk. We report four cases of ACE inhibitor-related angioedema that required immediate medical intervention. All four cases occurred in patients with a prior history of idiopathic angioedema, an otherwise uncommon clinical entity. These observations suggest that patients with a history of idiopathic angioedema are at increased risk for the development of ACE inhibitor-related angioedema and should be treated cautiously with this class of drugs.

Adult↗
PubMed1978

Acquired angioedema associated with rectal carcinoma and its response to danazol therapy. Acquired angioedema treated with danazol.

Cases of the acquired form of angioedema have been recognized as a separate entity since 1972. Previously reported cases have been related to various hematologic malignancies. We have recently studied a patient with rectal carcinoma who manifests a complement pattern compatible with the acquired form of angioedema. No previous personal or family history of allergic disease or angioedema was present. Because the episodes of angioedema were laryngeal in location and required emergency intubation to maintain an adequate airway, a trial of danazol prophylaxis, which has been shown to be effective in hereditary angioedema, was undertaken. His beneficial response to this form of therapy is also documented.

Adenocarcinoma↗
PubMed2006

Cytokine-associated angioedema syndromes including episodic angioedema with eosinophilia (Gleich's Syndrome).

Angioedema can be associated with many disorders and the presentation can be variable. Subsets of the angioedema syndromes are thought to be cytokine mediated (Table 1). Of these, the best described are the episodic angioedema with eosinophilia syndrome (Gleich's syndrome) and non-episodic angioedema with eosinophilia, which share some common features, but appear to have differences in pathophysiology. NERDS (nodules, eosinophilia, rheumatism, dermatitis and swelling), Clarkson syndrome (idiopathic capillary leak syndrome), and angioedema associated with aldesleukin (human recombinant IL-2) and IFN-alpha have also been reported in the literature, and have been discussed in this review. There is still much to be learned about the pathophysiology, diagnosis, and treatment of patients with these disorders. Our hope is that this review will be of help to those readers who care for patients with these disorders, and will stimulate interest in further research into the pathophysiology of these conditions.

Angioedema↗
PubMed2002

[Recurrent attacks of angioedema ascribed to the use of estrogen preparations and a pregnancy (hereditary angioedema type 3)].

A woman experienced recurrent attacks of angioedema from the age of 17 to 21 years and these appeared to be associated with the use of oestrogens. After stopping the medication her complaints disappeared, but they returned during her first pregnancy. Angioedema is a serious condition, which can lead to acute abdominal symptoms, oedema of the upper respiratory tract and death by asphyxiation. The most well-known cause is hereditary angioedema, an autosomal dominant disorder that is characterized by deficiency of C1 esterase inhibitor (C1-INH). Recently, a new type of hereditary angioedema (type 3) has been reported that occurs exclusively in women and is characterised by oestrogen dependency (both endogenous and exogenous), normal C1-INH concentrations and severe attacks of angioedema, which are clinically indistinguishable from the classic form.

Abdominal Pain↗
PubMed1980

Replacement therapy in hereditary angioedema: successful treatment of acute episodes of angioedema with partly purified C1 inhibitor.

Although considerable progress has been made during the past two decades in the use of androgens to prevent attacks of hereditary angioedema, replacement of the deficient C1-inhibitor protein would provide a useful menas of treatment once an attack has begun. We studied the clinical use of C1 inhibitor that was partly purified on a large scale from pooled plasma. The in vivo efficacy and safety of this protein concentrate were evaluated during 11 intravenous infusions in eight patients with hereditary angioedema. Three patients received the C1-inhibitor preparation during an asymptomatic period. Increases in serum C4 activity provided evidence of the biologic activity of the infused inhibitor. Intravenous administration of the concentrate during acute abdominal or laryngeal attacks of hereditary angioedema in five patients resulted in abatement of symptoms in addition to increased serum C4 activity. No untoward effects of the intravenous administration of the C1 inhibitor were observed in these eight patients. Thus, this C1-inhibitor preparation seems to offer the potential for safe, effective replacement therapy and may provide a means of controlling an attack of hereditary angioedema that is in progress.

Angioedema↗
PubMed2006

Hereditary angioedema with normal C1 inhibitor activity including hereditary angioedema with coagulation factor XII gene mutations.

Until recently it was assumed that hereditary angioedema is a disease that results exclusively from a deficiency of the C1 inhibitor. In 2000, families with hereditary angioedema, normal C1 inhibitor activity, and protein in plasma were described; all patients were women. In many of the affected women, oral contraceptives, hormone replacement therapy containing estrogens, and pregnancies triggered the clinical symptoms. Recently, in some families mutations in the coagulation factor XII (Hageman factor) gene were detected in the affected women.

Angioedema↗
PubMed1982

Familial angioedema associated with C1 esterase-inhibitor deficiency. A new genetic variant in hereditary angioedema?

In the absence of a positive family history for hereditary angioedema (HAE), both siblings in a family were found to have clinical and laboratory findings similar to those in HAE. Both siblings became symptom free after receiving danazol treatment, accompanied by a subnormal rise in C1 esterase inhibitor and C4 levels. As both siblings and their father share HLA haplotype A2, B7, the influence of other HLA loci on the clinical expression of this disorder should be considered. Although the disorder found in these siblings may be inherited as a recessive disorder, which to our knowledge has never been described before, or may have developed as the result of spontaneous genetic mutation, it is more appropriate to classify these two cases as familial angioedema until proved otherwise.

Adolescent↗
PubMed1978

Specific functional and immunologic assay of plasma plasminogen in hereditary angioedema, in hereditary angioedema treated with tranexamic acid, and in normal subjects.

Plasma plasminogen levels were determined by a specific esterolytic assay and a radial immunodiffusion assay, both of which were standardized on a weight basis by using highly purified plasminogen diluted in plasminogen-free plasma. In thirteen normal individuals the functional and antigenic levels were 275 +/- 61 microgram/ml and 285 +/- 61 microgram/ml, respectively (r = 0.95), whereas in 58 plasmas from individuals with hereditary angioedema the levels were 272 +/- 58 microgram/ml and 265 +/- 64 microgram/ml, respectively (r = 0.89). In two patients treated with tranexamic acid either acutely or chronically, both the functional and antigenic plasminogen levels were diminished.

Angioedema↗
PubMed1985

[Current diagnostic possibilities in hereditary angioedema and acquired angioedema].

Amidolytic assays for the determination of C1 esterase inhibitor have been proposed some years ago; however, the substrates employed lacked sensitivity. The recent development of a C1 esterase-sensitive substrate (N-alpha-methoxycarbonyl-l-lysyl(epsilon-CBO)-glycyl-arginyl-4-nit roanilide) provides a method that can be routinely used. Any interferences with other plasma proteases could not be observed. Normal range was ascertained to be 1.48 +/- 0.23 kU/l; within-run precision revealed C.V.'s of 1.74% (for the normal range) and 7.3% (for the pathological range). This method can be considered most suitable for functional determination of C1 esterase inhibitor and is superior to the determination of antikallikrein activity. To point out to the diagnostic relevance of a functional C1 esterase inhibitor assay some examples are illustrated.

Angioedema↗
PubMed2003

Recurrent episodes of skin angioedema and severe attacks of abdominal pain induced by oral contraceptives or hormone replacement therapy.

PURPOSE: Recurrent angioedema, characterized by skin swelling, colicky attacks of abdominal pain, and life-threatening laryngeal edema, can be either hereditary or acquired. According to anecdotal reports, it may be associated with use of oral contraceptives and hormone replacement therapy. We investigated potential interactions between these medications and various types of recurrent angioedema in a large cohort of women. METHODS: Women with recurrent angioedema (n = 516) underwent a thorough medical evaluation. They were then classified by type of angioedema, using standard criteria. RESULTS: Of the 516 women, 228 (44%) had used oral contraceptives or hormone replacement therapy, including 103 (45%) with urticaria-related angioedema, 50 (22%) with idiopathic angioedema, 39 (17%) with hereditary angioedema type III, 32 (14%) with hereditary angioedema type I, and 4 (2%) with angioedema induced by angiotensin-converting enzyme inhibitors. Oral contraceptives or hormone replacement therapy led to angioedema attacks in 46 women (20%), including 20 (63%) of the women with hereditary angioedema type I, 24 (62%) of those with hereditary angioedema type III, and 2 (4%) of those with idiopathic angioedema. These 46 women included 26 in whom symptoms occurred for the first time after use of these medications and 20 in whom pre-existing recurrent angioedema worsened considerably. CONCLUSION: Oral contraceptives or hormone replacement therapy can either induce or exacerbate symptoms of hereditary angioedema type I or type III, or idiopathic angioedema. However, many women with these diseases tolerate these medications without having any effects on their angioedema.

Abdominal Pain↗
PubMed2007

Investigation of angioedema associated with the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers.

BACKGROUND: Angiotensin-converting enzyme inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs) are known to cause angioedema. OBJECTIVE: To evaluate the time to onset of angioedema and the subsequent episodes of angioedema in patients initially experiencing ACE-I- or ARB-induced angioedema. METHODS: A manual medical record review was conducted on 64 patients with a diagnosis of urticaria, angioedema, or anaphylaxis as a result of taking an ACE-I or ARB. Data recorded included demographic characteristics; time to onset of symptoms; concomitant medication use; laboratory test results; recurrent episodes of angioedema, urticaria, or anaphylaxis; and morbidity and mortality. RESULTS: The mean age of patients with angioedema was 60.2 years (age range, 32-92 years). Women (60%) and African Americans (69%) were affected more commonly. The primary location for angioedema was the lips and tongue. Sixty-one of 64 patients developed at least one episode of angioedema as the result of taking an ACE-I, and 3 patients had angioedema associated with an ARB. The mean time to onset of angioedema after initiation of therapy in 51 patients was 1.8 years, with 13 patients (25%) presenting within the first month and 6 patients (12%) developing angioedema in the first week. No patients required a tracheostomy or died. Also, none of the 6 patients, whose angioedema was attributed to an ACE-I who then received an ARB, developed recurrent angioedema in more than 8.1 patient-years of follow-up. CONCLUSIONS: Angioedema attributable to an ACE-I or ARB resolves on discontinued use of the medication. It most commonly affects women and African Americans and did so in the first month of treatment in 25% of patients. Physicians should be aware but not deterred necessarily from recommending an ARB in patients with ACE-I-induced angioedema because of the benefits of control of hypertension or reducing albuminuria in selected patients.

Adult↗
PubMed1996

Epidemiological study of angioedema and ACE inhibitors.

BACKGROUND: Angioedema is an uncommon and poorly recognised adverse reaction to angiotensin converting enzyme inhibitors (ACE-Is). The epidemiology of this association has not been described. AIMS: To examine the epidemiology of angioedema and its relation to ACE inhibitor prescribing. To examine the characteristics of angioedema occurring in patients taking ACE inhibitors. METHODS: A retrospective case control study and a case note audit were conducted of 40 patients who presented to a teaching hospital Accident and Emergency Department with angioedema on 48 occasions. One hundred and sixty control subjects presenting to the same Accident and Emergency Department but without angioedema were matched to cases by age, sex and presentation date. An ecological study comparing the numbers of angioedema admissions by age cohorts to South Australian (SA) public hospitals with the prescription volumes of ACE-Is in Australia was also undertaken. RESULTS: Case control study: In patients presenting with angioedema compared with controls, the exposure odds ratio for ACE-Is was 5.1 (95% CI 2.03-12.89) and for non-steroidal anti-inflammatory drugs (NSAIDs) was 4.13 (95% CI 1.28-13.39). CASE NOTE AUDIT: 15/40 (38%) patients presenting with angioedema on 19/48 (40%) occasions were taking an ACE-I. These patients were older and less likely to have an atopic history than those not taking an ACE-I. The onset of angioedema after starting an ACE-I was delayed for greater than six months in nine patients. ACE-I therapy was continued after 53% of presentations. ECOLOGICAL STUDY: The number of admissions with angioedema to SA public hospitals increased between 1985-86 and 1994-95, predominantly in older patients, and paralleled the increasing prescription volumes of ACE-Is. CONCLUSIONS: A considerable proportion of patients presenting with angioedema will be taking an ACE-I or a NSAID. The association of ACE-Is and angioedema is not well recognised, partly because the onset of angioedema may be delayed for months or years after commencement of an ACE-I. A persisting risk of angioedema is present in patients who have initially commenced an ACE-I uneventfully. The epidemiology of angioedema is now changing in parallel with the increasing use of ACE-Is.

Adolescent↗