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At least 19 recordsLinked to original sources
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↗
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↗
PubMedDate not supplied

Long-acting ACE inhibitor-induced angioedema.

Angioedema is a known adverse reaction of the angiotensin converting enzyme (ACE) inhibitors. Although current investigations are in progress, the exact pathogenesis of ACE inhibitor-induced angioedema is still unclear. Most cases of angioedema we have seen remitting from the short-acting ACE inhibitor, captopril, have presented with mild angioedema, controlled with antihistamines and glucocorticosteroids. In contrast, the angioedema induced by the long-acting ACE inhibitors have been serious. Our five patients developed angioedema from either lisinopril or enalapril. Three of five patients presented with severe angioedema requiring intubation, and one of these patients had a tracheostomy. One patient with a history of mild angioedema secondary to captopril subsequently required intubation for his enalapril-induced angioedema.

Aged↗
PubMed1992

Urticaria and angioedema.

Urticaria and angioedema are usually the clinical consequence of vasoactive mediators derived from mast cells in the skin or mucosal tissues. Efforts to classify mast cell-mediated causes of urticaria and angioedema have generally been frustrated by their diverse pathogenesis and clinical course. The term acute is typically used to describe fleeting lesions whose recurrence does not extend beyond 6 weeks. Chronic is the term used to describe lesions that persist for more than a few hours but usually less than a day, and recurrences extend for more than 6 weeks. These definitions do not take histology into account. Skin biopsies of fleeting lesions demonstrate a paucity of inflammatory cells, whereas more persistent lesions display a spectrum of perivascular cuffing by predominantly T cells and monocytes. The presence of leukocytoclastic vasculitis in persistent lesions indicates an underlying immune complex disease. Many of the physical urticarias have fleeting lesions that can be induced with the appropriate stimulus for years. This review article has emphasized the clinical course and histology of urticaria and angioedema lesions in an effort to provide a more complete understanding of the pathogenesis and appropriate treatment. Clearly, avoidance of an identifiable inciting stimulus is optimum management, although most patients have no etiology defined or the cause is not realistically avoidable. At present, treatment options for these patients rely on antihistamines to control the immediate consequence of mast cell degranulation. Corticosteroids are reserved for the treatment of patients whose urticaria or angioedema lesions persist, reflecting the increasing involvement of mononuclear cells in the disease process. For leukocytoclastic vasculitis, corticosteroids are indicated, and cytotoxic drugs may be required for adequate treatment. Future treatments of urticaria and angioedema will evolve based on elucidation of the relevant cells and soluble mediators and will include counterregulatory or antagonistic peptides and drugs. C1 esterase inhibitor deficiency is a relatively uncommon cause of angioedema but is important to understand because of its ability to clinically mimic mast cell-mediated angioedemas and its unique pathogenesis and treatment. HAE can be divided into two serologic subtypes that simply reflect the location of the defect in one of the codominantly expressed C1-INH genes on chromosome 11. AAE can be divided into two serologic subtypes. AAE type I is due to massive consumption of C1-INH, presumably by tumor-related immune complexes. AAE type II is due to an anti-C1-INH autoantibody.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗
PubMed1991

Angioedema: manifestations and management.

Angioedema is characterized by localized swelling of sudden onset affecting the skin and/or mucous membranes. It can be classified into hereditary and acquired forms. Hereditary angioedema is a rare disease inherited as an autosomal dominant trait and caused by a deficiency of C1-esterase inhibitor. Acute attacks are life threatening and cannot be managed by antihistamines, corticosteroids, or adrenergic drugs. Prophylactic therapy is possible with danazol or stanozolol. Acquired angioedema includes nonhereditary C1-esterase inhibitor deficiency; idiopathic, allergic, and drug-induced forms; angioedema associated with lupus erythematosus and hypereosinophilia; and angioedema caused by physical stimuli. Treatment of these forms of angioedema depends on identifying and avoiding the cause, induction of tolerance, or symptomatic treatment with systemic antihistamines.

Angioedema↗
PubMed1991

Urticaria and angioedema: diagnosis and evaluation.

Because urticaria clears spontaneously in most patients, an extensive workup is not advised during the early weeks of an urticarial eruption. Whether and when to perform a screening workup or a more extensive workup depend on the degree of suspicion that the patient is ill, the urgency with which the patient presses for an answer, and the presence or absence of signs or symptoms that might lead the physician to pursue a diagnosis other than chronic idiopathic urticaria. Angioedema may occur with urticaria, and when it does, the prognosis is worse. Whereas urticaria manifests as circumscribed edema involving the superficial dermis, angioedema involves primarily the deep dermis or subcutaneous or deeper layers. Individual urticarial lesions usually disappear within 2 to 4 hours, whereas those of angioedema can persist for 72 hours. The workup for patients with chronic angioedema can be similar to that for patients with urticaria. However, several additional diagnostic possibilities should be pursued in patients with angioedema, such as hereditary angioedema caused by C1-esterase inhibitor deficiency, because anabolic steroids are effective in the treatment of these conditions.

Angioedema↗
PubMed1991

Oral manifestations and dental management of patients with hereditary angioedema.

Hereditary angioedema (HAE) is a genetic disorder in which affected individuals develop extensive, spontaneous angioedema of the extremities, gastrointestinal tract, and oropharynx. Dental treatment of unmedicated patients with HAE can trigger life-threatening pharyngeal edema. Previously, it was demonstrated that the administration of fresh frozen plasma (FFP) before surgery prevented angioedema attacks in 6 patients undergoing dental extractions. The present study examines the long term effectiveness of FFP in preventing angioedema from developing in 53 patients with HAE undergoing all types of dental treatment over a ten-year period. Only 3 of 45 patients (6.7%) covered with FFP had a minor angioedema attack after dental therapy in 10 yr. No attacks of moderate or severe swelling were seen. Attacks occurred independently of the disease activity of the patient and the trauma of the dental procedure. The use of fresh frozen plasma is effective in preventing attacks of angioedema in HAE patients undergoing all types of dental procedures.

Adolescent↗
PubMed1991

Acute and chronic urticaria and angioedema.

Urticaria and angioedema are clinical manifestations of various immunologic and inflammatory mechanisms, or they may be idiopathic. The respiratory and gastrointestinal tracts as well as the cardiovascular system may be involved in any combination. Patients with urticaria and/or angioedema can be classified based on pathophysiologic mechanisms into those with IgE-dependent or complement-mediated immunologic disorders, those with nonimmunologic disorders in which there is a direct effect on the mast cell or on arachidonic acid metabolism, and those whose condition is idiopathic. Evaluation of patients should focus on a thorough history. Laboratory tests provide minimal additional information. About one half of patients with urticaria alone and 25% with urticaria and angioedema or angioedema alone are free of lesions within 1 year. With urticaria, angioedema, or both, 20% of patients experience episodes for more than 20 years.

Acute Disease↗
PubMed1992

Angioedema associated with lisinopril.

Angioedema has been reported to occur in association with all angiotensin-converting enzyme inhibitors used in the United States. We reviewed nine cases of angioedema associated with lisinopril use seen in the emergency department at our hospital among 1,970 patients that had been prescribed lisinopril from March 1989 to May 1990. Cases were considered as probably (six cases) or possibly (three cases) drug related, depending on the temporal relationship of the initiation of therapy and the onset of angioedema. All of the cases had edema of the lips, buccal mucosa, and or face. None presented with laryngeal edema or stridor. The angioedema resolved within 1 to 2 days with diphenhydramine treatment and discontinuation of lisinopril. Our data suggest that the incidence of angioedema associated with lisinopril is greater than that associated with captopril or enalapril.

Adult↗
PubMed1992

Ophthalmic manifestations of chronic angioedema with necrotizing vasculitis.

Anatomic features unique to periocular tissues alter the clinical appearance of angioedema, making it difficult to distinguish from cellulitis and other inflammatory conditions. Two patients had prominent periocular manifestations of chronic angioedema with necrotizing vasculitis, a systemic disease often associated with multiorgan involvement. The diagnosis was established by exclusion of other inflammatory disorders and confirmed by biopsy. The scarcity of reports in the ophthalmic literature on chronic angioedema of the eyelids may be caused by its underrecognition. The distinction between chronic angioedema and typical angioedema or urticaria is important because of differences in their diagnostic evaluation, treatment, and prognosis.

Adult↗
PubMed1991

Clinical characteristics of angiotensin-converting enzyme inhibitor-induced angioedema.

We present the cases of two patients with angiotensin-converting enzyme (ACE) inhibitor-induced angioedema that required intubation for life-threatening airway compromise. This side effect has been previously reported with all ACE inhibitors, but its incidence and potential for a fatal outcome may not be fully appreciated. A review of the literature reveals 227 reports of this reaction with an overall incidence of approximately 0.1% to 0.2%. The etiology is nonimmunogenic and thought to be related to accentuated bradykinin activity. There is no clinical profile that identifies patients at increased risk for this side effect. There are unique clinical characteristics to this idiosyncratic reaction: angioedema may suddenly occur even though the drug has been well tolerated for months or years; symptoms may regress spontaneously while the patient continues the medication, erroneously prompting an alternative diagnosis; the pathology has a special predilection for the tongue, a circumstance that renders orotracheal and nasotracheal intubation difficult; symptoms may progress rapidly despite aggressive medical therapy, necessitating emergency airway procedures; and a rebound phenomenon following successful medical therapy has been described. We recommend intensive medical treatment before angioedema is severe enough to thwart standard methods to ensure a protected airway. Once even minor angioedema is attributed to an ACE inhibitor, an alternative class of antihypertensive medication should be chosen. Individuals with a history of idiopathic angioedema probably should not be given ACE inhibitors.

Angioedema↗
PubMed1990

Angioedema related to angiotensin-converting enzyme inhibitors.

Angioedema is a disorder characterized by well-demarcated nonpitting edema involving the tongue, floor of the mouth, larynx, lips, and face. This condition can progress to upper airway obstruction and death. Angiotensin-converting enzyme inhibitors (ACEIs), relatively new antihypertensive agents, act by blocking the formation of angiotensin II, a potent vasoconstrictor and stimulator of aldosterone formation. ACEIs also retard the breakdown of bradykinin, a potent vasodilator, which may lead to the edema seen in nonhereditary angioedema. These ACEIs include enalapril, captopril, lisinopril, saralasin acetate, and a combination of ACEI with diuretics (for example, Capozide). From August 1987 to January 1989, we treated six patients with a nonhereditary form of angioedema related to ingestion of angiotensin-converting enzyme inhibitors. Symptoms developed in all patients within 12 hours after their initial dose of an ACEI. They presented with shortness of breath and dysphagia associated with tongue and floor of the mouth edema. Two of the six required intubation and monitoring in the surgical intensive care unit for 36 to 48 hours. Three required supportive treatment and observation in an intermediate care unit, and one received supportive care in the clinic and was discharged the same day. Specifically, treatment consisted of cessation of inciting agent, steroids, antihistamines, and epinephrine, if not otherwise contraindicated. Assays of C1 esterase inhibitor levels and C4 were normal in all six patients; this was important in order to rule out hereditary forms of angioedema. These cases will be discussed, including a review of the literature, methods of diagnosis, pathophysiology, and treatment of angioedema.

Aged↗
PubMed1992

Fatal angioedema associated with lisinopril.

OBJECTIVE: To report a case of fatal angioedema associated with the use of lisinopril, a long-acting angiotensin-converting enzyme (ACE) inhibitor. DATA SOURCES: Case reports, review articles, short reports, and pertinent information from the patient's medical record. DATA EXTRACTION: Data was collected from contemporary medical journals and reviewed by both authors. DATA SYNTHESIS: Angioedema associated with ACE inhibitors (captopril and enalapril) is well documented in the literature. With increased prescribing of newer, longer-acting agents, this potentially lethal adverse reaction is of even greater concern. Because angioedema associated with ACE inhibitors is a class-related event, the number of reported cases would be expected to increase with increasing numbers of prescriptions written for these drugs. This report, describing a patient who developed angioedema following therapy with lisinopril, illustrates the severity of this adverse reaction. PATIENT: A 66-year-old man presented to the emergency room complaining of increased swelling of the back of his throat and difficulty breathing. Despite treatment with epinephrine, antihistamines, and corticosteroids, the patient's condition progressed from that of severe laryngeal edema to total laryngospasm and complete airway obstruction. Emergency measures to intubate the patient were complicated by severe swelling of his neck and oropharynx, forcing the physician to perform a grossly traumatic tracheotomy. The difficulty encountered during intubation deprived the patient of oxygen for a significant amount of time, precipitating cardiopulmonary arrest. The anoxic episode resulted in hypoxic, ischemic encephalopathy and, ultimately, death. CONCLUSIONS: Angioedema is a serious, potentially life-threatening adverse effect associated with the use of ACE inhibitors. Clinicians need to be aware of this effect when prescribing ACE inhibitors to treat hypertension and congestive heart failure, and when assessing patients presenting to the emergency room with complaints of tongue or pharyngeal swelling. Patients should be instructed to report immediately to an emergency room for medical attention if they experience any unexplained shortness of breath or swelling of the throat or tongue.

Aged↗
PubMed1992

Angioedema: 5 years' experience, with a review of the disorder's presentation and treatment.

Angioedema is a problem that the otolaryngologist-head and neck surgeon is often asked to treat. This report concerns 17 patients admitted for care during a 5-year period. At their initial presentation, 94% of these patients manifested signs and symptoms of angioedema in the head and neck; three of them required urgent tracheotomy or intubation. As treatment of complement-mediated angioedema is distinct, an etiology-specific diagnostic and treatment protocol is presented. Of the patients, 35% had recent initiation of angiotensin-converting enzyme (ACE) inhibitor therapy for hypertension, and 6% demonstrated classic hereditary angioedema. However, the majority of them (59%) had unclear etiologies for their symptoms. Since angioedema is the final result of several possible abnormalities, a thorough knowledge of the differential diagnosis and clinical presentation is vital to patient management.

Adolescent↗
PubMed1979

Urticaria and angioedema. Common clinical problems.

The cause of urticaria and angioedema often is difficult to ascertain. In most cases the conditions are transient, but a chronic idiopathic form does occur and may be intractable. Acute urticaria and angioedema usually result from an IgE-mediated mechanism; success in treatment depends on recognition of the underlying factor. Chronic urticaria may ultimately necessitate use of corticosteroids. Hereditary angioedema is easily differentiated from idiopathic angioedema by the family history and absence of pruritus.

Angioedema↗
PubMed1990

Autoimmune angioedema: a new role for autoantibody in disease pathogenesis.

Angioedema may be due to hereditary forms of Cl-Inh deficiency, but recently an autoimmune form of angioedema has been described in which the mechanism is novel. While the peripheral blood monocytes of patients with autoimmune angioedema produce a normal, functionally active, 105 KD Cl-Inh in normal quantities, the Cl-Inh isolated from the patient's plasma exists in a dysfunctional lower molecular weight (96 KD) performance. Rather than bind and biologically inactivate the enzyme, a relatively common phenomenon in autoimmune disease, the autoimmune angioedema cleave the Cl-Inh molecule. The following sequence of events is proposed: structural and functionally normal Cl-Inh is synthesised and secreted, this secreted inhibitor is complexed by autoantibody and following enzyme interaction, denatured 96 KD Cl-Inh is proposed. This process depletes the pool of normal, functional Cl-Inh to critical levels and predisposes patients to episodes of oedema.

Angioedema↗
PubMed1990

Angiotensin-converting enzyme inhibitor induced angioedema of the head and neck.

Angiotensin-converting enzyme (ACE) inhibitors are now in widespread use for the treatment of essential and renovascular hypertension. Consequently, angioedema, an uncommon complication of ACE inhibitor therapy is being encountered with increasing frequency. Since ACE inhibitor angioedema predominantly involves the face, lips, oral cavity, and occasionally the larynx the otolaryngologist is often consulted to evaluate affected patients. Treatment ranges from simple cessation of the drug to emergent airway intervention. The pertinent pharmacologic properties of ACE inhibitors and the pathophysiology of angioedema are discussed. The authors' experience with the evaluation and treatment of ACE inhibitor induced angioedema is presented.

Adrenal Cortex Hormones↗