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Results for “Angioedema”

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At least 19 recordsLinked to original sources

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

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

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↗

PubMed1979

Prophylaxis of attacks of hereditary angioedema.

Danazol, an attentuated androgen, has been suggested as an effective agent for the prophylaxis of attacks of hereditary angioedema. Four patients, with a clinical history of hereditary angioedema and a demonstrated depression of the serum inhibitor of the first component of complement (C1 INH) and the fourth component of complement (C4), were entered into a study to determine the minimum effective dose of this agent. All four of the patients had been experiencing attacks at least monthly, but they had only six attacks during a total of 60 patient months of Danazol therapy. The minimum effective dose varied from 100 to 400 mg/day. The drug appeared to work by increasing the level of serum C1 INH which reached the normal range in two of four patients. Side effects were only the anticipated menstrual irregularities in the female patients. Danazol appears to be an efficacious drug for prophylaxis of hereditary angioedema.

Adult↗

PubMed1979

Hereditary angioedema controlled with danazol. Report of a case.

Hereditary angioedema is a condition which should be approached with caution and concern for the patient. The fact that the disease can be fatal cannot be overemphasized. The routine medical history should include questions aimed at identifying these patients. If the angioedema patient is to be treated, provisions must be made for maintenance of an adequate airway. This should include intubation if deemed necessary, and the practitioner should be prepared for a tracheostomy. Close observation following extubation is indicated. A case report in which the patient was controlled with danazol, a synthetic androgen, has been presented. The primary advantage of this drug is a decrease in the various side effects which have been associated with other therapeutic agents used previously in the treatment of hereditary angioedema.

Adult↗

PubMed1977

C1q levels in hereditary angioedema.

In 21 affected members from 4 kindreds with hereditary angioedema, serum C1q levels generally were in the lower part of the normal range, with some values clearly below the lower limit of normal. The serum C1q levels in patients with hereditary angioedema were significantly depressed when compared with those in unaffected family members (p less than 0.001) and healthy control subjects (p less than 0.05). serum C1q levels were significantly (p less than 0.01) related to serum C4 levels which have been used as an indicator of disease activity in individual patients. C1q was stable during storage of serum samples at --20 degrees C for 60 days compared to storage at --70 degrees C. These studies indicate that depressed serum C1q concentrations may be seen in patients with hereditary angioedema and that the finding of this abnormality does not exclude the diagnosis.

Angioedema↗

PubMed1992

Angiotensin-converting enzyme inhibitor-induced angioedema: still unrecognized.

Angiotensin-converting enzyme inhibitors are a widely used antihypertensive modality. While they have a favorable side effect profile, there is a .1% to .2% incidence of potentially life threatening angioedema. The edema usually presents in the head and neck, especially the face, lips, tongue, and glottis. Patients may initially be treated with standard anti-allergic therapy; however, the situation may dictate a more aggressive therapeutic approach. The authors present the case of a patient who presented with angioedema 18 times over a 3-year period to qualified emergency physicians before the correct diagnosis of angiotensin-converting enzyme inhibitor-induced angioedema was made. Despite recent literature on the subject, there appears to be a lack of familiarization among emergency department physicians regarding this relatively common adverse effect.

Adult↗

PubMed1979

Acquired C1 esterase inhibitor deficiency and angioedema: a review.

A case of acquired C1INH deficiency with angioedema is described. Fifteen cases are thus far recorded. The clinical syndrome of angioedema in these patients closely resembles hereditary angioedema (HAE). Most cases are associated with a paraprotein, cryoglobulin, or autoantibody, which presumably initiates C1 activation and C1 Inhibitor consumption. C1INH, C4 and C2 levels are low in acquired C1INH deficiency, as in HAE. A distinguishing feature is that C1 titers are very low in the acquired disease and only minimally depressed, if at all, in HAE. Most cases have appeared in patients with an underlying lymphoproliferative or autoimmune disease. Therapy is directed at the underlying disorder, but androgen therapy may be helpful in preventing attacks. Future potential therapeutic approaches are discussed.

Angioedema↗

PubMed1976

Acquired angioedema with lymphoproliferative disorder: association of C1 inhibitor deficiency with cellular abnormality.

A patient with a lymphoproliferative disorder, angioedema, and an acquired deficiency of the inhibitor of the activated first component of complement was studied. The patient's complement profile revealed depletion of the first component of complement, which has not been seen in angioedema of the hereditary type. There was no evidence for C1-depleting activity in the patient's plasma. The majority of the patient's peripheral blood mononuclear cells resembled B cells in their memebrane receptor properties and in that they carried easily detectable immunoglobulin, predominantly IgM. However, these cells were unusual in that they phagocytosed both latex particles and C3-coated erythrocytes. Morphological study of the cells infiltrating the patient's lung revealed immature, atypical, and plasmacytoid lymphocytes and immunoblasts. Both the patient's peripheral blood mononuclear cells and a suspension of cells from the pulmonary infiltrate were capable of depleting the first component of complement and its inhibitor from homologous plasma. Normal ABO-compatible cells did not possess this property. The data suggested that the patient's abnormal lymphoid cells may have interacted with the complement system to produce a biochemical defect and a clinical syndrome closely resembling angioedema of the hereditary type.

Aged↗

PubMed1992

Angioedema complicating lisinopril therapy.

A case of angioedema induced by antihypertensive therapy with lisinopril is presented. The patient was a 70 year old black woman, with a history of hypertension for 15 years. The patient presented with acute onset of swelling involving the oro-facial region and respiratory distress after ingestion of three doses of lisinopril over a three day period. A clinical diagnosis of drug induced angioedema was made based on clinical presentation. The patient was treated with diphenhydramine, 50 mg intravenously, and hydrocortisone 100 mg every eight hours with resolution of her symptoms over a 24 hour period. Angioedema should be recognized as a possible life threatening complication of therapy with lisinopril, and other angiotensin converting enzyme (ACE) inhibitors. This usually responds to therapy with antihistamines and steroids if recognized early.

Aged↗

PubMed1992

[Hereditary angioedema. Control and treatment in 7 cases].

Hereditary angioedema (HAE) is due to a deficit of the C1 inhibitor (C1 INH) of a dominant autosomic inheritance. Seven patients are presented from a family with HAE, four of whom with poor prognosis due to the frequency and site of the angioedema. Prophylaxis was obtained with long-term danazol since antifibrinolytic drugs are not efficient in the prevention of outbreaks of angioedema. In three cases a concentrate of C1 INH was administered and in another as short term prophylaxis prior to surgery. C1 INH was more efficient under these indications than fresh plasma or antifibrinolytic drugs.

Adult↗

PubMedDate not supplied

[Hereditary angioedema by defict of C1 esterase. Our experience in 8 cases].

Eight cases of hereditary angioedema, all of them with low values of C1-sterase inhibitor are analyzed. In 7 cases the C3 and C4 components of the complement were assessed; the results showed marked descent of C4. The 8 patients came from 4 different families; only 2 of them were males. Six patients presented digestive disorders, reporting colic pain, nausea and vomiting. In 1 of them the abdominal picture was the only evidence of the disease. In 5 patients the angioedema episodes occurred following traumatisms and in 3 because of emotional states. The duration of the attacks varied from several hours to six days. There was a familial history in all cases. Three of the patients had repeated episodes of pharyngolaryngeal angioedema, two of them requiring emergency tracheotomy because of suffocating crisis. Six patients were treated with Epsilon aminocaproic acid (16 to 20 gr daily) or with tranexamic acid (1 to 3 gr. daily). In 4 cases the results were excellent with either of these antifibrinolytic drugs. No side effects were observed in the tranexamic acid therapy whilst they were frequent in the treatment with Epsilon aminocaproic acid.

Adolescent↗

PubMed1976

Hereditary vibratory angioedema: confirmation of histamine release in a type of physical hypersensitivity.

A new syndrome called hereditary vibratory angioedema (HVA), characterized by pyruritis and angioedema at the site of a vibratory stimulus, was recently reported as a model of nonimmunologic immediate hypersensitivity. The biochemical mediator of this syndrome was not defined initially. This study now demonstrates that in vivo histamine release occurs in conjunction with the local and systemic clinical manifestations following a controlled vibratory stimulus. Histamine is suggested as the major mediator in this inherited physical hypersensitivity state.

Angioedema↗

PubMed1976

Treatment of hereditary angioedema with danazol. Reversal of clinical and biochemical abnormalities.

Danazol, an androgen derivative, was evaluated for its effectiveness in preventing attacks of hereditary angioedema in a double-blind study with nine patients. Of 47 placebo courses, 44 ended with attacks, but during 46 danazol courses only one attack occurred. Side effects were minimal, and virilization was not observed in the women studied. C1 esterase inhibitor levels increased three to four times, and levels of the fourth component of complement (C4) increased 15 times. These changes began during the first day of therapy and were maximal by one to two weeks. After therapy was stopped, C1 esterase inhibitor and C4 levels rapidly decreased. Danazol effectively prevents attacks in hereditary angioedema and acts to correct the underlying biochemical abnormality.

Adult↗