1/73. Rapid oral challenge-desensitization for patients with aspirin-related urticaria-angioedema.BACKGROUND: Acetylsalicylic acid (ASA), commonly known as aspirin, is indicated in the treatment of coronary artery disease (CAD). Many patients are denied treatment with ASA because of a history of ASA or nonsteroidal anti-inflammatory drug (NSAID)-induced urticaria or angioedema. OBJECTIVE: We sought to develop a safe and practical protocol to allow the administration of ASA to patients with a history of ASA- or NSAID-induced urticaria-angioedema. methods: Eleven subjects with a history of ASA- or NSAID-induced urticaria-angioedema were challenged-desensitized by oral protocols based on rapidly escalating doses of ASA. Most had CAD, one had a history of pulmonary embolism, and one had refractory chronic sinusitis and asthma. Starting doses ranged from 0.1 to 10 mg and were administered at intervals of 10 to 30 minutes. Dosing was individualized for each patient but followed this general sequence (in milligrams): 0.1, 0.3, 1, 3, 10, 20, 40, 81, 162, 325. RESULTS: Nine patients tolerated the procedure without adverse effects and continued taking ASA for periods ranging from 1 to 24 months, without development of urticaria or angioedema. A patient who had a history of chronic idiopathic urticaria in addition to aspirin-induced urticaria had chest tightness during the protocol. Another patient who had continuing urticaria and angioedema associated with antithyroid antibodies developed angioedema several hours after completing the protocol. CONCLUSION: In patients with historical ASA- or NSAID-induced urticaria-angioedema reactions but who did not have urticaria and angioedema independent of ASA/NSAID, rapid oral challenge-desensitization to ASA was performed safely and permitted patients with CAD and other diseases to receive treatment with ASA.- - - - - - - - - - ranking = 1keywords = angioedema (Clic here for more details about this article) |
2/73. Leukotriene receptor antagonists may prevent NSAID-induced exacerbations in patients with chronic urticaria.BACKGROUND: About 30% of patients with chronic urticaria experience flares of hives and/or angioedema after ingesting either aspirin or nonsteroidal anti-inflammatory drugs. In such patients, cross-reactivity to all NSAIDs seems to occur suggesting a mechanism dependent on cyclooxygenase inhibition. OBJECTIVE: To evaluate the preventive effect of leukotriene receptor antagonists on urticaria exacerbations induced by NSAIDs in a patient with chronic urticaria. methods: A 59-year-old woman with a 2-year history of recurrent urticaria exacerbated by different NSAIDs including aspirin 500 mg (2 episodes), piroxicam 20 mg, and nimesulide 100 mg (1 episode each) was studied. acetaminophen 375 mg and floctafenine 50 mg induced a marked flare of urticaria/angioedema in a single-blind, placebo-controlled challenge. RESULTS: The patient was totally urticaria free during a 3-week course of montelukast 10 mg once a day. After montelukast withdrawal, a gradual relapse of urticaria/angioedema occurred along with a further acute urticaria/angioedema episode after a single piroxicam, 20-mg tablet. Zafirlukast 20 mg twice daily was started. After some days the patient was urticaria-free again, and after 3 weeks she tolerated a 6-day course of injective piroxicam (20 mg once a day) without any problem. To date the patient is still urticaria-free. CONCLUSION: Leukotriene receptor antagonists may prevent the severe urticaria/angioedema exacerbations which follow the use of NSAIDs in some patients with chronic urticaria.- - - - - - - - - - ranking = 0.41666666666667keywords = angioedema (Clic here for more details about this article) |
3/73. hypersensitivity reactions associated with recombinant tissue-type plasminogen activator and urokinase.anaphylaxis or angioedema in response to recombinant tissue-type plasminogen activator or urokinase have been reported in only a few isolated cases. Both agents are endogenous proteins and thus considered non-antigenic. Activation of fibrinolysis may per se facilitate anaphylactoid reactions by pathophysiologic pathways that are not well understood. We report a unique case, review the literature and discuss implication for the clinician. The 25-year-old patient underwent thrombolytic treatment for extensive thrombosis of pelvic and deep lower extremity veins. The patient developed protracted anaphylactoid reactions during recombinant tissue-type plasminogen activator continuous intravenous infusion. After changing treatment to urokinase, the same symptoms recurred with more severe intensity, despite corticosteroid premedication. Symptoms resolved within hours after treatment with histamine receptor blockers. This unique observation, i.e. sequential occurrence of anaphylactoid reactions during recombinant tissue plasminogen activator and urokinase treatments, adds to existing evidence for an unspecific non-antigenic pathomechanism, and for a class effect of thrombolytics. steroids do not prevent, but histamine receptor blockers seem to be an effective treatment of this unusual complication of thrombolytic therapy.- - - - - - - - - - ranking = 0.083333333333333keywords = angioedema (Clic here for more details about this article) |
4/73. Allergic contact urticaria from raw potato.A 19-year-old man exhibited symptoms of immediate urticaria and angioedema related to contact with raw potato. A prick-by-prick test with potato pulp and rub test were positive. Specific IgE to potato was positive (class 2).- - - - - - - - - - ranking = 0.083333333333333keywords = angioedema (Clic here for more details about this article) |
5/73. urticaria and angioedema from cyclooxygenase-2 inhibitors.Cyclooxygenase-2 (COX-2) inhibitors celecoxib and rofecoxib have generally been well tolerated. It has been unclear if specific COX-2 inhibitors would cross react with acetylsalicylic acid and typical nonsteroidal antiinflammatory drugs to cause urticaria or angioedema. There are no reports in the literature of hives or angioedema resulting from their use. We describe 3 patients who developed urticaria and/or angioedema from COX-2 inhibitors. With the increasing use of COX-2 inhibitors, one needs to be aware of these side effects and of possible cross reactivity between celecoxib and rofecoxib.- - - - - - - - - - ranking = 0.58333333333333keywords = angioedema (Clic here for more details about this article) |
6/73. angioedema and systemic sclerosis. A review of the literature.We report a case of chronic idiopathic recurrent urticaria-angioedema and gastroesophageal reflux disease in a 35-years-old man, followed after 2 years by Raynaud's phenomenon and esophageal dysphagia, recurrent cough and dyspnoea, and after 4 years by systemic sclerosis. A review of the literature and possible correlated pathogenetic mechanisms are presented.- - - - - - - - - - ranking = 0.083333333333333keywords = angioedema (Clic here for more details about this article) |
7/73. Successful treatment of autoimmune chronic idiopathic urticaria with intravenous cyclophosphamide.BACKGROUND: A 45-year-old woman presented with a 20-year history of chronic idiopathic urticaria (CIU) unresponsive to H1- and H2-antagonists and combinations of other anti-inflammatory agents but controlled with daily prednisone (35 mg) for more than 13 years. Intracutaneous testing to autologous serum revealed an 8 x 10-mm wheal/flare reaction consistent with the presence of anti-Fc epsilonRIalpha autoantibodies. These autoantibodies have been reported to be present in >45% of patients with CIU. Their functional role in the pathogenesis of CIU remains poorly understood. OBJECTIVE: Because of the therapeutic refractory nature of this patient's CIU requiring high doses of corticosteroids, it was decided to initiate treatment with intravenous cyclophosphamide (CTX) in an attempt to eradicate autoantibody-producing B-lymphocyte clones. This therapeutic approach has been previously successful in other autoantibody-mediated disorders such as type II acquired angioedema and factor viii deficiency. RESULTS: Initial treatment consisted of 500 mg CTX intravenously followed by increases of 100 mg every 2 weeks, with the maximum dose reaching 1,500 mg once a month, which represents approximately 20% of the dose administered during systemic cancer chemotherapy. Within 7 months there was a complete clinical remission and prednisone was discontinued. Repeat intracutaneous testing to autologous serum was negative, consistent with an abrogated autoantibody response. The patient has not experienced a recurrence of CIU at the time of this report. CONCLUSION: This index case suggests that intravenous CTX may be effective in alleviating autoantibody-associated CIU in corticosteroid-dependent patients refractory to conventional therapies.- - - - - - - - - - ranking = 0.083333333333333keywords = angioedema (Clic here for more details about this article) |
8/73. hypersensitivity to procarbazine associated with angioedema, urticaria, and low serum complement activity.hypersensitivity to procarbazine associated with urticaria, angioedema, and painful joint swelling was found in a 20-year-old student being treated for Hodgkin's disease. A marked fall in complement component activity occurred simultaneously with the development of symtoms. It is suggested that generation of products of complement component activation could be important in the pathogenesis of hypersensitivity to some drugs.- - - - - - - - - - ranking = 0.41666666666667keywords = angioedema (Clic here for more details about this article) |
9/73. Autoimmune progesterone dermatitis and its manifestation as anaphylaxis: a case report and literature review.OBJECTIVE: Autoimmune progesterone dermatitis is a rare cyclic premenstrual reaction to progesterone produced during the luteal phase of a woman's menstrual cycle with a variety of presentations including erythema multiforme, eczema, urticaria, angioedema, and progesterone-induced anaphylaxis. We present a case of progesterone-induced anaphylaxis and a review of literature focusing on its diagnosis and therapy. DATA SOURCES: We surveyed all the literature in English back to 1921 when the first case was published. First, we researched the terms progesterone anaphylaxis, autoimmune progesterone dermatitis, cyclic urticaria, using the pubmed resource. Then we included articles found within these publications' reference sections. STUDY SELECTION: We selected articles based on whether the cases described appeared to fit the description of the entity autoimmune progesterone dermatitis. All cases included had dermatologic reactions occurring during the luteal phase of the menstrual period, positive skin or intramuscular reactions to progesterone, and treatment amenable to anovulatory agents and/or hysterectomy with bilateral salpingo-oophorectomy. RESULTS: We found approximately 50 published cases of autoimmune progesterone dermatitis, and only nine known cases of its manifestation as anaphylaxis. These cases, including the case described by us, are summarized, and successful diagnostic and therapeutic approaches in the literature are reviewed. CONCLUSIONS: Autoimmune progesterone dermatitis is a rare entity associated with progesterone production of the luteal phase of a woman's menstrual cycle. It can be diagnosed using intradermal or intramuscular progesterone tests and can be treated by disrupting the ovulation cycle using specific medications or by oopherectomy.- - - - - - - - - - ranking = 0.083333333333333keywords = angioedema (Clic here for more details about this article) |
10/73. The syndrome of thyroid autoimmunity and idiopathic chronic urticaria and angioedema presenting as anaphylaxis.Previous observations have shown that the syndrome of thyroid autoimmunity and idiopathic urticaria and angioedema (ICUA) can be associated with a marked worsening of reactive airway disease. Possibly, mediators released in this syndrome may contribute to acute bronchospasm and associated respiratory symptoms in some patients. In this study, two patients presenting with overlapping clinical presentations of the syndrome of thyroid immunity and ICUA are described in whom a diagnosis of anaphylaxis to food and antibiotics, respectively, was initially suspected but ruled out by testing and challenges. These cases illustrate clinical overlap between presentations of ICUA and anaphylaxis. We suggest that patients with idiopathic anaphylaxis be evaluated for the presence of antithyroid microsomal (peroxidase) antibodies or antithyroglobulin antibodies, particularly because the diagnosis of thyroid antibody-positive ICUA may suggest additional therapeutic options.- - - - - - - - - - ranking = 0.41666666666667keywords = angioedema (Clic here for more details about this article) |
| | Next -> |