Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Angioedema Medication

  • Author: Huamin Henry Li, MD, PhD, CPI; Chief Editor: Michael A Kaliner, MD  more...
 
Updated: Apr 01, 2015
 

Medication Summary

The primary goal of medical therapy for angioedema is to reduce and prevent swelling. Reducing discomfort and minimizing complications are also extremely important goals. Most of the drugs used for urticaria and anaphylaxis are also used for many types of angioedema.

In histamine-mediated angioedema, second-generation antihistamines are often first-line treatment. Corticosteroids can be used in severe cases of this form of the disease, but long-term use of these agents should be avoided in outpatient treatment.

Antihistamines do not work for patients with bradykinin-mediated angioedema, and corticosteroids have limited or no value in this type of angioedema. However, fresh frozen plasma (FFP), antifibrinolytics, C1 esterase inhibitor (C1-INH), ecallantide, and icatibant can be used to manage bradykinin-mediated angioedema.

Limited small studies of anti-inflammatory agents have shown dapsone, sulfasalazine, hydroxychloroquine, and colchicine to provide clinical benefit in patients with chronic urticaria or angioedema.[7] This group of medications is associated with higher risk than antihistamines or H2 antagonists and leukotriene receptor antagonists. However, for those requiring corticosteroids, selecting one of these drugs may offer better side effect profile. Special safety monitoring is recommended for each individual medication.

Recalcitrant angioedema

Immunosuppressants such as calcineurin inhibitors (cyclosporine and tacrolimus), methotrexate, mycophenolate mofetil, cyclophosphamide, azathioprine, and sirolimus have been tried in treating antihistamine-resistant chronic urticaria or angioedema. Of these, cyclosporine has been most thoroughly studied in this setting.[62] Although clear benefit has been shown with cyclosporine, concerns for its side effects (which may outweigh the benefit) still pose a challenge for clinicians.

Intravenous immunoglobulin (IVIg) has also shown to be effective for some patients who are antihistamine-unresponsive. Evidence of its efficacy is limited to a few open-label case studies, and the appropriate dosage, dosing interval, and treatment duration have not been well established. At this time, IVIg use is limited to a carefully selected group of patients who do not have an adequate treatment response or who not tolerate alternative treatment.

Next

Alpha/Beta-Adrenergic Agonists

Class Summary

Adrenergic agonist agents cause vasoconstriction and bronchodilation and reduce vascular permeability. They are vitally important in treating acute angioedema associated with an allergic reaction affecting the upper airways. Their benefit in other types of laryngeal edema (eg, acute hereditary angioedema [HAE]) is less certain.

Epinephrine (EpiPen, Twinject, EpiPen Jr, Adrenaclick, Auvi-Q, Adrenalin)

 

Use epinephrine in case of laryngeal edema. It has alpha-agonist effects that include increased peripheral vascular resistance and reduced vascular permeability.

Previous
Next

Antihistamines, 1st-Generation

Class Summary

Antihistamines (H1 and H2) generally work well for urticaria. However, the great majority of angioedema cases, especially when not accompanied by urticaria, do not respond adequately to antihistamine treatment. In certain types of angioedema, such as hereditary angioedema (HAE), angiotensin-converting enzyme (ACE) inhibitor–acquired angioedema (AIIA), and acquired angioedema (AAE), antihistamines are ineffective and are not recommended for treatment.

The first-generation H1 antagonists (eg, diphenhydramine, hydroxyzine, doxepin, chlorpheniramine, and cyproheptadine) are inexpensive and effective in reducing pruritus, but drowsiness and anticholinergic effects can be troublesome. Because of the potential sedative effects, patients should be cautioned about driving and operating heavy machinery.

Diphenhydramine (Benadryl, Benadryl Allergy Dye-Free LiquiGels, Children's Benadryl Allergy, Children's Triaminic Thin Strips Allergy, PediaCare Children's Allergy)

 

Diphenhydramine is used for the relief of symptoms caused by the release of histamine. It is the most commonly used first-generation antihistamine and is available without a prescription in the United States.

Chlorpheniramine (ChlorTrimeton)

 

Chlorpheniramine is a first-generation agent. It competes with histamine for H1-receptor sites on effector cells in blood vessels and the respiratory tract. Chlorpheniramine is one of the safest antihistamines to use during pregnancy.

Cyproheptadine

 

Cyproheptadine is a first-generation agent. It is used for the symptomatic relief of allergic symptoms caused by histamine release. Cyproheptadine prevents histamine release in blood vessels and is more effective in preventing histamine response than in reversing it. It may be useful in patients with syndromes sustained by histamine-producing tumors.

Hydroxyzine hydrochloride (Vistaril)

 

Hydroxyzine hydrochloride antagonizes H1 receptors in the periphery. It may suppress histamine activity in the subcortical region of the central nervous system (CNS).

Previous
Next

Antihistamines, 2nd Generation

Class Summary

The second-generation antihistamines have much lower sedative effects. Nevertheless, any patient who is taking a medication that has potential sedative effects should be cautioned about driving and operating heavy machinery.

Fexofenadine (Allegra)

 

Fexofenadine is a nonsedating second-generation antihistamine. It is tolerated very well, with a rate of sedation that does not differ significantly from that of placebo.

Cetirizine (Zyrtec)

 

Cetirizine selectively inhibits histamine H1 receptor sites in blood vessels and in the gastrointestinal (GI) and respiratory tracts, and this action, in turn, inhibits the physiologic effects that histamine normally induces at H1 receptor sites. The once-daily dosing is convenient. Bedtime dosing may be useful if sedation is a problem.

Desloratadine (Clarinex)

 

Desloratadine is a long-acting, tricyclic histamine antagonist that is selective for the H1 receptor. It is a major metabolite of loratadine, which, after ingestion, is extensively metabolized to the active metabolite 3-hydroxydesloratadine.

Loratadine (Claritin, Alavert, Loradamed)

 

Loratadine selectively inhibits peripheral histamine H1 receptors. It is tolerated very well, with a rate of sedation that does not differ significantly from that of placebo. The once-daily dosing makes it convenient.

Levocetirizine (Xyzal)

 

Levocetirizine is an H1-receptor antagonist that is an active enantiomer of cetirizine. This agent is available as a 5-mg breakable (scored) tab and a 0.5 mg/mL oral solution.

Previous
Next

Histamine H2 Antagonists

Class Summary

These drugs are usually used to decrease gastric acid secretion. When used as a single agent for urticaria and angioedema, they are not effective. However, the combination of an H1 antagonist with an H2 antagonist has been shown to be more effective than an H1 antagonist alone. Any of the H2 blockers can be used. Two of the most commonly used agents are ranitidine and cimetidine.

Cimetidine (Tagamet)

 

Cimetidine is a nonprescription antihistamine H2-receptor antagonist. Its use can increase the serum concentration of hydroxyzine but not of cetirizine.[73]

Ranitidine (Zantac)

 

Ranitidine is a nonprescription antihistamine H2-receptor antagonist. It has a better safety profile, a longer duration of action, and considerably (10 times) stronger H2-receptor binding than cimetidine does, and it does not suppress cytochrome P450 isoenzymes. Its clinical efficacy as add-on therapy to antihistamine in urticaria has not been conclusively determined.[74, 75, 76]

Previous
Next

Leukotriene Receptor Antagonists

Class Summary

Leukotriene receptor antagonists may be used as add-on therapy for histamine-mediated angioedema with or without urticaria. A subset of patients, especially those with sensitivity to aspirin or nonsteroidal anti-inflammatory agents (NSAIDs) or food additive intolerance, may benefit more from this treatment; however, this is not supported by strong clinical evidence.[77]

Montelukast (Singulair)

 

Montelukast blocks binding of leukotriene D4 to its receptor. It is used off label to treat chronic urticaria.

Zafirlukast (Accolate)

 

Zafirlukast is a competitive receptor antagonist of leukotrienes C4, D4, and E4.

Previous
Next

Tricyclic Antidepressants

Class Summary

Tricyclic antidepressants (TCAs) have potent H1 antihistamine activity that may be beneficial in treating angioedema.

Doxepin

 

Doxepin is a TCA that has potent H1-blocking activity.

Previous
Next

Corticosteroids

Class Summary

Despite the paucity of well controlled clinical studies, the efficacy of corticosteroids in histamine-mediated angioedema and some forms of idiopathic angioedema (IAE) appears to be evident. However, because of their well-recognized side effects, long-term use of corticosteroids is generally not advisable.

The optimal dosage and duration of treatment are not well established. Most experts are in favor of their short-term use, preferably with the lowest effective dosage over a limited time period (eg, 15 mg/day, reduced by 1 mg weekly). Corticosteroids should only be used when other treatments cannot provide adequate clinical benefits or symptom control.{[14]

Corticosteroids may be used when antihistamines are inadequate or ineffective at controlling an acute episode of angioedema. These agents usually reduce inflammation and reduce vascular permeability in allergic angioedema and in some cases of idiopathic angioedema. However, they usually have very limited or no benefit in ACE inhibitor ̶ induced angioedema (AIIA), hereditary angioedema (HAE), and acquired angioedema (AAE).

Corticosteroids can be given as a short course of an oral agent (administered daily for 5-7 days, with or without a taper) or as a single dose of a long-acting, injectable agent. Such regimens are not usually associated with long-term sequelae.

Long-term corticosteroid use should be avoided in chronic angioedema, when possible. If angioedema is severe and cannot be safely controlled with other medications, low-dose therapy and/or alternate-day therapy can be considered.

Prednisone (Deltasone, Rayos, Prednisone Intensol, Sterapred, Sterapred DS)

 

Prednisone, a commonly used oral agent, may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte (PMN) activity. To have an effect, it must be metabolized to the active metabolite prednisolone. Conversion may be impaired in liver disease.

Prednisolone (Pediapred, Prelone, Orapred, Millipred)

 

Prednisolone, available in tablet and liquid forms, reduces vascular permeability.

Methylprednisolone (Medrol, Medrol Dosepak, DepoMedrol, SoluMedrol)

 

Methylprednisolone, available in intravenous (IV)/intramuscular (IM) and oral forms, reduces vascular permeability.

Previous
Next

Androgens

Class Summary

Androgens are particularly useful in patients with HAE and perhaps in some patients with AAE. They are not useful in angioedema due to allergy or to drug sensitivity or intolerance. There is limited experience with these drugs in IAE. They may induce the synthesis of messenger ribonucleic acid (mRNA) in the liver and directly increase C1-INH.

Danazol

 

Danazol increases levels of C4 and C1-INH and reduces attacks associated with angioedema.

Oxandrolone (Oxandrin)

 

Oxandrolone is a synthetic androgen derivative with a pediatric indication. It is used primarily in HAE prophylaxis.

Previous
Next

Antifibrinolytic Agents

Class Summary

The exact mechanism by which hemostatic agents act against angioedema is uncertain, but it is most likely related to the inhibition of plasmin, with subsequent effects on bradykinin metabolism. Hemostatic agents have shown benefit in treating HAE, AAE, and certain forms of IAE. They are not indicated in the treatment of allergic angioedema.

Aminocaproic acid (Amicar)

 

Aminocaproic acid inhibits fibrinolysis through inhibition of plasminogen activator substances and, to a lesser degree, through antiplasmin activity. It may be used in HAE and AAE as prophylaxis and to relieve acute attacks. The clinical benefit is marginal.

Tranexamic acid (Cyklokapron, Lysteda)

 

Tranexamic acid is an alternative to aminocaproic acid. It inhibits fibrinolysis by displacing plasminogen from fibrin. In Europe, it is used primarily for HAE prophylaxis, though some authors believe that it is also helpful for treating acute HAE attacks.

Previous
Next

Immunomodulators

Class Summary

Immunomodulating agents are used for treating acute HAE attacks and as routine prophylaxis against HAE attacks.

Ecallantide (Kalbitor)

 

Ecallantide is a potent, selective, reversible inhibitor of plasma kallikrein. It treats acute, episodic attacks of HAE by binding to plasma kallikrein and blocking its binding site, thus inhibiting the conversion of high-molecular-weight kininogen to bradykinin.

Icatibant (Firazyr)

 

Icatibant inhibits the binding of bradykinin to the B2 receptor and thereby treats the clinical symptoms of an acute attack of angioedema. The recommended dose is 30 mg subcutaneously in the abdominal area. The drug is available in a single-use prefilled syringe, which delivers a dose of 30 mg (10 mg/mL). Syringes can be carried and stored at room temperature, and the medication can be self-injected by the patient.

C1 inhibitor, human (Cinryze, Berinert)

 

C1-INH is a serine protease inhibitor (serpin) and a normal constituent of human blood that regulates activation of the complement pathway, the intrinsic coagulation system, and the fibrinolytic system. It binds to and neutralizes substrates that activate these systems, suppressing conversion of tissue high- molecular-weight kininogen to bradykinin and thereby reducing bradykinin-mediated angioedema. Pharmacologic preparations of C1-INH are pasteurized, lyophilized products derived from purified human plasma.

Cinryze is approved by the US Food and Drug Administration (FDA) for prophylaxis of HAE attacks. It is available as a freeze-dried powder that is reconstituted for IV administration. Berinert is indicated for the treatment of acute laryngeal, abdominal, and facial angioedema attacks in adolescents and adults with HAE. It is approved for patient self-administration after proper training by a healthcare professional.

C1 esterase inhibitor recombinant (Ruconest)

 

Recombinant C1 esterase inhibitor is from the milk of genetically modified (transgenic) rabbits. It restores the level of functional C1 esterase inhibitor in a patient's plasma, thereby treating the acute attack of swelling. It is indicated for adolescents and adults to treat acute attacks of hereditary angioedema (HAE). Efficacy for treatment of laryngeal attack was not established.

Previous
 
Contributor Information and Disclosures
Author

Huamin Henry Li, MD, PhD, CPI Director of Chevy Chase Clinical Research, Institute for Asthma and Allergy; Assistant Professor, George Washington University Hospital; Clinical Faculty, Johns Hopkins Asthma and Allergy Center, Johns Hopkins Hospital

Huamin Henry Li, MD, PhD, CPI is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, Joint Council of Allergy, Asthma and Immunology, MedChi The Maryland State Medical Society

Disclosure: Received consulting fee from Dyax for consulting; Received consulting fee from Pharming/Salix for consulting; Received consulting fee from CSL Behring for consulting; Received honoraria from Viropharma/Shire for speaking and teaching; Received consulting fee from Viropharma/Shire for consulting; Received honoraria from Dyax for speaking and teaching.

Chief Editor

Michael A Kaliner, MD Clinical Professor of Medicine, George Washington University School of Medicine; Medical Director, Institute for Asthma and Allergy

Michael A Kaliner, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association of Immunologists, American College of Allergy, Asthma and Immunology, American Society for Clinical Investigation, American Thoracic Society, Association of American Physicians

Disclosure: Nothing to disclose.

Acknowledgements

Stephen C Dreskin, MD, PhD Professor of Medicine, Departments of Internal Medicine, Director of Allergy, Asthma, and Immunology Practice, University of Colorado Health Sciences Center

Stephen C Dreskin, MD, PhD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association for the Advancement of Science, American Association of Immunologists, American College of Allergy, Asthma and Immunology, Clinical Immunology Society, and Joint Council of Allergy, Asthma and Immunology

Disclosure: Genentech Consulting fee Consulting; American Health Insurance Plans Consulting fee Consulting; Johns Hopkins School of Public Health Consulting fee Consulting; Array BioPharma Consulting fee Consulting

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Wakisaka M, Shuto M, Abe H, et al. Computed tomography of the gastrointestinal manifestation of hereditary angioedema. Radiat Med. 2008 Dec. 26(10):618-21. [Medline].

  2. Scheirey CD, Scholz FJ, Shortsleeve MJ, Katz DS. Angiotensin-converting enzyme inhibitor-induced small-bowel angioedema: clinical and imaging findings in 20 patients. AJR Am J Roentgenol. 2011 Aug. 197(2):393-8. [Medline].

  3. Kaplan AP. Urticaria and angioedema. Adkinson Jr, NF. Middleton's Allergy: Principle and Practice. 7th ed. Mosby; 2009. 1061-81.

  4. Nakamura S, Nagao A, Kishino M, Konishi H, Shiratori K. Education and Imaging. Gastrointestinal: angioedema of the small bowel. J Gastroenterol Hepatol. 2008 Jul. 23(7 Pt 1):1158. [Medline].

  5. Raman SP, Lehnert BE, Pruthi S. Unusual radiographic appearance of drug-induced pharyngeal angioedema and differential considerations. AJNR Am J Neuroradiol. 2009 Jan. 30(1):77-8. [Medline].

  6. Donati M. De medica historia mirabili. Mantuae, per Fr. Osanam. 1586.

  7. Milton JL. On giant urticaria. Edinburgh Med J. 1876. 22:513-26.

  8. Quincke H. Uber Akutes Umschreibenes H Autodem. Monatusschr Pract Dermatol. 1882. 129-31.

  9. Osler W. Hereditary angio-neurotic edema. Am J Med Sci. 1888. 95:362-7.

  10. Adhikari SP, Schneider JI. An unusual cause of abdominal pain and hypotension: angioedema of the bowel. J Emerg Med. 2009 Jan. 36(1):23-5. [Medline].

  11. Kaplan AP. Angioedema. World Allergy Organ J. 2008 Jun. 1(6):103-13. [Medline].

  12. Rye Rasmussen EH, Bindslev-Jensen C, Bygum A. Angioedema--assessment and treatment. Tidsskr Nor Laegeforen. 2012 Nov 12. 132(21):2391-5. [Medline].

  13. Marx J, Hockberger R, Walls R. Urticaria and angioedema. Rosen's Emergency Medicine. 7th ed. Mosby; 2009. [Full Text].

  14. Mansi M, Zanichelli A, Coerezza A, Suffritti C, Wu MA, Vacchini R, et al. Presentation, diagnosis and treatment of angioedema without wheals: a retrospective analysis of a cohort of 1058 patients. J Intern Med. 2014 Sep 4. [Medline].

  15. [Guideline] Cicardi M, Aberer W, Banerji A, Bas M, Bernstein JA, Bork K, et al. Classification, diagnosis, and approach to treatment for angioedema: consensus report from the Hereditary Angioedema International Working Group. Allergy. 2014 May. 69(5):602-16. [Medline].

  16. Oschatz C, Maas C, Lecher B, Jansen T, Björkqvist J, Tradler T, et al. Mast cells increase vascular permeability by heparin-initiated bradykinin formation in vivo. Immunity. 2011 Feb 25. 34(2):258-68. [Medline].

  17. Asero R, Bavbek S, Blanca M, Blanca-Lopez N, Cortellini G, Nizankowska-Mogilnicka E, et al. Clinical management of patients with a history of urticaria/angioedema induced by multiple NSAIDs: an expert panel review. Int Arch Allergy Immunol. 2013. 160(2):126-33. [Medline].

  18. Fonacier LS, Dreskin SC, Leung DY. Allergic skin diseases. J Allergy Clin Immunol. 2010 Feb. 125(2 Suppl 2):S138-49. [Medline].

  19. Bas M, Adams V, Suvorava T, Niehues T, Hoffmann TK, Kojda G. Nonallergic angioedema: role of bradykinin. Allergy. 2007 Aug. 62(8):842-56. [Medline].

  20. Cugno M, Marzano AV, Asero R, Tedeschi A. Activation of blood coagulation in chronic urticaria: pathophysiological and clinical implications. Intern Emerg Med. 2010 Apr. 5(2):97-101. [Medline].

  21. Zuraw BL. Clinical practice. Hereditary angioedema. N Engl J Med. 2008 Sep 4. 359(10):1027-36. [Medline].

  22. Champion RH, Roberts SO, Carpenter RG, Roger JH. Urticaria and angio-oedema. A review of 554 patients. Br J Dermatol. 1969 Aug. 81(8):588-97. [Medline].

  23. Galli SJ, Tsai M. IgE and mast cells in allergic disease. Nat Med. 2012 May 4. 18(5):693-704. [Medline]. [Full Text].

  24. Frigas E, Nzeako UC. Angioedema. Pathogenesis, differential diagnosis, and treatment. Clin Rev Allergy Immunol. 2002 Oct. 23(2):217-31. [Medline].

  25. Banerji A, Sheffer AL. The spectrum of chronic angioedema. Allergy Asthma Proc. 2009 Jan-Feb. 30(1):11-6. [Medline].

  26. Cugno M, Zanichelli A, Foieni F, Caccia S, Cicardi M. C1-inhibitor deficiency and angioedema: molecular mechanisms and clinical progress. Trends Mol Med. 2009 Feb. 15(2):69-78. [Medline].

  27. Kaplan AP, Greaves M. Pathogenesis of chronic urticaria. Clin Exp Allergy. 2009 Jun. 39(6):777-87. [Medline].

  28. Zingale LC, Castelli R, Zanichelli A, Cicardi M. Acquired deficiency of the inhibitor of the first complement component: presentation, diagnosis, course, and conventional management. Immunol Allergy Clin North Am. 2006 Nov. 26(4):669-90. [Medline].

  29. Byrd JB, Adam A, Brown NJ. Angiotensin-converting enzyme inhibitor-associated angioedema. Immunol Allergy Clin North Am. 2006 Nov. 26(4):725-37. [Medline].

  30. Bork K, Barnstedt SE, Koch P, Traupe H. Hereditary angioedema with normal C1-inhibitor activity in women. Lancet. 2000 Jul 15. 356(9225):213-7. [Medline].

  31. Bowen T, Cicardi M, Bork K, Zuraw B, Frank M, Ritchie B, et al. Hereditary angiodema: a current state-of-the-art review, VII: Canadian Hungarian 2007 International Consensus Algorithm for the Diagnosis, Therapy, and Management of Hereditary Angioedema. Ann Allergy Asthma Immunol. 2008 Jan. 100(1 Suppl 2):S30-40. [Medline].

  32. Dewald G, Bork K. Missense mutations in the coagulation factor XII (Hageman factor) gene in hereditary angioedema with normal C1 inhibitor. Biochem Biophys Res Commun. 2006 May 19. 343(4):1286-9. [Medline].

  33. Bork K, Gül D, Dewald G. Hereditary angio-oedema with normal C1 inhibitor in a family with affected women and men. Br J Dermatol. 2006 Mar. 154(3):542-5. [Medline].

  34. Craig TJ, Levy RJ, Wasserman RL, et al. Efficacy of human C1 esterase inhibitor concentrate compared with placebo in acute hereditary angioedema attacks. J Allergy Clin Immunol. 2009 Oct. 124(4):801-8. [Medline].

  35. Bossi F, Fischetti F, Regoli D, et al. Novel pathogenic mechanism and therapeutic approaches to angioedema associated with C1 inhibitor deficiency. J Allergy Clin Immunol. 2009 Dec. 124(6):1303-10.e4. [Medline]. [Full Text].

  36. Banerji A, Weller PF, Sheikh J. Cytokine-associated angioedema syndromes including episodic angioedema with eosinophilia (Gleich's Syndrome). Immunol Allergy Clin North Am. 2006 Nov. 26(4):769-81. [Medline].

  37. Ferreli C, Pinna AL, Atzori L, Aste N. Eosinophilic cellulitis (Well's syndrome): a new case description. J Eur Acad Dermatol Venereol. 1999 Jul. 13(1):41-5. [Medline].

  38. Brown AF, McKinnon D, Chu K. Emergency department anaphylaxis: A review of 142 patients in a single year. J Allergy Clin Immunol. 2001 Nov. 108(5):861-6. [Medline].

  39. Yang MS, Lee SH, Kim TW, et al. Epidemiologic and clinical features of anaphylaxis in Korea. Ann Allergy Asthma Immunol. 2008 Jan. 100(1):31-6. [Medline].

  40. Kalmár L, Hegedüs T, Farkas H, Nagy M, Tordai A. HAEdb: a novel interactive, locus-specific mutation database for the C1 inhibitor gene. Hum Mutat. 2005 Jan. 25(1):1-5. [Medline].

  41. Banerji A, Clark S, Blanda M, LoVecchio F, Snyder B, Camargo CA Jr. Multicenter study of patients with angiotensin-converting enzyme inhibitor-induced angioedema who present to the emergency department. Ann Allergy Asthma Immunol. 2008 Apr. 100(4):327-32. [Medline].

  42. Frigas E, Park M. Idiopathic recurrent angioedema. Immunol Allergy Clin North Am. 2006 Nov. 26(4):739-51. [Medline].

  43. Hentges F, Hilger C, Kohnen M, Gilson G. Angioedema and estrogen-dependent angioedema with activation of the contact system. J Allergy Clin Immunol. 2009 Jan. 123(1):262-4. [Medline].

  44. Cichon S, Martin L, Hennies HC, et al. Increased activity of coagulation factor XII (Hageman factor) causes hereditary angioedema type III. Am J Hum Genet. 2006 Dec. 79(6):1098-104. [Medline]. [Full Text].

  45. Gleich GJ, Leiferman KM. The hypereosinophilic syndromes: current concepts and treatments. Br J Haematol. 2009 May. 145(3):271-85. [Medline].

  46. Morgan M, Khan DA. Therapeutic alternatives for chronic urticaria: an evidence-based review, Part 2. Ann Allergy Asthma Immunol. 2008 Jun. 100(6):517-26; quiz 526-8, 544. [Medline].

  47. Bouillet L, Longhurst H, Boccon-Gibod I, Bork K, Bucher C, Bygum A, et al. Disease expression in women with hereditary angioedema. Am J Obstet Gynecol. 2008 Nov. 199(5):484.e1-4. [Medline].

  48. Sánchez-Borges M, Asero R, Ansotegui IJ, Baiardini I, Bernstein JA, Canonica GW, et al. Diagnosis and treatment of urticaria and angioedema: a worldwide perspective. World Allergy Organ J. 2012 Nov. 5(11):125-47. [Medline].

  49. Joint Taskforce on Practice Parameters Website. Available at http://www.allergyparameters.org/. Accessed: June 5, 2013.

  50. Joint Taskforce on Practice Parameters. Angioedema practice parameters: 2013 update. J Allergy Clin Immunol. [in press] June 2013.

  51. Cugno M, Zanichelli A, Bellatorre AG, Griffini S, Cicardi M. Plasma biomarkers of acute attacks in patients with angioedema due to C1-inhibitor deficiency. Allergy. 2009 Feb. 64(2):254-7. [Medline].

  52. Lang DM, Aberer W, Bernstein JA, Chng HH, Grumach AS, Hide M, et al. International consensus on hereditary and acquired angioedema. Ann Allergy Asthma Immunol. 2012 Dec. 109(6):395-402. [Medline].

  53. Powell RJ, Leech SC, Till S, Huber PA, Nasser SM, Clark AT. BSACI guideline for the management of chronic urticaria and angioedema. Clin Exp Allergy. 2015 Mar. 45(3):547-65. [Medline].

  54. Craig T, Pürsün EA, Bork K, Bowen T, Boysen H, Farkas H, et al. WAO Guideline for the Management of Hereditary Angioedema. World Allergy Organ J. 2012 Dec. 5(12):182-199. [Medline].

  55. Zuberbier T, Asero R, Bindslev-Jensen C, Walter Canonica G, Church MK, Giménez-Arnau A, et al. EAACI/GA(2)LEN/EDF/WAO guideline: definition, classification and diagnosis of urticaria. Allergy. 2009 Oct. 64(10):1417-26. [Medline].

  56. Ferrer M, Sastre J, Jáuregui I, Dávila I, Montoro J, del Cuvillo A, et al. Effect of antihistamine up-dosing in chronic urticaria. J Investig Allergol Clin Immunol. 2011. 21 Suppl 3:34-9. [Medline].

  57. Handa S, Dogra S, Kumar B. Comparative efficacy of cetirizine and fexofenadine in the treatment of chronic idiopathic urticaria. J Dermatolog Treat. 2004 Jan. 15(1):55-7. [Medline].

  58. Potter PC, Kapp A, Maurer M, Guillet G, Jian AM, Hauptmann P, et al. Comparison of the efficacy of levocetirizine 5 mg and desloratadine 5 mg in chronic idiopathic urticaria patients. Allergy. 2009 Apr. 64(4):596-604. [Medline].

  59. Curran MP, Scott LJ, Perry CM. Cetirizine: a review of its use in allergic disorders. Drugs. 2004. 64(5):523-61. [Medline].

  60. Hindmarch I, Johnson S, Meadows R, Kirkpatrick T, Shamsi Z. The acute and sub-chronic effects of levocetirizine, cetirizine, loratadine, promethazine and placebo on cognitive function, psychomotor performance, and weal and flare. Curr Med Res Opin. 2001. 17(4):241-55. [Medline].

  61. Asero R, Tedeschi A, Lorini M. Leukotriene receptor antagonists in chronic urticaria. Allergy. 2001 May. 56(5):456-7. [Medline].

  62. Maurer M, Rosén K, Hsieh HJ, Saini S, Grattan C, Gimenéz-Arnau A, et al. Omalizumab for the treatment of chronic idiopathic or spontaneous urticaria. N Engl J Med. 2013 Mar 7. 368(10):924-35. [Medline].

  63. Spector SL, Tan RA. Advances in allergic skin disease: omalizumab is a promising therapy for urticaria and angioedema. J Allergy Clin Immunol. 2009 Jan. 123(1):273-4. [Medline].

  64. Song CH, Stern S, Giruparajah M, Berlin N, Sussman GL. Long-term efficacy of fixed-dose omalizumab for patients with severe chronic spontaneous urticaria. Ann Allergy Asthma Immunol. 2013 Feb. 110(2):113-7. [Medline].

  65. Zuraw BL et al. Nanofiltered C1 inhibitor concentrate for treatment of hereditary angioedema. N Engl J Med. Aug 2010. 363:513-22.

  66. Riedl MA, Hurewitz DS, Levy R, Busse PJ, Fitts D, Kalfus I. Nanofiltered C1 esterase inhibitor (human) for the treatment of acute attacks of hereditary angioedema: an open-label trial. Ann Allergy Asthma Immunol. 2012 Jan. 108(1):49-53. [Medline].

  67. Cicardi M et al. Ecallantide for the treatment of acute attacks in hereditary angioedema. N Engl J Med. Aug 2010. 363:523-31.

  68. Cicardi M, et al. Icatibant, a new bradykinin-receptor antagonist, in hereditary angioedema. N Engl J Med. 2010 Aug 5. 363(6):532-41. [Medline].

  69. US Food and Drug Administration. FDA approves Firazyr to treat acute attacks of hereditary angioedema. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm269616.htm. Accessed: January 3, 2013.

  70. [Guideline] Cicardi M, Bork K, Caballero T, Craig T, Li HH, Longhurst H, et al. Evidence-based recommendations for the therapeutic management of angioedema owing to hereditary C1 inhibitor deficiency: consensus report of an International Working Group. Allergy. 2012 Feb. 67(2):147-57. [Medline].

  71. [Guideline] Caballero T, Farkas H, Bouillet L, Bowen T, Gompel A, Fagerberg C, et al. International consensus and practical guidelines on the gynecologic and obstetric management of female patients with hereditary angioedema caused by C1 inhibitor deficiency. J Allergy Clin Immunol. 2012 Feb. 129(2):308-20. [Medline].

  72. Simons FE, Sussman GL, Simons KJ. Effect of the H2-antagonist cimetidine on the pharmacokinetics and pharmacodynamics of the H1-antagonists hydroxyzine and cetirizine in patients with chronic urticaria. J Allergy Clin Immunol. 1995 Mar. 95(3):685-93. [Medline].

  73. Paul E, Bödeker RH. Treatment of chronic urticaria with terfenadine and ranitidine. A randomized double-blind study in 45 patients. Eur J Clin Pharmacol. 1986. 31(3):277-80. [Medline].

  74. Sharpe GR, Shuster S. In dermographic urticaria H2 receptor antagonists have a small but therapeutically irrelevant additional effect compared with H1 antagonists alone. Br J Dermatol. 1993 Nov. 129(5):575-9. [Medline].

  75. Fedorowicz Z, van Zuuren EJ, Hu N. Histamine H2-receptor antagonists for urticaria. Cochrane Database Syst Rev. 2012 Mar 14. 3:CD008596. [Medline].

  76. Trojan TD, Khan DA. Calcineurin inhibitors in chronic urticaria. Curr Opin Allergy Clin Immunol. 2012 Aug. 12(4):412-20. [Medline].

 
Previous
Next
 
Photographic documentation of swelling.
Bradykinin production and metabolism.
Classification of angioedema without urticaria based on clinical or etiopathologic features. AAE = acquired angioedema; ACEI = angiotensin-converting enzyme inhibitors; HAE = hereditary angioedema; Specific triggers = food, drug, insect bite, environmental allergen, or other physical stimulus. Based on data from Zingale LC, Beltrami L, Zanichelli A, et al. Angioedema without urticaria: a large clinical survey. CMAJ. Oct 24 2006; 175(9): 1065–70.
Angioedema secondary to angiotensin-converting enzyme (ACE) inhibitors.
Types of angioedema.
Pathways for production of prostaglandins and leukotrine from mobilized arachidonic acid.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.