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Acute Urticaria Treatment & Management

  • Author: Henry K Wong, MD, PhD; Chief Editor: Michael A Kaliner, MD  more...
 
Updated: Jun 19, 2015
 

Approach Considerations

Identify the etiology of the acute urticaria if possible. If an inciting agent can be identified, instruct the patient to avoid it. The major goal is to control the severity of acute urticaria lesions until the process resolves over 4-6 weeks.

Inpatient therapy may be required rarely if the urticaria is severe and does not respond to antihistamine therapy, or if the patient's condition progresses to laryngeal angioedema and/or anaphylactic shock.

The EAACI/GA2LEN/EDF/WAO panel consensus released an updated guideline in 2013 on the management of urticaria including a treatment algorithm for symptomatic management of chronic spontaneous urticaria.[76, 48, 49]

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Pharmacologic Therapies

As advised in the 2013 EAACI/GA2LEN/EDF/WAO management guideline, due to the fluctuating nature of acute urticaria and the chance that spontaneous remission can occur at any time, continued or alternative drug treatment should be reevaluated every 3-6 months.[76, 48, 49]

In children, if a case is confirmed to involve streptococcal infection, penicillin G should be given either orally or by injection, depending on the patient’s age and circumstances.[12]

H1 antagonists (first-generation antihistamines)

Antihistamines are the primary agents used to treat urticaria.[11] The older, first-generation H1 antagonists (eg, diphenhydramine, hydroxyzine) are effective in reducing the lesions and pruritus but can produce a number of adverse effects, such as drowsiness, anticholinergic effects, and cognitive effects, which may continue until the next day.[50] Thus, these agents can be useful if administered at bedtime.

According to the EAACI/GA2LEN/EDF/WAO management guideline, first-generation sedating antihistamines should no longer be used as the first choice therapy except where second-generation antihistamines are not available or where their benefits outweigh their risks. The guideline advises against using older, sedating first-generation antihistamines in patients with urticaria who have no special indications.[76, 48, 49]

Any patient who is taking a medication that has potential sedative effects should be cautioned about driving and operating heavy machinery. Commonly used first-generation agents include diphenhydramine, hydroxyzine, chlorpheniramine, and cyproheptadine.

Most patients with urticaria can be treated with oral (PO) H1 antihistamines. Modern second-generation antihistamines are the first choice. Increasing the dose up to fourfold is permitted in patients who do not respond sufficiently to the standard dosing. For refractory cases, use a combination of H1 and H2 antihistamines.

The experimental evidence comparing the various possible regimens and rates of adverse effects in the long term is still minimal.

H1 antagonists (second-generation antihistamines)

The newer second-generation antihistamines are nonsedating in most patients, with very few adverse effects reported (cetirizine can cause drowsiness in up to 10% of patients).[51, 48, 49] Therefore, many specialists prefer the use of these agents for chronic urticaria, with first-generation agents reserved for acute or refractory cases. Commonly used second-generation antihistamines are cetirizine, levocetirizine, desloratadine, loratadine, and fexofenadine. Four times the approved doses can be used if needed in cases where standard dose is insufficient to control the symptom.

H2 antagonists

These drugs are usually used to decrease gastric acid secretion. H2 antagonists are not effective when used as single agents for urticaria; however, the combination of an H1 antagonist with an H2 antagonist has been shown to be more effective than an H1 antagonist alone.[52, 53] Any of the H2 blockers can be used. Two of the most commonly used agents are ranitidine and cimetidine.

Corticosteroids

In some instances of acute or chronic urticaria, antihistamines may fail, even at high doses, or adverse effects may be problematic. In addition, mediators other than histamine may be involved. In such situations, corticosteroids can be highly effective. Corticosteroids may also be used in urticarial vasculitis, which usually does not respond to antihistamines.

The EAACI/GA2LEN/EDF/WAO management guideline recommends the use of corticosteroids only in severely affected patients.[48, 49]

A short course of an oral corticosteroid (administered daily for 5-7 d, with or without a taper) or a single dose of a long-acting injectable steroid is not usually associated with long-term sequelae and can be helpful when used for an acute episode of urticaria nonresponsive to antihistamines.[24] Examples of corticosteroid preparations include prednisolone, methylprednisolone, and prednisone

Because of adverse effects of chronic or recurrent use of systemic corticosteroids, the long-term use of these agents should be avoided, when possible. If urticaria is severe and cannot be safely controlled with other medications, low-dose therapy and/or alternate-day therapy can be considered.

Corticosteroids stabilize mast cell membranes and inhibit further histamine release, as well as reduce the inflammatory effect of histamine and other mediators. The efficacy of corticosteroids in acute urticaria remains controversial. In one study, acute urticaria improved more quickly in the group treated with prednisone than in the group treated with placebo.[54]

In adults, 40-60 mg daily of prednisone for 5 days is a reasonable therapeutic regimen. In children, the treatment is 1 mg/kg/d for 5 days. Tapering of the corticosteroid dose is not necessary in most cases of acute urticaria.[1]

ympathomimetic agents

Sympathomimetic agents cause vasoconstriction and reduction in vascular dilation, which contributes to urticaria formation.

The efficacy of epinephrine in acute urticaria is controversial.[48, 49] If angioedema is present with urticaria, epinephrine should be administered via the IM route. Remember that converting enzyme inhibitor (ACEI)–induced angioedema usually does not respond to epinephrine or most other common therapies, as it is not an IgE-mediated process.[55]

Immunomodulatory and anti-inflammatory therapy

Cyclosporine has been shown to be effective in 2 double-blind placebo-controlled studies.[56, 57] IV gammaglobulin and plasmapheresis have been described as useful in a limited number of case studies.[58, 59] These therapies can be a consideration in severe urticaria, particularly of the autoimmune type that is unresponsive to medications, but such treatment is usually only initiated by specialists with considerable expertise in urticaria.

Colchicine and dapsone have also been reported to be useful for refractory urticaria and urticarial vasculitis,[60, 61] perhaps because of their ability to modulate polymorphonuclear lymphocyte (PMN) function. PMNs and a mixed infiltrate can be present in some urticarial lesions, particularly urticaria that is severe or refractory to antihistamine treatment.

Some reports describe the effectiveness of the antileukotriene agents in urticaria,[62, 63] but extensive clinical trials have not been performed, so their usefulness is still questionable. Clinical trials might in the future support the theory that the antileukotriene agents can provide a synergistic response when used in conjunction with antihistamines.

Omalizumab (monoclonal antibody to IgE) is a recombinant biologic molecule effective for chronic urticaria based on two large positive phase III studies and is currently FDA approved for treatment of chronic urticaria. Patients can be treated with 150 or 300 mg subcutaneously every four weeks.[77] The role in acute urticaria has not been determined and further studies are needed. 

Because the use of the aforementioned agents is not widespread, details of dosage and administration are not provided, but references are listed in the bibliography. The use of corticosteroids is more common and is discussed in Medication.

Tricyclic antidepressants

Tricyclic antidepressants (TCAs) are a complex group of drugs that have central and peripheral anticholinergic effects, as well as sedative effects. TCAs block the active reuptake of norepinephrine and serotonin; and some (eg, doxepin) have antihistamine effects, blocking both the H1 and H2 receptors, and have been used in the treatment of allergic reactions, especially urticaria.

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Nonpharmacologic Therapies

Food and symptom diaries

Suspected food allergies can be confirmed or disproved with the use of food diaries. A food or symptom diary for a fixed duration (eg, 2-4 wk) may be helpful. Note all activities in which the patient was involved for 6-8 hours before the onset of urticaria. Cases have been reported in which a food or activity (such as jogging) by itself results in no symptoms but when combined (eg, eating a shrimp cocktail and then jogging) may result in urticaria with or without progression to anaphylaxis. Excessive or prolonged use of a food or symptom diary is unlikely to be of benefit.

Avoidance

If a trigger can be identified, avoidance is the most effective form of management. This would include any food, medication, physical agent, or other factor that triggers the urticaria.

Aspirin,[65, 66] NSAIDs,[67] opiates, and alcohol have been reported to be nonspecific triggers of urticaria and might lower the threshold for urticaria in selected patients. Therefore, some specialists advise all patients with urticaria to avoid these agents. However, little experimental evidence is available to support this recommendation.

Removing offending ectoparasites can prevent papular urticaria, and insect repellent may lessen the chance of bites or stings from offending insects. Desensitization strategies are not recommended, except for stinging insect venoms.

Although the need for cold cardiopulmonary bypass surgery in patients with cold-induced urticaria is uncommon, one study reported success using an anti-inflammatory regimen before surgery and during recovery to prevent a systemic reaction of urticaria.[68]

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Emergency Care and Complications

Acute urticaria is a common disorder that often prompts patients to seek treatment in the emergency department (ED). In fact, acute urticaria is the most common cutaneous disease treated in the ED.[69] Determining whether urticaria is part of an anaphylactic reaction is important. If an anaphylactic reaction occurs, the patient needs prompt treatment and careful monitoring

The management of urticaria in the ED is straightforward and typically is not altered by underlying etiology. The mainstay is avoidance of further exposure to the antigen and antihistamines.

Most cases of acute urticaria respond to pharmacotherapy (see Medication). Antihistamines are the first line of therapy for urticaria.[48, 49] Modern second-generation antihistamines are also effective as first-line treatment. Diphenhydramine (25 mg IV or 50 mg IM or PO) or hydroxyzine (50 mg IM or PO) can be administered also and have benefit in helping patients sleep at nights.[48, 49]

If any features of anaphylaxis (eg, hypotension, respiratory distress, stridor, gastrointestinal distress, swallowing problems, joint swelling, joint pain) are present, immediate medical intervention should occur.

Acute urticaria may progress to life-threatening angioedema and/or anaphylactic shock in a very short time, although it usually presents as rapid-onset shock with no urticaria or angioedema.[70]

If associated angioedema is present, especially if laryngeal angioedema (eg, hoarseness, stridor) is suspected, prehospital administration of 0.3-0.5 mg of intramuscular [IM] epinephrine may be warranted. If associated bronchospasm is present, prehospital nebulized albuterol may be warranted.

Other measures may be appropriate, such as continuous electrocardiography (ECG); blood pressure and pulse oximetry monitoring; administering IV crystalloids if the patient is hypotensive; and administering oxygen. If the patient has angioedema that is treated successfully in the ED, the patient should be sent home with an EpiPen prescription. The patient should be instructed to keep the EpiPen with him or her at all times and to use it if swelling of the lips, tongue, or face develops or if his or her voice becomes acutely hoarse.

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Diet

Dietary modification is only necessary if food allergy or food additive hypersensitivity has been established. If such hypersensitivity is identified, the patient should avoid the offending food or food additive.

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Activity

If the patient has physical urticaria, activity should be carefully monitored, depending on the trigger (eg, cold or hot temperatures, exposure to sun or water, pressure or vibration).

Individuals with cold urticaria must be particularly cautious and not immerse themselves suddenly in cold water. Patients should avoid swimming in lakes, streams, or oceans.

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Consultations

A primary care provider can manage most cases of acute urticaria. If a trigger is easily identified and avoidance leads to resolution, then referral is not necessary. If an allergic trigger is suspected but not easily identified, then referral to an allergy specialist is warranted.[71] Similarly, if avoidance of a trigger does not lead to resolution or if the patient does not respond well to antihistamines, then referral to an allergist or dermatologist is warranted.[71]

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Long-term Monitoring

Identify the etiology of the acute urticaria if possible. If an inciting agent can be identified, instruct the patient to avoid it. The major goal is to control the severity of acute urticaria lesions until the process resolves over 4-6 weeks.

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Contributor Information and Disclosures
Author

Henry K Wong, MD, PhD Professor and Chairman, Department of Dermatology, University of Arkansas for Medical Sciences College of Medicine

Henry K Wong, MD, PhD is a member of the following medical societies: American Academy of Dermatology, International Society for Cutaneous Lymphomas, Society for Investigative Dermatology, Medical Dermatology Society

Disclosure: Received income in an amount equal to or greater than $250 from: Celgene<br/>Received honoraria from Amgen for speaking and teaching; Received grant/ Received grant/research funds from Celgene for none; Received grant/research funds from Abbott Labs for independent contractor; Received grant/research funds from Amgen for none; Received honoraria from Seattle Genetics for consulting. for: Actelion-Advisory board, grants.

Coauthor(s)

Javed Sheikh, MD Assistant Professor of Medicine, Harvard Medical School; Clinical Director, Division of Allergy and Inflammation, Clinical Director, Center for Eosinophilic Disorders, Beth Israel Deaconess Medical Center

Javed Sheikh, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology

Disclosure: Received grant/research funds from Genentech for other.

Umer Najib, MD Clinical Research Fellow, Department of Medicine, Division of Allergy and Inflammation, Beth Israel Deaconess Medical Center

Disclosure: Nothing to disclose.

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

Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Consulting fee Consulting; Celgene Honoraria Safety Monitoring Committee; GSK - Glaxo Smith Kline Consulting fee Consulting; TenXBioPharma Consulting fee Safety Monitoring Committee

Kevin P Connelly, DO Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency Care, Virginia Commonwealth University School of Medicine; Medical Director, Paws for Health Pet Visitation Program of the Richmond SPCA; Pediatric Emergency Physician, Emergency Consultants Inc, Chippenham Medical Center

Kevin P Connelly, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association

Disclosure: Nothing to disclose.

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

Dirk M Elston, MD Director, Department of Dermatology, Geisinger Medical Center

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Daniel J Hogan, MD Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center

Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, and Canadian Dermatology Association

Disclosure: Nothing to disclose.

Shih-Wen Huang, MD Professor Emeritus, Pulmonology and Allergy, Department of Pediatrics University of Florida College of Medicine

Shih-Wen Huang, MD, is a member of the following medical societies: American Academy of Allergy Asthma and Immunology

Disclosure: Nothing to disclose.

Harumi Jyonouchi, MD Associate Professor, Division of Pulmonary Allergy/Immunology and Infectious Diseases, Department of Pediatrics, UMDNJ-New Jersey Medical School

Harumi Jyonouchi, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American Association of Immunologists, American Medical Association, Clinical Immunology Society, New York Academy of Sciences, Society for Experimental Biology and Medicine, Society for Mucosal Immunology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

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. Frigas E, Park MA. Acute urticaria and angioedema: diagnostic and treatment considerations. Am J Clin Dermatol. 2009. 10(4):239-50. [Medline].

  2. Hide M, Francis DM, Grattan CE, Hakimi J, Kochan JP, Greaves MW. Autoantibodies against the high-affinity IgE receptor as a cause of histamine release in chronic urticaria. N Engl J Med. 1993 Jun 3. 328(22):1599-604. [Medline].

  3. Zuberbier T, Maurer M. Urticaria: current opinions about etiology, diagnosis and therapy. Acta Derm Venereol. 2007. 87(3):196-205. [Medline].

  4. Kaplan AP, Joseph K, Maykut RJ, Geba GP, Zeldin RK. Treatment of chronic autoimmune urticaria with omalizumab. J Allergy Clin Immunol. 2008 Sep. 122(3):569-73. [Medline].

  5. Criado PR, Criado RF, Takakura CF, Pagliari C, de Carvalho JF, Sotto MN, et al. Ultrastructure of vascular permeability in urticaria. Isr Med Assoc J. 2013 Apr. 15(4):173-7. [Medline].

  6. Viola M, Quaratino D, Gaeta F, Rumi G, Caruso C, Romano A. Cross-reactive reactions to nonsteroidal anti-inflammatory drugs. Curr Pharm Des. 2008. 14(27):2826-32. [Medline].

  7. Kalogeromitros D, Kempuraj D, Katsarou-Katsari A, Gregoriou S, Makris M, Boucher W, et al. Theophylline as "add-on" therapy in patients with delayed pressure urticaria: a prospective self-controlled study. Int J Immunopathol Pharmacol. 2005 Jul-Sep. 18(3):595-602. [Medline].

  8. [Guideline] Magerl M, Borzova E, Giménez-Arnau A, Grattan CE, Lawlor F, Mathelier-Fusade P, et al. The definition and diagnostic testing of physical and cholinergic urticarias--EAACI/GA2LEN/EDF/UNEV consensus panel recommendations. Allergy. 2009 Dec. 64(12):1715-21. [Medline].

  9. Tong LJ, Balakrishnan G, Kochan JP, Kinét JP, Kaplan AP. Assessment of autoimmunity in patients with chronic urticaria. J Allergy Clin Immunol. 1997 Apr. 99(4):461-5. [Medline].

  10. Cardinale F, Mangini F, Berardi M, Sterpeta Loffredo M, Chinellato I, Dellino A, et al. [Intolerance to food additives: an update]. Minerva Pediatr. 2008 Dec. 60(6):1401-9. [Medline].

  11. Sheikh J. Advances in the treatment of chronic urticaria. Immunol Allergy Clin North Am. 2004 May. 24(2):317-34, vii-viii. [Medline].

  12. Schuller DE. Acute urticaria in children: causes and an aggressive diagnostic approach. Postgrad Med. 1982 Aug. 72(2):179-85. [Medline].

  13. Wedi B, Raap U, Wieczorek D, Kapp A. Urticaria and infections. Allergy Asthma Clin Immunol. 2009 Dec 1. 5(1):10. [Medline]. [Full Text].

  14. Kaplan AP. What the first 10,000 patients with chronic urticaria have taught me: a personal journey. J Allergy Clin Immunol. 2009 Mar. 123(3):713-7. [Medline].

  15. Valsecchi R, Pigatto P. Chronic urticaria and Helicobacter pylori. Acta Derm Venereol. 1998 Nov. 78(6):440-2. [Medline].

  16. Ozkaya-Bayazit E, Demir K, Ozgüroglu E, Kaymakoglu S, Ozarmagan G. Helicobacter pylori eradication in patients with chronic urticaria. Arch Dermatol. 1998 Sep. 134(9):1165-6. [Medline].

  17. Di Campli C, Gasbarrini A, Nucera E, Franceschi F, Ojetti V, Sanz Torre E, et al. Beneficial effects of Helicobacter pylori eradication on idiopathic chronic urticaria. Dig Dis Sci. 1998 Jun. 43(6):1226-9. [Medline].

  18. Schnyder B, Helbling A, Pichler WJ. Chronic idiopathic urticaria: natural course and association with Helicobacter pylori infection. Int Arch Allergy Immunol. 1999 May. 119(1):60-3. [Medline].

  19. Leznoff A, Josse RG, Denburg J, Dolovich J. Association of chronic urticaria and angioedema with thyroid autoimmunity. Arch Dermatol. 1983 Aug. 119(8):636-40. [Medline].

  20. Rose RF, Bhushan M, King CM, Rhodes LE. Solar angioedema: an uncommonly recognized condition?. Photodermatol Photoimmunol Photomed. 2005 Oct. 21(5):226-8. [Medline].

  21. Botto NC, Warshaw EM. Solar urticaria. J Am Acad Dermatol. 2008 Dec. 59(6):909-20; quiz 921-2. [Medline].

  22. Kaplan AP. Urticaria angioedema. Adkinson NFY Jr, Busse WW, Bochner BS, Holgate ST, Simons FER, eds. Allergy: Principles and Practice. Philadelphia, Pa: Mosby; 2003. 1537-58.

  23. Sackesen C, Sekerel BE, Orhan F, Kocabas CN, Tuncer A, Adalioglu G. The etiology of different forms of urticaria in childhood. Pediatr Dermatol. 2004 Mar-Apr. 21(2):102-8. [Medline].

  24. Kaplan AP. Chronic urticaria and angioedema. N Engl J Med. 2002. Vol. 346:175-9.

  25. Beltrani VS. Urticaria and angioedema. Dermatol Clin. 1996 Jan. 14(1):171-198. [Medline].

  26. Soter NA. Acute and chronic urticaria and angioedema. J Am Acad Dermatol. 1991 Jul. 25(1 Pt 2):146-54. [Medline].

  27. Varadarajulu S. Urticaria and angioedema. Controlling acute episodes, coping with chronic cases. Postgrad Med. 2005 May. 117(5):25-31. [Medline].

  28. O'Donnell BF, Lawlor F, Simpson J, Morgan M, Greaves MW. The impact of chronic urticaria on the quality of life. Br J Dermatol. 1997 Feb. 136(2):197-201. [Medline].

  29. Zuberbier T, Iffländer J, Semmler C, Henz BM. Acute urticaria: clinical aspects and therapeutic responsiveness. Acta Derm Venereol. 1996 Jul. 76(4):295-7. [Medline].

  30. Davis MD, Brewer JD. Urticarial vasculitis and hypocomplementemic urticarial vasculitis syndrome. Immunol Allergy Clin North Am. 2004 May. 24(2):183-213, vi. [Medline].

  31. Kaplan AP. Urticaria and angioedema. Middleton E, Reed CE, Ellis EF, et al, eds. Allergy: Principles and Practices. St. Louis, Mo: Mosby-Year Book; 1998. 1104-18.

  32. Sheila MA, Stephen CD. Urticaria. Prim Care Clin Office Pract. 2008. Vol. 35:141-57.

  33. Charlesworth EN. Urticaria and angioedema: a clinical spectrum. Ann Allergy Asthma Immunol Jun. 1996. 76(6):484-95.

  34. Greaves M. Chronic urticaria. J Allergy Clin Immunol. 2000 Apr. 105(4):664-72. [Medline].

  35. Hirschmann JV, Lawlor F, English JS, Louback JB, Winkelmann RK, Greaves MW. Cholinergic urticaria. A clinical and histologic study. Arch Dermatol. 1987 Apr. 123(4):462-7. [Medline].

  36. Wong RC, Fairley JA, Ellis CN. Dermographism: a review. J Am Acad Dermatol. 1984 Oct. 11(4 Pt 1):643-52. [Medline].

  37. Belani H, Gensler L, Bajpai U, Meinhardt E, Graf J, Pincus L, et al. Neutrophilic urticaria with systemic inflammation: a case series. JAMA Dermatol. 2013 Apr 1. 149(4):453-8. [Medline].

  38. Schoepke N, Doumoulakis G, Maurer M. Diagnosis of urticaria. Indian J Dermatol. 2013 May. 58(3):211-8. [Medline]. [Full Text].

  39. Dibbern DA Jr. Urticaria: selected highlights and recent advances. Med Clin North Am. 2006 Jan. 90(1):187-209. [Medline].

  40. Dibbern DA Jr, Dreskin SC. Urticaria and angioedema: an overview. Immunol Allergy Clin North Am. 2004 May. 24(2):141-62, v. [Medline].

  41. [Guideline] American Academy of Allergy, Asthma & Immunology. Consultation and referral guidelines citing the evidence: how the allergist-immunologist can help. J Allergy Clin Immunol. 2006 Feb. 117(2 Suppl Consultation):S495-523. [Medline].

  42. Beltrani VS. Urticaria: reassessed. Allergy Asthma Proc. 2004 May-Jun. 25(3):143-9. [Medline].

  43. Mortureux P, Léauté-Labrèze C, Legrain-Lifermann V, Lamireau T, Sarlangue J, Taïeb A. Acute urticaria in infancy and early childhood: a prospective study. Arch Dermatol. 1998 Mar. 134(3):319-23. [Medline].

  44. Irinyi B, Széles G, Gyimesi E, Tumpek J, Herédi E, Dimitrios G, et al. Clinical and laboratory examinations in the subgroups of chronic urticaria. Int Arch Allergy Immunol. 2007. 144(3):217-25. [Medline].

  45. [Guideline] 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]. [Full Text].

  46. Brown NA, Carter JD. Urticarial vasculitis. Curr Rheumatol Rep. 2007 Aug. 9(4):312-9. [Medline].

  47. Haas N, Toppe E, Henz BM. Microscopic morphology of different types of urticaria. Arch Dermatol. 1998 Jan. 134(1):41-6. [Medline].

  48. [Guideline] Zuberbier T, Asero R, Bindslev-Jensen C, Walter Canonica G, Church MK, Giménez-Arnau AM, et al. EAACI/GA(2)LEN/EDF/WAO guideline: management of urticaria. Allergy. 2009 Oct. 64(10):1427-43. [Medline]. [Full Text].

  49. [Guideline] Zuberbier T. A Summary of the New International EAACI/GA2LEN/EDF/WAO Guidelines in Urticaria. World Allergy Organ J. 2012 Jan. 5 Suppl 1:S1-5. [Medline].

  50. Slater JW, Zechnich AD, Haxby DG. Second-generation antihistamines: a comparative review. Drugs. 1999 Jan. 57(1):31-47. [Medline].

  51. Breneman DL. Cetirizine versus hydroxyzine and placebo in chronic idiopathic urticaria. Ann Pharmacother. 1996 Oct. 30(10):1075-9. [Medline].

  52. Bleehen SS, Thomas SE, Greaves MW, Newton J, Kennedy CT, Hindley F, et al. Cimetidine and chlorpheniramine in the treatment of chronic idiopathic urticaria: a multi-centre randomized double-blind study. Br J Dermatol. 1987 Jul. 117(1):81-8. [Medline].

  53. Lin RY, Curry A, Pesola GR, Knight RJ, Lee HS, Bakalchuk L, et al. Improved outcomes in patients with acute allergic syndromes who are treated with combined H1 and H2 antagonists. Ann Emerg Med. 2000 Nov. 36(5):462-8. [Medline].

  54. Pollack CV Jr, Romano TJ. Outpatient management of acute urticaria: the role of prednisone. Ann Emerg Med. 1995 Nov. 26(5):547-51. [Medline].

  55. Bluestein HM, Hoover TA, Banerji AS, Camargo CA Jr, Reshef A, Herscu P. Angiotensin-converting enzyme inhibitor-induced angioedema in a community hospital emergency department. Ann Allergy Asthma Immunol. 2009 Dec. 103(6):502-7. [Medline].

  56. Grattan CE, O'Donnell BF, Francis DM, Niimi N, Barlow RJ, Seed PT, et al. Randomized double-blind study of cyclosporin in chronic 'idiopathic' urticaria. Br J Dermatol. 2000 Aug. 143(2):365-72. [Medline].

  57. Vena GA, Cassano N, Colombo D, Peruzzi E, Pigatto P. Cyclosporine in chronic idiopathic urticaria: a double-blind, randomized, placebo-controlled trial. J Am Acad Dermatol. 2006 Oct. 55(4):705-9. [Medline].

  58. O'Donnell BF, Barr RM, Black AK, Francis DM, Kermani F, Niimi N, et al. Intravenous immunoglobulin in autoimmune chronic urticaria. Br J Dermatol. 1998 Jan. 138(1):101-6. [Medline].

  59. Grattan CE, Francis DM, Slater NG, Barlow RJ, Greaves MW. Plasmapheresis for severe, unremitting, chronic urticaria. Lancet. 1992 May 2. 339(8801):1078-80. [Medline].

  60. Werni R, Schwarz T, Gschnait F. Colchicine treatment of urticarial vasculitis. Dermatologica. 1986. 172(1):36-40. [Medline].

  61. Ruzicka T, Goerz G. Systemic lupus erythematosus and vasculitic urticaria. Effect of dapsone and complement levels. Dermatologica. 1981. 162(3):203-5. [Medline].

  62. Nettis E, Dambra P, D'Oronzio L, Loria MP, Ferrannini A, Tursi A. Comparison of montelukast and fexofenadine for chronic idiopathic urticaria. Arch Dermatol. 2001 Jan. 137(1):99-100. [Medline].

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

  64. Gober LM, Sterba PM, Eckman JA, Saini SS. Effect of anti-IgE (omalizumab) in chronic idiopathic urticaria (CIU) patients. J Allergy Clin Immunol. 2008. 121(2 supp 1):S147. [Full Text].

  65. Wong JT, Nagy CS, Krinzman SJ, Maclean JA, Bloch KJ. Rapid oral challenge-desensitization for patients with aspirin-related urticaria-angioedema. J Allergy Clin Immunol. 2000 May. 105(5):997-1001. [Medline].

  66. Grattan CE. Aspirin sensitivity and urticaria. Clin Exp Dermatol. 2003 Mar. 28(2):123-7. [Medline].

  67. Díaz Jara M, Pérez Montero A, Gracia Bara MT, Cabrerizo S, Zapatero L, Martínez Molero MI. Allergic reactions due to ibuprofen in children. Pediatr Dermatol. 2001 Jan-Feb. 18(1):66-7. [Medline].

  68. Lancey RA, Schaefer OP, McCormick MJ. Coronary artery bypass grafting and aortic valve replacement with cold cardioplegia in a patient with cold-induced urticaria. Ann Allergy Asthma Immunol. 2004 Feb. 92(2):273-5. [Medline].

  69. Simonart T, Askenasi R, Lheureux P. Particularities of urticaria seen in the emergency department. Eur J Emerg Med. 1994 Jun. 1(2):80-2. [Medline].

  70. Simons FE. Anaphylaxis. J Allergy Clin Immunol. 2010 Feb. 125(2 Suppl 2):S161-81. [Medline].

  71. Najib U, Sheikh J. An update on acute and chronic urticaria for the primary care provider. Postgrad Med. 2009 Jan. 121(1):141-51. [Medline].

  72. Poonawalla T, Kelly B. Urticaria : a review. Am J Clin Dermatol. 2009. 10(1):9-21. [Medline].

  73. Simons FE. H1-Antihistamines: more relevant than ever in the treatment of allergic disorders. J Allergy Clin Immunol. 2003 Oct. 112(4 Suppl):S42-52. [Medline].

  74. Bains SN, Hsieh FH. Current approaches to the diagnosis and treatment of systemic mastocytosis. Ann Allergy Asthma Immunol. 2010 Jan. 104(1):1-10; quiz 10-2, 41. [Medline].

  75. Baek YS, Jeon J, Kim JH, Oh CH. Severity of acute and chronic urticaria correlates with D-dimer level, but not C-reactive protein or total IgE. Clin Exp Dermatol. 2014 Oct. 39 (7):795-800. [Medline].

  76. Zuberbier T, et al. European Academy of Allergy and Clinical Immunology, Global Allergy and Asthma European Network, European Dermatology Forum, World Allergy Organization. The EAACI/GA(2) LEN/EDF/WAO Guideline for the definition, classification, diagnosis, and management of urticaria: the 2013 revision and update. Allergy. 2014 Jul. 69 (7):868-87. [Medline].

  77. Cooke A, Bulkhi A, Casale TB. Role of biologics in intractable urticaria. Biologics. 2015. 9:25-33. [Medline].

 
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Urticaria associated with a drug reaction.
Urticaria developed after bites from an imported fire ant.
Local urticaria on a patient with latex allergy who was touched with a latex glove.
Urticaria from drug reaction.
Photograph of dermographism.
Pressure urticaria (dermatographia) developed after strokes.
Acute urticaria associated with dermatographism.
Urticaria associated with acute group A beta-hemolytic streptococci infection.
Acute urticaria in a toddler affecting the face. Likely cause is postviral syndrome.
 
 
 
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