Answer: A

Urticaria, also referred to as hives or wheals, is a relatively common skin rash that often occurs in the setting of exposure to an allergen but may also present secondary to a specific physical trigger. Urticarial rashes have been recognized for an extremely long time, with initial descriptions made by Hippocrates as early as the 400s BC. Today, approximately 20% of the population experience urticaria at some point in their life.6 The initial presentation of acute urticaria often occurs in children, especially after exposure to a new potential allergen. In the case of chronic urticaria, a number of comorbidities have been described, particularly in children, including atopy, low vitamin D levels, and psychiatric disorders.7


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The development of urticaria is primarily thought to occur via an allergic or autoimmune pathway. Allergens or recognition of self-antigens by IgE results in the activation of mast cells and basophils. The activation of these cells, as well as subsequent degranulation of mast cells, leads to massive histamine release.8 Histamine release in the dermis results in urticarial lesions, while release in the deeper dermis and subcutaneous tissue leads to angioedema.9

Multiple ideas have been proposed to describe the etiology of urticaria; the most common involves exposure to allergens, such as pollen and peanuts, which then stimulates the allergic pathway resulting in urticaria.9 Additionally, food pseudo-allergens, or substances that either contain histamine-like molecules or directly release endogenous histamine, have also been identified as possible causal agents for urticaria.9 Infections caused by a broad range of common viruses and bacteria have been known to cause urticaria as well, particularly in children.9 Similarly, allergic drug reactions may cause urticaria, such as seen with beta-lactam antibiotics and NSAIDs. It has also been noted that physical stimuli such as mechanical pressure or heat may reliably produce urticaria in some susceptible patients.10

Urticaria typically presents as a wheal with characteristic features including central swelling, surrounding reflex erythema, and associated burning or pruritus.11 The skin rash can be accompanied by angioedema, or swelling of the underlying dermis and/or mucosal tissue; associated signs and symptoms such as flushing or wheezing may also be present.10 Urticaria typically resolves within a few hours of onset and almost always within 24 hours.11 Urticaria is classified as either acute or chronic based on whether episodes of the rash have occurred continuously for less than 6 weeks or more than 6 weeks, respectively.11 Urticaria can also be subdivided into inducible and spontaneous based on whether a specific trigger or precipitating factor can be identified. Examples of inducible urticaria include urticaria that occurs in response to temperature changes or to specific substance exposure (contact urticaria).10,11

The time frame of presentation is important when establishing a differential diagnosis for urticaria, as it may provide clues to a specific trigger or exposure to an allergen that leads to the rash, such as with new drug exposures or physical precipitants like mechanical pressure or heat.10 Autoimmune diseases including bullous pemphigoid and systemic lupus erythematosus should also be considered, especially in the setting of a positive family history or rheumatologic findings such as uveitis or joint pain.10 A viral exanthem is another potential diagnosis to consider when a patient presents with new-onset rash in addition to other clinical signs of infection.10 Due to its life-threatening nature, anaphylaxis must be immediately considered and ruled out; a lack of involvement of other organ systems can help to quickly remove this possibility from the differential diagnosis.9 Insect bites may also produce urticarial-like lesions, although the diagnosis of urticaria is much less likely when the lesions continue to persist beyond a day or a history of insect bites is present.9

Diagnosis of an urticarial rash is primarily clinical, with a detailed exposure history, timing of the onset of the rash, and rash progression being the most helpful historical elements.9 A complete review of systems is important in for identifying any associated signs and symptoms that may be associated with urticaria, as well as to rule out other potential infectious or systemic causes of rash.

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The primary method for treating urticaria is to eliminate or avoid the trigger, if it is known, to as great of a degree as is possible.9 The first-line agent for the medical management of acute urticaria is a second-generation H1 blocker or an antihistamine, such as loratadine or cetirizine.9 In cases of severe or prolonged urticaria, a brief course of oral corticosteroids, such as prednisone at a dosage of 0.5 to 1 mg/kg for 3 to 10 days, may also be considered.9 Prescribing an epinephrine autoinjector may also be prudent for patients who have a history of severe allergic reactions involving anaphylaxis or angioedema of the airways.9 The first-line management approach chronic urticaria is also second-generation H1 blockers and antihistamines; however, if these agents fail to control symptoms, a trial of a leukotriene receptor antagonist should be considered.9 For cases of recalcitrant urticaria, a high-potency antihistamine such as hydroxyzine or doxepin, or immunomodulatory therapy such as the anti-IgE antibody omalizumab may be required.9

In the case scenario provided, the patient had no symptoms beyond the itchy wheals. The rash fully resolved within the next few hours. He was discharged with instructions for antihistamine use in the event of a recurrence, and he was counseled to avoid areas with wasps and to use insect repellent when he is outdoors. 

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Sirus Jesudasen, BA, is a medical student; Joan Fernandez, BA, is a medical student; and Christopher Rizk, MD, is a dermatology resident at Baylor College of Medicine, in Houston, Texas.

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References

  1. Gerson D, Sriganeshan V, Alexis JB. Cutaneous drug eruptions: a 5-year experience. J Am Acad Dermatol.  2008;59(6):995-999.
  2. Pichler WJ, Adam J, Daubner B, Gentinetta T, Keller M, Yerly D. Drug hypersensitivity reactions: pathomechanism and clinical symptoms. Med Clin North Am. 2010;94(4):645-664.
  3. Stern RS. Exanthematous drug eruptions. N Engl J Med. 2012;366:2492-2501.
  4. Ramdial PK, Naidoo DK. Drug-induced cutaneous pathology. J Clin Pathol. 2009;62(6):493-504.
  5. Dyall-Smith D. Morbilliform drug reaction. DermNet NZ website. www.dermnetnz.org/topics/morbilliform-drug-reaction/. Updated January 2016.  Accessed November 5, 2018.
  6. Jafilan L, James C. Urticaria and allergy-mediated conditions. Prim Care. 2015;42(4):473-483.
  7. Cornillier H, Giraudeau B, Munck S, et al. Chronic spontaneous urticaria in children – a systematic review on interventions and comorbidities. Pediatr Allergy Immunol. 2018;29(3):303-310.
  8. Church MK, Kolkhir P, Metz M, Maurer M. The role and relevance of mast cells in urticaria. Immunol Rev. 2018;282(1):232-247.
  9. Schaefer P. Acute and chronic urticaria: evaluation and treatment. Am Fam Physician. 2017;95(11):717-724.
  10. Radonjic-Hoesli S, Hofmeier KS, Micaletto S, Schmid-Grendelmeier P, Bircher A, Simon D. Urticaria and angioedema: an update on classification and pathogenesis. Clin Rev Allergy Immunol. 2018;54(1,):88-101.
  11. Godse K, Abhishek D, Zawar V, et al. Consensus statement for the diagnosis and treatment of urticaria: a 2017 update. Indian J Dermatol. 2018;63(1):2-15.

This article originally appeared on Clinical Advisor