Histamine produces a prototypic, short-lived urticaria. However, the clinical spectrum and pattern of lesions indicate that other molecules, including prostaglandins, leukotrienes, cytokines, and chemokines, produced at different times after mast cell activation contribute to the polymorphism of this symptom and the variable evolution of this disease.

It is a common practice to distinguish immunological and nonimmunological urticaria.

Immunological urticaria is a hypersensitivity reaction mediated by antibodies and/or T-cells that results in mast cell activation.

It is now well established that urticaria may result from the binding of IgG auto-antibodies to IgE and/or to the receptor for IgE molecules on mast cells, thus corresponding to a type II HS reaction. These auto-immune urticarias represent up to 50% of patients with chronic urticaria. Mast cell activation can also result from type III HS through the binding of circulating immune complexes to mast cell-expressing Fc receptors for IgG and IgM.

Under certain circumstances, T-cells can induce activation of mast cells, as well as histamine release (type IV HS).

Nonimmunological urticarias result from mast cell activation through membrane receptors involved in innate immunity (e.g., complement, Toll-like, cytokine/chemokine, opioid) or by direct toxicity of xenobiotics (haptens, drugs).


Many acute urticarial reactions are due to viruses, especially in children, or present as hives persisting or recurring for more than 24 hours.

In conclusion, urticaria may result from different pathophysiological mechanisms that explain the great heterogeneity of clinical symptoms and the variable responses to treatment.



Urticaria, or hives, is a cutaneous reaction marked by acute onset of pruritic, erythemic wheals of varying size that generally are described as "fleeting."

Erythema multiforme is a more pronounced variation of urticaria, characterized by typical "target" skin lesions.

Urticaria is dermal edema resulting from vascular dilatation and leakage of fluid into the skin in response to molecules released from mast cells.





Obtain a detailed history; if an etiologic agent can be identified, future reactions may be avoided, although many acute urticarial reactions are viral in nature.

Treatment of urticarial reactions is generally supportive and symptomatic, with attempts to identify and remove the offending agent. H1-antihistamines, with or without corticosteroids, are usually sufficient, although epinephrine can be considered in severe or refractory cases. The addition of an H2-antihistamine, such as ranitidine, may also be useful in more severe, chronic, or unresponsive cases. Cold compresses may be soothing to affected areas. Referral to an allergy specialist is indicated in severe, recurrent, or refractory cases.


Most people with pyelonephritis do not have complications if appropriately treated with bacteria-fighting medications called antibiotics.

In rare cases, pyelonephritis may cause permanent kidney scars, which can lead to chronic kidney disease, high blood pressure, and kidney failure. These problems usually occur in people with a structural problem in the urinary tract, kidney disease from other causes, or repeated episodes of pyelonephritis.

Infection in the kidneys may spread to the bloodstream—a serious condition called sepsis—though this is also uncommon.



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Which of the following medications is/are associated with urticaria?

The correct answer is D.



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