Pressure Urticaria Medication

The results of treatment of delayed pressure urticaria (DPU) are relatively disappointing. Antihistamines are helpful but may not completely control symptoms of delayed pressure urticaria. Some authors have used up to 4 times the recommended dose of nonsedating antihistamines to achieve control.^[19]

Combination therapy may decrease disease activity. Reported successful adjunctive agents include leukotriene antagonists (eg, montelukast, zafirlukast) and H2-receptor antagonists (eg, famotidine, ranitidine).^[28]

Prednisone and NSAIDs produce variable responses. NSAIDs as a treatment may be suboptimal because they, along with aspirin, may worsen urticaria and angioedema. Indomethacin has not demonstrated efficacy for the treatment of delayed pressure urticaria. Similarly, colchicine has been ineffective as a therapy.

Prednisone has some clinical efficacy, but long-term therapy is problematic because of its many adverse effects. One study of a small group of patients showed efficacy of high-potency topical steroids for reducing edema, erythema, and pruritus associated with delayed pressure urticaria lesions.^[29]

Class Summary

These agents may be useful in helping control symptoms of chronic urticaria, which frequently coexists with delayed pressure urticaria. Many H1 antagonists are metabolized through the P450 system. Important exceptions include cetirizine, levocetirizine, and fexofenadine.

Levocetirizine (Xyzal)

Histamine1-receptor antagonist. Active enantiomer of cetirizine. Peak plasma levels reached within 1 h and half-life approximately 8 h. Available as a 5-mg breakable (scored) tab and 0.5 mg/mL oral sol. Indicated for uncomplicated skin manifestations of chronic idiopathic urticaria

Fexofenadine (Allegra)

Nonsedating second-generation medication with fewer adverse effects than first-generation medications. Competes with histamine for H1 receptors on GI tract, blood vessels, and respiratory tract, reducing hypersensitivity reactions. Does not sedate. Available in qd and bid preparations.

Diphenhydramine (Benadryl)

First-generation antihistamine with anticholinergic effects that binds to H1 receptors in the CNS and the body.

Competitively blocks histamine from binding to H1 receptors. Has significant antimuscarinic activity and penetrates CNS, which causes pronounced tendency to induce sedation. Approximately half of those treated with conventional doses experience some degree of somnolence. A small percentage of children paradoxically respond to diphenhydramine with agitation.

For symptomatic relief of pruritus caused by release of histamine in inflammatory reactions.

Loratadine (Claritin)

Selectively inhibits peripheral histamine H1 receptors.

Desloratadine (Clarinex)

Long-acting tricyclic histamine antagonist selective for H1 receptor. Major metabolite of loratadine, which, after ingestion, is extensively metabolized to active metabolite 3-hydroxydesloratadine.

Cetirizine (Zyrtec)

Selectively inhibits histamine H1 receptor sites in blood vessels, GI tract, and respiratory tract, which, in turn, inhibits physiologic effects that histamine normally induces at H1 receptor sites. Once-daily dosing is convenient. Bedtime dosing may be useful if sedation is a problem.

Hydroxyzine (Atarax, Vistaril)

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS.

Doxepin (Adapin, Sinequan)

A tricyclic antidepressant that has potent H1-blocking activity, making it quite useful for urticaria. However, has very potent sedative and anticholinergic effects. Can be quite effective if used at bedtime because sedative effects can help patients with pruritus sleep.

Class Summary

Can be used as an adjunctive agent to H1 antagonist therapy.

Famotidine (Pepcid)

H2 antagonist that when combined with an H1 type may be useful in treating allergic reactions that do not respond to H1 antagonists alone.

Ranitidine (Zantac)

Second-generation agent that is effective in urticaria. Tolerated very well, with a rate of sedation that is not significantly different from placebo.

Class Summary

Small reports^[8] have demonstrated the efficacy for delayed pressure urticaria of leukotriene antagonists, alone or in combination. Other forms of chronic urticaria have not demonstrated similar responses to this treatment.

Montelukast (Singulair)

Leukotriene inhibitors can be a helpful addition to asthma and allergic rhinitis not well controlled with H1-receptor blockers and inhaled corticosteroids.

Zafirlukast (Accolate)

Inhibits effects by leukotriene receptor, whose activity has been associated with airway edema, smooth muscle contraction, and cellular activity associated with symptoms.

Class Summary

These agents have been used with variable success for their anti-inflammatory properties.

Prednisone (Deltasone, Sterapred)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and suppresses lymphocyte and antibody production.

Class Summary

Some small studies have shown efficacy in reducing the size, erythema, and pruritus associated with pressure urticaria lesions.

Clobetasol propionate (Clobex, Olux, Embeline, Temovate)

Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Decreases inflammation by stabilizing lysosomal membranes, inhibiting PMN leukocytes and mast cell degranulation.

Class Summary

NSAIDs are the most commonly used medications to control mild to moderate pain and to decrease inflammation. Sulfasalazine, steroids, and immunosuppressive agents are sometimes used. These agents have been used with variable success. NSAIDs can also be a nonimmunologic trigger of mast cell degranulation and subsequent urticaria.

Ibuprofen (Ibuprin, Advil, Motrin)

NSAID with analgesic, anti-inflammatory, and antipyretic properties. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Naproxen (Aleve, Naprelan, Anaprox)

Inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.