Pressure Urticaria

Back

Background

Pressure urticaria is an uncommon form of physical urticaria. Patients who have had urticaria for more than 6 weeks are given the diagnosis of chronic urticaria. This distinction is important because an inciting event or etiology is not identified for the majority of patients with chronic urticaria—hence the often-used term chronic idiopathic urticaria (CIU). A proportion of patients with chronic urticaria have physical urticaria,[1] which is urticaria incited by a physical stimulus, such as cold, vibration, or pressure.

Pressure urticaria may occur immediately (within minutes) after a pressure stimulus.[2] More commonly, however, it develops 4-6 hours after a pressure stimulus. For this reason, the term delayed pressure urticaria (DPU) is commonly used. The wheals may last for 8-72 hours. The hands, feet, trunk, buttocks, legs, and face are the areas most commonly affected. Lesions can be induced by a variety of stimuli, including standing, walking, wearing of tight clothes, or sitting on a hard surface.[3]

For further information on urticaria, see Contact Syndrome Urticaria, Dermographism Urticaria, and Solar Urticaria. For patient education resources, see the Allergy Center and the Skin, Hair, and Nails Center, as well as Hives and Angioedema.

Pathophysiology

The pathogenesis of DPU is unknown. In most cases, no allergen can be identified. Mast cells and histamine release are believed to play roles because the injection of compound 48/80, which causes depletion of mast cell mediators, prevents the induction of lesions in the injected area.[4]

Histamine levels are increased in lesional skin, and intracellular histamine levels are decreased in peripheral white blood cells.[5] Despite these findings and the finding of increased stimulated histamine release, histamine is not likely to be the sole mediator in pressure urticaria, given the relative unresponsiveness of the condition to antihistamine treatment.

Other possible mediators include eosinophils (as suggested by the presence of eosinophilia), eosinophil cationic protein (ECP), and eosinophil cationic factor (ECF) found in biopsy specimens from some patients with DPU, particularly bullous DPU.[6] Elevated concentrations of interleukin (IL)-5 and IL-6 and of leukotrienes have also been found in lesional skin of pressure urticaria patients.[7, 8] Abnormalities in platelets and fibrin or fibrinolysis are also being investigated.[9, 10]

Etiology

Pressure stimuli may include the following:

Occasionally, DPU is aggravated by heat, aspirin, or menstruation. Exacerbation of the condition during medical procedures is a reasonable possibility; urticaria flares following endoscopy have been described.[11]

Epidemiology

DPU is generally considered a rare entity; some investigators suggest that it is less uncommon than is usually assumed but appears to be rare because it is not consistently recognized. One study of 2310 patients with urticaria seen over 32 years found the prevalence of DPU to be 2%.[12]

The peak age of onset of DPU is in the 20s and 30s (range, 5-63 y).[13] DPU is slightly more common in men than in women.

Prognosis

DPU is a chronic disease that can last for years (mean, 9 y; range, 1-40 y).[13] One study reported that 28% and 48% of patients with DPU were free of lesions after 5 and 10 years, respectively. The morbidity of DPU varies, depending on the severity and the response to treatment. In some patients, this condition can be disabling, especially in patients who perform manual labor.

Quality-of-life (QOL) tools have demonstrated that patients with urticaria can show impairments in QOL scores similar to those seen in patients with cardiac disease or chronic dermatoses such as psoriasis and atopic eczema. QOL scores were lowest for energy, social isolation, emotional reaction, and sleep disturbance. The dimension of daily living activities was more profoundly impaired in patients with CIU than in those with atopic eczema or psoriasis.[14]

History and Physical Examination

The clinical manifestations of delayed pressure urticaria (DPU) differ from those typical of most types of urticaria. Onset is typically delayed, most commonly occurring 4 hours after the pressure stimulus. Less commonly, wheals due to pressure develop within minutes, in which case they may be confused with dermatographism. The lesions of DPU can persist for several hours and sometimes for as long as 48 hours, unlike those in typical urticaria, which resolve within 24 hours.

The lesions may be pruritic, painful, or burning. They can occur on any cutaneous surface and may mimic angioedema. With severe episodes, patients may experience fever, malaise, fatigue, chills, headache, and generalized arthralgias. Affected areas can be refractory to the development of new lesions for 1-2 days.

As many as 60% of individuals with DPU have concomitant chronic idiopathic urticaria (CIU), immediate or delayed dermographism (dermatographism), or angioedema. In some reports, the incidence of DPU in patients with CIU varies considerably, ranging from 2% to 40%; other reports estimate the rate to be 2-4%.[1, 12, 15]

The physical findings in DPU include wheals, typically involving the palms, soles, legs, and waist. DPU lesions may also involve the genitals. The wheals, which appear as deep dermal and subcutaneous swellings, often resemble angioedema more than they do typical urticaria. Typical urticaria may also be present as a result of coexisting CIU or some other chronic physical urticaria.

Laboratory Studies

An elevated white blood cell (WBC) count or neutrophilia may be present.[16, 17] Complement levels are normal.

Some patients with delayed pressure urticaria (DPU) also have concomitant chronic idiopathic urticaria (CIU). The following ancillary testing can be helpful in patients with CIU[18, 19] :

Pressure Challenge Testing

Pressure challenge testing (with the dermographometer or the suspended-weight method) may be performed for DPU.[20] Because therapy may influence test results, it is recommended that testing be performed at a time when therapy has been interrupted or stopped; however, some patients may have more severe disease that does not allow this. Repetitive testing can be used to assess response to therapy.

Multiple methods of applying measured amounts of pressure can be used to test for the development of DPU. A consensus conference review suggests using the following approaches[18] :

The tests are most often applied to the shoulders, upper back, posterior thighs, or volar forearm. Pressure provocation tests should be read at 6 hours. Both the weight and the application time should be recorded. The duration of application is inversely related to the pressure applied; for example, wheals will take longer to develop with a lower pressure than with a higher pressure.

Assessment of Urticaria Severity

Several scoring systems are used to measure the severity of chronic urticaria, both in research settings and in clinical practice. A useful assessment tool was suggested by a European panel (see Table 1 below).[19]

Table 1. Assessment Tool for Scoring Severity of Disease*


View Table

See Table

The severity of DPU can vary throughout the day and from day to day. Overall disease activity is best assessed by having patients determine a severity score several times a day for several days before coming to their appointments.

Histologic Findings

The histologic features of DPU lesions are variable, often depending on the age of the lesion. Biopsy within hours demonstrates moderate-to-heavy infiltration of eosinophils with neutrophils and lymphocytes in a perivascular and interstitial pattern in the dermis and subcutaneous fat. Degranulated mast cells may be noted. Biopsy of an older DPU lesion (> 24 h) demonstrates eosinophils and lymphocytes.

No vessel-related changes (eg, leukocytoclasia or fibrinoid necrosis), such as those noted in urticarial vasculitis, are seen. Direct immunofluorescence test results are negative.

Several reports of bullous pressure urticaria have been reported, and histologic findings show spongiosis and intraepidermal bullae associated with an eosinophil-rich inflammatory infiltrate in the superficial and deep dermis.[6]

Approach Considerations

Patients should attempt to limit pressure stimuli. A simple intervention is to broaden the handles on heavy items or straps on clothing to disperse the pressure over a larger area. However, avoidance is not easy and may not be helpful in patients with moderate-to-severe disease.

The results of pharmacologic treatment of delayed pressure urticaria (DPU) are somewhat disappointing. Besides antihistamines, agents used have included systemic corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, dapsone, sulfasalazine, montelukast, chloroquine, cyclosporine, intravenous immunoglobulin (IVIg), and omalizumab.

Restrictions in activity depend on the severity of the disease. Consult a dermatologist or allergist for evaluation for other causes of urticaria.

Pharmacologic Therapy

Antihistamines can reduce the severity of symptoms and are helpful in controlling associated chronic idiopathic urticaria (CIU), but they may not control the symptoms completely. Some authors have used up to 4 times the recommended dose of nonsedating antihistamines to achieve control.[19]

NSAIDs produce variable responses. As treatment, they may be suboptimal because they, along with aspirin, may worsen urticaria and angioedema. Indomethacin has not demonstrated efficacy in the treatment of DPU.

Steroids also yield variable results. 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 found high-potency topical steroids to be efficacious for reducing edema, erythema, and pruritus associated with DPU lesions.[21]

Patients who see improvement with systemic steroid therapy often relapse when these agents are discontinued. The adverse effects of steroids must also be considered and managed. Patients may already be taking H2 blockers in an attempt to manage their urticaria; however, these are also used to treat gastritis from systemic steroid therapy. Long-term steroid use also affects the bones, and patients are often advised to take calcium with vitamin D daily, with additional consideration given to adding a bisphosphonate such as alendronate.[22]

Other therapeutic agents that have been tried include colchicine, dapsone, sulfasalazine, and montelukast.[23, 24] Colchicine has been largely ineffective as a therapy. Reports from small studies have found leukotriene antagonists, alone or in combination, to be efficacious for treatment of DPU[8] ; other forms of chronic urticaria have not demonstrated similar responses to this treatment.

Case reports have demonstrated successful treatment with chloroquine.[25] Cyclosporine, IVIg, and omalizumab have each been used in a small number of patients with severe and refractory disease.[26, 27, 28]

Combination therapy may decrease disease activity. Adjunctive agents that reportedly have been successfully employed in this context include leukotriene antagonists (eg, montelukast and zafirlukast) and H2 -receptor antagonists (eg, famotidine and ranitidine).[29]

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Agents used in the management of pressure urticaria include antihistamines, leukotriene antagonists, corticosteroids, and nonsteroidal anti-inflammatory drugs (NSAIDs).

Levocetirizine (Xyzal)

Clinical Context:  Levocetirizine is an H1-receptor antagonist and an active enantiomer of cetirizine. Peak plasma levels are reached within 1 hour, and the half-life is approximately 8 hours. Levocetirizine is available as a 5-mg breakable (scored) tablet and a 0.5 mg/mL oral solution. It is indicated for uncomplicated skin manifestations of chronic idiopathic urticaria (CIU).

Fexofenadine (Allegra)

Clinical Context:  Fexofenadine is a nonsedating second-generation medication that has fewer adverse effects than first-generation medications. It competes with histamine for H1 receptors in the gastrointestinal (GI) tract, blood vessels, and the respiratory tract, reducing hypersensitivity reactions. Fexofenadine does not sedate. It is available in once-daily and twice-daily preparations.

Loratadine (Claritin, Alavert)

Clinical Context:  Loratadine selectively inhibits peripheral histamine H1 receptors.

Desloratadine (Clarinex)

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

Cetirizine (Zyrtec)

Clinical Context:  Cetirizine selectively inhibits H1 receptor sites in blood vessels, the GI tract, and the respiratory tract, thereby inhibiting the 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.

Class Summary

Antihistamines may be useful in helping control symptoms of chronic urticaria, which frequently coexists with delayed pressure urticaria (DPU). Second-generation antihistamines, also known as less-sedating or low-sedation antihistamines, produce less sedation than traditional H1 blockers because they are less lipid-soluble and only cross the blood-brain barrier in small amounts. They also have longer half-lives, allowing less frequent dosing. Many H1 antagonists are metabolized through the cytochrome P-450 system. Important exceptions include cetirizine, levocetirizine, and fexofenadine.

Diphenhydramine (Benadryl, Diphenhist, Allerdryl)

Clinical Context:  Diphenhydramine is a first-generation antihistamine with anticholinergic effects. It binds to H1 receptors in the central nervous system (CNS) and the body, competitively blocking histamine from binding to these receptors.

Diphenhydramine is employed for symptomatic relief of pruritus caused by release of histamine in inflammatory reactions. It has significant antimuscarinic activity and penetrates the CNS and thus has a 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.

Hydroxyzine (Vistaril)

Clinical Context:  Hydroxyzine antagonizes H1 receptors in the periphery. It may suppress histamine activity in the subcortical region of the CNS.

Class Summary

First-generation antihistamines compete with histamine at the tissue-receptor level, preventing it from carrying out its mediator functions in urticaria.

Doxepin

Clinical Context:  Doxepin is a tricyclic antidepressant that has potent H1-blocking activity, which makes it quite useful for urticaria. However, doxepin has very potent sedative and anticholinergic effects. It can be quite effective if given at bedtime because its sedative effects can make it easier for patients with pruritus to sleep.

Class Summary

Agents in this class that antagonize the H1 receptor preventing histamine from causing urticaria. The tricyclic antidepressant doxepin is used in urticaria for its sedative and antihistaminic properties. Oral doxepin may be considered if oral antihistamines are not helpful.

Famotidine (Pepcid)

Clinical Context:  Famotidine is an 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)

Clinical Context:  Ranitidine is a second-generation agent that is effective for the treatment of urticaria. It is tolerated very well, with a rate of sedation that is not significantly different from that seen with placebo.

Nizatidine (Axid, Axid AR)

Clinical Context:  This agent competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.

Cimetidine (Tagamet HB 200)

Clinical Context:  This agent inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

Class Summary

H2 antagonist therapy can be used as an adjunct to H1 antagonist therapy.

Montelukast (Singulair)

Clinical Context:  Leukotriene inhibitors can be a helpful addition to therapy in patients with asthma and allergic rhinitis that are not well controlled with H1-receptor blockers and inhaled corticosteroids.

Zafirlukast (Accolate)

Clinical Context:  Zafirkulast inhibits effects mediated by leukotriene receptors, the activity of which has been associated with airway edema, smooth muscle contraction, and cellular activity associated with symptoms.

Class Summary

Leukotriene antagonists, alone or in combination, have been found to be efficacious for treating DPU. Other forms of chronic urticaria have not demonstrated similar responses to this treatment.

Prednisone

Clinical Context:  Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte (PMN) activity. It stabilizes lysosomal membranes and suppresses lymphocyte and antibody production.

Prednisolone (Pediapred, Orapred, Flo-Pred)

Clinical Context:  This glucosteroid occurs naturally and synthetically. It is used for both acute and chronic asthma. It may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity.

Class Summary

Because of their anti-inflammatory properties, corticosteroids have been used in the management of pressure urticaria, with variable success.

Clobetasol propionate (Clobex, Olux, Temovate)

Clinical Context:  Clobetasol propionate is a class I superpotent topical steroid; it suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Clobetasol decreases inflammation by stabilizing lysosomal membranes, inhibiting PMN leukocytes and mast cell degranulation.

Class Summary

Some small studies have shown topical corticosteroids to be efficacious in reducing the size of pressure urticaria lesions, as well as the erythema and pruritus associated with them.

Ibuprofen (Advil, Motrin IB, NeoProfen, Addaprin)

Clinical Context:  Ibuprofen is an NSAID with analgesic, anti-inflammatory, and antipyretic properties. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Naproxen (Aleve, Naprelan, Anaprox, Naprosyn)

Clinical Context:  Naproxen inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Class Summary

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

Author

Joslyn S Kirby, MD, Assistant Professor, Department of Dermatology, Milton S Hershey Penn State Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Ellen J Kim, MD, Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania

Disclosure: Nothing to disclose.

Robin M Levin, MD, Staff Physician, Assistant Professor, Department of Family Medicine, Division of Dermatology, Kennedy Hospital at Stratford

Disclosure: Nothing to disclose.

Warren R Heymann, MD, Head, Division of Dermatology, Professor, Department of Internal Medicine, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Ackerman Academy of Dermatopathology, New York

Disclosure: Nothing to disclose.

Additional Contributors

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.

Jeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society

Disclosure: Nothing to disclose.

Michael J Wells, MD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

References

  1. Barlow RJ, Warburton F, Watson K, Black AK, Greaves MW. Diagnosis and incidence of delayed pressure urticaria in patients with chronic urticaria. J Am Acad Dermatol. Dec 1993;29(6):954-8. [View Abstract]
  2. Commins SP, Kaplan AP. Immediate pressure urticaria. Allergy. Jan 2002;57(1):56-7. [View Abstract]
  3. Lawlor F, Black AK. Delayed pressure urticaria. Immunol Allergy Clin North Am. May 2004;24(2):247-58, vi-vii. [View Abstract]
  4. Ryan TJ, Shim-Young N, Turk JL. Delayed pressure urticaria. Br J Dermatol. Aug 1968;80(8):485-90. [View Abstract]
  5. Kaplan AP, Horakova Z, Katz SI. Assessment of tissue fluid histamine levels in patients with urticaria. J Allergy Clin Immunol. Jun 1978;61(6):350-4. [View Abstract]
  6. Kerstan A, Rose C, Simon D, et al. Bullous delayed pressure urticaria: pathogenic role for eosinophilic granulocytes?. Br J Dermatol. Aug 2005;153(2):435-9. [View Abstract]
  7. Lawlor F, Bird C, Camp RD, et al. Increased interleukin 6, but reduced interleukin 1, in delayed pressure urticaria. Br J Dermatol. May 1993;128(5):500-3. [View Abstract]
  8. Di Lorenzo G, Pacor ML, Mansueto P, et al. Is there a role for antileukotrienes in urticaria?. Clin Exp Dermatol. Mar 2006;31(3):327-34.
  9. Kasperska-Zajac A, Brzoza Z, Rogala B. Increased concentration of platelet-derived chemokines in serum of patients with delayed pressure urticaria. Eur Cytokine Netw. Jun 2008;19(2):89-91. [View Abstract]
  10. Kasperska-Zajac A, Jasinska T. Analysis of plasma D-dimer concentration in patients with delayed pressure urticaria. J Eur Acad Dermatol Venereol. Feb 2011;25(2):232-4. [View Abstract]
  11. Czecior E, Grzanka A, Kurak J, Misiolek M, Kasperska-Zajac A. Late Dysphagia and Dyspnea as Complications of Esophagogastroduodenoscopy in Delayed Pressure Urticaria: Case Report. Dysphagia. Jun 5 2011;[View Abstract]
  12. Champion RH. Urticaria: then and now. Br J Dermatol. Oct 1988;119(4):427-36. [View Abstract]
  13. Dover JS, Black AK, Ward AM, Greaves MW. Delayed pressure urticaria. Clinical features, laboratory investigations, and response to therapy of 44 patients. J Am Acad Dermatol. Jun 1988;18(6):1289-98. [View Abstract]
  14. Grob JJ, Gaudy-Marqueste C. Urticaria and quality of life. Clin Rev Allergy Immunol. Feb 2006;30(1):47-51. [View Abstract]
  15. Morioke S, Takahagi S, Iwamoto K, Shindo H, Mihara S, Kameyoshi Y. Pressure challenge test and histopathological inspections for 17 Japanese cases with clinically diagnosed delayed pressure urticaria. Arch Dermatol Res. Oct 2010;302(8):613-7. [View Abstract]
  16. Barlow RJ, Ross EL, MacDonald D, Black AK, Greaves MW. Adhesion molecule expression and the inflammatory cell infiltrate in delayed pressure urticaria. Br J Dermatol. Sep 1994;131(3):341-7. [View Abstract]
  17. Barlow RJ, Ross EL, MacDonald DM, Kobza Black A, Greaves MW. Mast cells and T lymphocytes in chronic urticaria. Clin Exp Allergy. Apr 1995;25(4):317-22. [View Abstract]
  18. Magerl M, Borzova E, Giménez-Arnau A, Grattan CE, Lawlor F, Mathelier-Fusade P. The definition and diagnostic testing of physical and cholinergic urticarias--EAACI/GA2LEN/EDF/UNEV consensus panel recommendations. Allergy. Dec 2009;64(12):1715-21. [View Abstract]
  19. Zuberbier T, Bindslev-Jensen C, Canonica W, et al. EAACI/GA2LEN/EDF guideline: management of urticaria. Allergy. Mar 2006;61(3):321-31. [View Abstract]
  20. Lawlor F, Black AK, Ward AM, Morris R, Greaves MW. Delayed pressure urticaria, objective evaluation of a variable disease using a dermographometer and assessment of treatment using colchicine. Br J Dermatol. Mar 1989;120(3):403-8. [View Abstract]
  21. Vena GA, Cassano N, D'Argento V, Milani M. Clobetasol propionate 0.05% in a novel foam formulation is safe and effective in the short-term treatment of patients with delayed pressure urticaria: a randomized, double-blind, placebo-controlled trial. Br J Dermatol. Feb 2006;154(2):353-6. [View Abstract]
  22. Liu RH, Werth VP. What is new in the treatment of steroid-induced osteoporosis?. Semin Cutan Med Surg. Dec 2007;26(4):203-9. [View Abstract]
  23. Hartmann K, Hani N, Hinrichs R, Hunzelmann N, Scharffetter-Kochanek K. Successful sulfasalazine treatment of severe chronic idiopathic urticaria associated with pressure urticaria. Acta Derm Venereol. Jan-Feb 2001;81(1):71. [View Abstract]
  24. Kozel MM, Sabroe RA. Chronic urticaria: aetiology, management and current and future treatment options. Drugs. 2004;64(22):2515-36. [View Abstract]
  25. Kulthanan K, Thumpimukvatana N. Positive impact of chloroquine on delayed pressure urticaria. J Drugs Dermatol. Apr 2007;6(4):445-6. [View Abstract]
  26. Dawn G, Urcelay M, Ah-Weng A, O'Neill SM, Douglas WS. Effect of high-dose intravenous immunoglobulin in delayed pressure urticaria. Br J Dermatol. Oct 2003;149(4):836-40. [View Abstract]
  27. Metz M, Altrichter S, Ardelean E, Kessler B, Krause K, Magerl M, et al. Anti-immunoglobulin E treatment of patients with recalcitrant physical urticaria. Int Arch Allergy Immunol. 2011;154:177-80.
  28. Mitzel-Kaoukhov H, Staubach P, Müller-Brenne T. Effect of high-dose intravenous immunoglobulin treatment in therapy-resistant chronic spontaneous urticaria. Ann Allergy Asthma Immunol. Mar 2010;104(3):253-8. [View Abstract]
  29. Nettis E, Colanardi MC, Soccio AL, Ferrannini A, Vacca A. Desloratadine in combination with montelukast suppresses the dermographometer challenge test papule, and is effective in the treatment of delayed pressure urticaria: a randomized, double-blind, placebo-controlled study. Br J Dermatol. Dec 2006;155(6):1279-82. [View Abstract]
Score Wheals Pruritus
0NoneNone
1Mild (< 20 wheals/24 h)Mild
2Moderate (21-50 wheals/24 h)Moderate
3Intense (>50 wheals/24 h) or large confluent areasIntense
*Score = wheal score (0-3) + pruritus score (0-3); thus, the overall score for severity ranges from 0 to 6.