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Pressure Urticaria

  • Author: Sarah Beggs; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Sep 09, 2014
 

Background

Pressure urticaria is an uncommon form of physical urticaria, a subset of chronic urticaria, which presents with erythematous swelling at sites of pressure. Patients who have urticaria for more than 6 weeks are given the diagnosis of chronic urticaria. This distinction is important as an inciting event or etiology is not identified for the majority of patients with chronic urticaria—hence, the term chronic idiopathic urticaria (CIU) is often used. A proportion of patients diagnosed with chronic urticaria have physical urticaria,[1] which is urticaria incited by a physical stimulus, such as mechanical (friction, vibration, pressure), thermal, or electromagnetic waves.[2]

Pressure urticaria may occur immediately (within minutes) after a pressure stimulus.[3] However, more commonly, erythema and cutaneous (and often subcutaneous) edema develops 4-6 hours after a pressure stimulus. For this reason, the term delayed pressure urticaria (DPU) is commonly used. The reaction may last up to 72 hours and can be associated with pruritus, burning, and pain.[4] Pressure sites, including the hands, feet, trunk, buttocks, and legs, are most commonly affected. Lesions can be induced by a variety of stimuli, including standing, walking, wearing of tight clothes, and sitting or leaning on a hard surface.[5]

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.

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Pathophysiology

The pathogenesis of delayed pressure urticaria (DPU) is relatively unknown. Although the trigger stimulus is typically identified, no allergen has been established. The general pathogenesis of urticaria (hives) can be mediated immunologically or nonimmunologically; usually antibodies against immunoglobulin E (IgE) molecules are involved. IgE molecules bind to mast cells. When an antibody or autoantibody attaches to the antigen-binding site of the IgE molecule, a bridge is formed between two or more IgE molecules. This induces mast cell degranulation, releasing multiple proinflammatory mediators, including histamine. In chronic idiopathic urticaria (CIU), the mast cells are inappropriately activated.[6]

In DPU, mast cells and histamine are believed to play a role in the disease pathogenesis. Injections of compound 48/80, a mast cell degranulator, lead to the formation of wheals in patients with DPU both 15 minutes after injection and at 6-8 hours after injection. Injections in patients with chronic urticaria, but without DPU, produce wheals at 15 minutes that diminish over time. Histamine injections in both patients lead to initial wheal formation with no late-phase reaction.[7]

Histamine levels are increased in the lesional skin, while intracellular histamine levels are decreased in peripheral white blood cells.[8] There is also an increased stimulation of histamine release. Despite these findings, histamine is unlikely to be the sole mediator in pressure urticaria. This is further demonstrated in the relative unresponsiveness of pressure urticaria to antihistamine treatment.

Other mediators are believed to be involved. This includes 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.[9] In addition, elevated concentrations of interleukin (IL)–1a, IL-5, and IL-6; tumor necrosis factor (TNF)–alpha; and leukotrienes have also been found in lesional skin of pressure urticaria patients.[10, 11, 12] Abnormalities in platelets and fibrin or fibrinolysis have also been investigated.[13, 14] Systemic inflammation has also been suggested with elevation seen of C-reactive protein (CRP) and sCD40L, a platelet activator.[15, 16]

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Etiology

Pressure stimuli may include the following:

  • Standing, walking, or sitting on a hard surface
  • Using tools (eg, a screwdriver or a hammer)
  • Hand clapping
  • Carrying a handbag
  • Wearing tight-fitting clothes (eg, bra straps, belts, shoes, cuffs, or watches)
  • Dental work
  • Kissing
  • Sexual intercourse
  • Tampon use

Occasionally, delayed pressure urticaria (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.[17]

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Epidemiology

Delayed pressure urticaria (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%.[18] The peak age of onset of DPU is in the 20s and 30s (range, 5-63 y).[19] DPU is slightly more common in men than in women.

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Prognosis

Delayed pressure urticaria (DPU) is a chronic disease that can last for years (mean, 9 y; range, 1-40 y).[19] 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 chronic idiopathic urticaria (CIU) than in those with atopic eczema or psoriasis.[20]

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Contributor Information and Disclosures
Author

Sarah Beggs George Washington University School of Medicine and Health Sciences

Disclosure: Nothing to disclose.

Coauthor(s)

Warren R Heymann, MD Head, Division of Dermatology, Professor, Department of Internal Medicine, Rutgers New Jersey Medical School

Warren R Heymann, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Niraj Butala, MD Resident Physician, Department of Dermatology, Cooper University Hospital

Niraj Butala, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Medical Association, American Society for Dermatologic Surgery

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

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

Disclosure: Nothing to disclose.

Acknowledgements

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.

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

Joslyn S Kirby, MD is a member of the following medical societies: American Academy of Dermatology, International Society for Cutaneous Lymphomas, Pennsylvania Academy of Dermatology, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

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

Ellen J Kim, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Dermatology Foundation, Medical Dermatology Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

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

Robin M Levin, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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Table. Assessment Tool for Scoring Severity of Disease*
Score Wheals Pruritus
0 None None
1 Mild (< 20 wheals/24 h) Mild
2 Moderate (21-50 wheals/24 h) Moderate
3 Intense (>50 wheals/24 h) or large confluent areas Intense
*Score = wheal score (0-3) + pruritus score (0-3); thus, the overall score for severity ranges from 0 to 6.
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