What causes pressure urticaria?

Many people may have heard of urticaria. It is a common and serious skin disease in life. It is divided into many types. Compression urticaria is one of them. It may be found at any age and may even be accompanied by other urticaria. Therefore, people must understand the cause of compression urticaria and achieve fundamental treatment.

1. Relationship with inflammatory mediators

Ryan et al. injected mast cell degranulation agent 48/80 complex into the patient's compressed skin, which could produce delayed wheals locally. High concentrations of histamine and kinins have been isolated from pressure wheals, but treatment with antihistamines and antikinins is ineffective. Leukotrienes are not found in pressure wheals. Therefore, leukotrienes are not the main pathogenic mediators in this disease. Patients were compared with normal subjects. White blood cells can release more histamine and leukocyte chemotactic factor, but this change is non-specific.

2. Relationship with serum proteins

The lack of serum protease inhibitors will lead to prolonged mediator action, which may explain the formation of delayed wheals, but the tests of various serum proteases are normal. Because the wheals in this disease are large and painful, similar to congenital angioedema, complement deficiency was considered, but the test results were normal, and no abnormalities were found in serum cellulose, IgC, IgM, and ISA. One quarter of patients have a deficiency of serum factor vIII, but they do not have a bleeding tendency.

Skin lesions often occur on pressure-bearing areas of the body, such as the palms, soles, buttocks, and upper back, and rarely on the face. Local wheals occur 4-8 hours after skin pressure and the lesions last for 8-72 hours, with an average of about 20 hours. The lesions are large erythematous plaques with deep edema and central vascular compression that appears white. Lesions rarely extend beyond the site of compression.