An otherwise healthy 10-month-old boy was brought to an allergy clinic for evaluation of atopic dermatitis and chronic rhinitis. On arrival at the clinic for aeroallergen and milk prick skin testing, a rash was noted that was different from his usual atopic dermatitis. The rash had not been present 2 hours earlier when the mother dressed the child and placed him in his car seat during the ride to the clinic.
The rash was present only in the distribution shown here. The skin folds of the patient's back were spared. There were no discrete lesions. The rash was slightly raised and blanched with pressure.
The child had been in his usual state of good health, without fevers or any change in appetite or activity level. The mother reported that he had had a similar rash in the past, but that it had not appeared for several months.
Amy L. Parker, MD, and Rajiv Arora, MD, of Lackland Air Force Base in Texas,* diagnosed immediate pressure urticaria (IPU). Key features supporting the diagnosis included the rash's raised, erythematous nature, distribution, and acute onset.1,2 The child's car seat was the apparent source of pressure.
IPU is typically accompanied by pruritus and a burning sensation.1 Because this baby was unable to verbally express himself, it is difficult to say whether these symptoms were present. The patient did not seem bothered by the rash.
Pressure urticaria is synonymous with delayed pressure urticaria (DPU), which has a latent period of onset within 1 to 4 hours after exposure to pressure.3 In contrast, IPU occurs within minutes after pressure is applied to the skin.1,2 Studies of DPU are far more common than studies of IPU; however, both entities appear to be rare in children. In one study of 226 children with chronic urticaria, pressure urticaria accounted for only 0.4% of the cases.4
The histopathology of DPU is characterized by the presence ofCD4+ T cells, eosinophils, mast-cell degranulation, and adhesion molecule expression.5 One histopathologic sample featured in a case report of IPU revealed perivascular infiltration consisting of lymphocytes and histiocytes without eosinophilia.1 Other histopathologic features of this case, including T-cell subsets, were not discussed inthat report.
The cause of IPU is unknown, although it can occur in conjunction with hypereosinophilic syndrome.6 Chronic urticaria has been rarely reported in association with autoimmune disorders.4,7,8 Pressure urticaria is often refractory to treatment, but antihistamines and/or leukotriene antagonists are often tried.7,9
Corticosteroids will suppress the rash, but the risk-benefit ratio of such therapy may not be acceptable.7 The long-term outcome for patients with IPU has not been published, but chronic urticaria is known to be a persistent entity for many. One study demonstrated that 42% of children continued to have recurrent urticaria after 1 year of follow-up.9
The patient described in this report was not treated because the rash occurred infrequently, resolved spontaneously, and did not appear to be bothersome. One study suggested that atopy may play a role in chronic urticaria in children: the authors documented rates of 2.2% and 4% for aeroallergen sensitivity and food allergen sensitivity, respectively.4 However, skin testing of this patient, which was completed at a later date, was negative for cow's milk (whole and casein), tree mix, grass mix, weed mix, mold mix, dust mite mix, and dog and cat extracts. Therefore, it is not possible to say definitively whether his atopic dermatitis or chronic rhinitis was related to his IPU. The patient and his family moved and were subsequently lost to follow-up.
The opinions and views contained herein are the private views of the authors and are not to be construed as reflecting the views of the Department of the Air Force, the Department of Defense, or the United States Government.