Pressure urticaria L50.4

Polyetiological clinical picture triggered by pressure mechanisms. Pressure urticaria can occur residual after acute urticaria, can accompany acute or chronic urticaria or can occur without a precursor stage with a delay of 4-8 hours. (delayed pressure urticaria) can occur after the skin has been exposed to weights, e.g. after standing, walking, sitting on a hard surface or vibration.

S.a.u. Urticaria factitia; s.a.u. Urticaria, physical.

f:m=1:1; beginning around the age of 30 (average: 40 years). Years of progression.

At the place of application of force: palms of hands, soles of feet, buttocks, back, shoulders

4-8 hours after exposure to the traumatic stimulus, development of a deep redness and swelling in the affected area, accompanied by painful or burning, less often itching. The formation of blisters after the trauma is rare (bullous pressure urticaria of the delayed type). In delayed type pressure urticaria, the swelling can remain for up to 2 days.

Often urticarial dermographism. The reaction reaches its maximum after hours and lasts longer than 1 day.

Frequently accompanying general symptoms such as fatigue, fever, myalgia, arthralgia, joint effusion, headache, nausea.

In delayed pressure urticaria, systemic signs such as: BSG acceleration, CRP and IL-6 elevations, leukocytosis (relevance?) may occur.

Wherever possible, avoid triggering mechanisms (e.g. wearing insoles made of foam or silicone or relieving shoes) In daily life (especially at work) trigger factors are often unavoidable. In individual cases, severe pressure urticaria can lead to work and occupational disability.

An effective therapy is the administration of systemic glucocorticoids such as prednisolone (e.g. Decortin H). Initially 50-80 mg/day p.o., aim for the lowest possible maintenance dose. Many patients manage with very low doses (2.0-5.0 mg prednisolon/day). Problem: NW with long-term therapy!

Alternative: Therapy with DADPS (50-100 mg/day p.o.) should be initiated early, overlapping with glucocorticoid therapy if necessary. Own results are positive.

Alternative: Positive case studies with leukotriene antagonists ( montelukast) exist in the literature (own experiences are negative).

Alternative: In individual cases, therapy with TNF-alpha-blockers ( Infliximab; dosage scheme as for psoriasis therapy) as well as IVIG(cave! costs) has been successfully described.

Alternative: Sulfasalazine as a cost-effective approach

Alternative: Omalizumab. The positive effect was described in smaller studies (Müller S et al. 2014)

Antihistamines (non-sedating H1-blockers) are generally not very effective and should only be given in high doses as additives.

Accompanying robotic measures such as alternating hot and cold baths and sauna sessions can be carried out. S.a.u. Urticaria.

The delayed pressure urticaria is extremely resistant to therapy. The use of omalizumab is indicated for severe forms of the disease.

1. Cap JP et al (1985) The effect of ketotifen in Urticaria factitia and Urticaria cholinergica in a crossed double-blind experiment. Dermatologist 36: 509-511
2. Debus D et al (2007) Successful use of Infliximab in therapy-resistant delayed pressure urticaria. Allergo J 16: 507-511
3. Butcher M, grave J (2004) Physical urticaria. dermatologist 55: 344-349
4. Kasperska-Zajac A et al (2013) Markers of systemic inflammation in delayed pressure urticaria. Int J Dermatol 52:309-310
5. Kontou-Fili K et al (1997) Physical urticaria:classification and diagnostic guidelines. Allergy 552: 504-513
6. Müller S et al (2014) Bullous delayed pressure urticaria responding to omalizumab. Allergo J Int 23:237
7. Rodríguez-Rodríguez M et al (2014) Successful treatment of severe delayed pressure angio-oedema with omalizumab. Allergol Immunopathol (Madr) 42:78-80
8. Swerlick RA et al (2015) Delayed pressure urticaria: response to treatment with sulfasalazine in a case series of seventeen patients. Dermatol Ther 28:318-322