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Delayed pressure urticaria is a mechanical urticaria in which pressure causes whealing. Delayed cutaneous erythema and edema occur in association with marked subcutaneous swelling after the application of a sustained pressure stimulus to the skin. The earliest reports and theories of the pathogenesis of delayed pressure urticaria are summarized. Detailed attention is given to making the diagnosis by taking a history and provoking the lesions. The clinical features and natural history are considered. The effects of the disorder on quality of life are delineated, and management strategies are suggested.

Circulating functional autoantibodies to the high-affinity IgE receptor (Fc(epsilon)RI) or to IgE have been found in approximately one third of patients with chronic idiopathic urticaria (CIU).We sought to compare basophil histamine release and basophil numbers in patients with CIU with and without autoantibodies.Basophil histamine release to the anti-Fc(epsilon)RI mAb 22E7, anti-IgE, and formyl-methionyl-leucyl-phenylalanine (fMLP); basophil numbers; and total cellular histamine were measured in 26 patients with CIU and 18 healthy control subjects. Twelve patients were classified as having functional anti-Fc(epsilon)RI and/or anti-IgE autoantibodies on the basis of their serum-evoked histamine release from the basophils of 2 healthy donors.22E7 and anti-IgE, but not fMLP, released less histamine from basophils of patients with CIU than from those of control subjects. Mean+/-SEM maximum histamine release to 22E7 from basophils of control subjects and patients with CIU with and without autoantibodies was 38.5%+/-5.0%, 17.9%+/-6.0% (P =.01), and 1.0%+/-0.3% (P.0001), respectively. Similar results were obtained with anti-IgE, which is dependent on and cross-links cell bound IgE, and 22E7, which directly cross-links the IgE receptor. The mean+/-SEM basophil counts for control subjects and patients with CIU without and with autoantibodies were 52+/-7, 34+/-9 (P =.04), and 5+/-1 (P.0001) x 10(6) cells/L, respectively, and similar changes were found in measurements of total cellular histamine.Patients with autoantibodies have both markedly reduced basophil numbers and basophil histamine release to factors acting through Fc(epsilon)RI, which indicates either a residual pool of functionally distinct basophils or may be a consequence of desensitization of the Fc(epsilon)RI pathway.

The pharmacologic and clinical effects of the 5-lipoxygenase inhibitor, lonapalene, have been determined in a double-blind, placebo-controlled, topical study in ten volunteers with psoriasis. A statistically significant clinical improvement was seen in lesions treated with 2% lonapalene ointment as compared with vehicle-treated sites. Although there was a statistically significant reduction in the levels of material similar or identical to the chemoattractant arachidonate 5-lipoxygenase product, leukotriene B4>, in skin chamber fluid samples from lonapalene versus vehicle treated lesions, no significant reduction in arachidonic acid or 12-hydroxy-5,8,10,14-eicosatetraenoic acid was seen. The reduction in leukotriene B4 equivalents occurred before significant clinical improvement in lesions was seen. This and the selectivity of the pharmacologic response suggest that the therapeutic effect of topical lonapalene in psoriasis might be related to inhibition of leukotriene B4 synthesis. These results support the view that 5-lipoxygenase inhibitors may be useful in the treatment of psoriasis, and that leukotriene B4 is a relevant mediator of the pathology of this disease.

We studied 44 patients with delayed pressure urticaria. The mean age at onset of the disease was 33 years (range, 5 to 63 years) and the mean duration of disease was 9 years (range, 1 to 40 years). After pressure stimulus, the mean onset of whealing occurred in 3 1/2 hours, the mean peak swelling occurred after 10 hours, and the mean lesion duration was 36 hours. Two thirds of patients had generalized flulike symptoms. Sixty percent had disabling nonremitting delayed pressure urticaria. Sixty-two percent had coexistent chronic idiopathic urticaria, and 27% had angioedema. Delayed pressure urticaria was confirmed by pressure tests with either a calibrated dermographometer or suspended weights. More than 50% of patients tested also had delayed dermographism. A double-blind, controlled, crossover trial of indomethacin therapy in 14 patients revealed no Significant subjective improvement or reduction in area of induced wheals. We conclude: (1) The diagnosis of delayed pressure urticaria can be easily made by dermographometer testing. (2) Delayed dermographism may be the same entity as delayed pressure urticaria induced by a different method of pressure application. (3) Systemic corticosteroids remain the only known effective treatment for disabling delayed pressure urticaria.

The 5,12-dihydroxy metabolite of arachidonic acid, leukotriene B 4 , is a highly potent neutrophil chemoattractant. In view of the characteristic epidermal neutrophil infiltrate in psoriasis, the presence of leukotriene B 4 in samples from untreated lesional and uninvolved skin has been sought. Chambers were fixed to abraded skin and filled with phosphate-buffered saline (PBS). After 35 mm, the fluid was removed, and acidic lipids were extracted and subjected to high-performance liquid chromatography (HPLC). Extracts were purified by both straight- and reversed-phase HPLC, and assay of evaporated fractions by an agarose microdroplet chemokinesis technique indicated the presence of leukotriene B 4 -like material. No significant leukotriene B 4 - like activity was found in samples from uninvolved skin. Subsequent experiments using a modification of the initial skin chamber method indicated that leukotriene B 4 was being released from deeper layers of lesional skin and not only from superficial scale. Monohydroxy-ei- cosatetraenoic acid-like activity was also seen in lesional samples as determined by straight-phase HPLC and chemokinesis assay. These findings and the proinflammatory properties of these compounds in human skin suggest that they may play a role in the pathogenesis of the psoriatic neutrophil infiltrate.