Cutaneous inflammatory cell infiltrate in chronic idiopathic urticaria: Comparison of patients with and without anti-Fc epsilon RI or anti-IgE autoantibodies
Ra. Sabroe et al., Cutaneous inflammatory cell infiltrate in chronic idiopathic urticaria: Comparison of patients with and without anti-Fc epsilon RI or anti-IgE autoantibodies, J ALLERG CL, 103(3), 1999, pp. 484-493
Background: Previous studies defining the histopathologic features of patie
nts with chronic idiopathic urticaria (CIU) were performed on wheals of unc
ertain duration and before the identification of functional autoantibodies
against Fc epsilon RI and/or IgE, now known to be present in approximately
30% of patients with CIU.
Objective: We sought to determine the timing of the inflammatory infiltrate
in the wheals of patients with CIU and to detect differences between patie
nts with and without autoantibodies.
Methods: Immunohistochemistry was used to identify neutrophils (neutrophil
elastase), T lymphocytes (CD3), and activated eosinophils (EG2) in biopsy s
pecimens from uninvolved skin and wheals present for less than 4 hours and
greater than 12 hours in 22 patients with CIU,as wed as in biopsy specimens
from the skin of 12 healthy control subjects. Patients were identified as
having functional autoantibodies on the basis of their serum-evoked histami
ne release in vitro from the basophils of 2 healthy donors
Results: EG2(+), neutrophil elastase(+), and, to a lesser extent, CD3(+) ce
lls were found in greater numbers in wheals undergoing biopsy at less than
4 and greater than IZ hours than in uninvolved skin (P < .05). Patients wit
hout autoantibodies (n = 12) had significantly more EG2(+) cells in wheals
of greater than 12 hours' duration than patients with autoantibodies (n = 1
0; P = .02). There was no other difference between patients with and withou
t autoantibodies in the cutaneous cellular infiltrate.
Conclusion: Neutrophil and eosinophil accumulation occurs early in the evol
ution of a wheal in patients with CIU but eosinophil activation may occur l
ater or be more persistent in patients without autoantibodies.