Clinicopathologic findings in (anti-FcepsilonR1alpha) autoimmune-related chronic urticaria.

One cause of chronic urticaria is autoreactivity which is diagnosed by detecting autoantibodies against the IgE receptor alpha subunit (anti-Fc R1alpha).
To compare the histopathologic features of chronic urticaria patients testing positive for anti-IgE receptor antibody (Ab) to those testing negative.
Totally, 438 patients with a clinical presentation of chronic urticaria (2011-2013) had anti-IgE receptor Ab tested and 37 of those patients had skin biopsy. We evaluated microscopic features including: spongiosis, dermal edema, presence of mast cells, density of lymphocytic infiltration, predomination of eosinophils/neutrophils; intravascular neutrophils and presence of vasculitis. The aforementioned features were compared between negative and positive anti-IgE receptor Ab groups.
Of 37 patients , 69% were women and 31% were men. 49% had positive anti-IgE receptor Ab and 51% had negative anti-IgE receptor Ab. In the positive anti-IgE receptor Ab group, 83% showed intravascular neutrophils. Eosinophil predominance was identified in 72% and neutrophil predominance was identified in 28%. In the negative anti-IgE receptor Ab group, 89% showed intravascular neutrophils. Eosinophil predominance was identified in 53% and neutrophil predominance was identified in 47%. There was no evidence of vasculitis in either group.
There were no significant histopathologic differences between the anti-IgE receptor Ab positive and negative cases. Therefore, serum testing for anti-IgE receptor Ab is required to identify this subgroup of chronic urticaria patients.
AuthorsTheera Rojanapremsuk, Sarah Kasprowicz, Ewa Schafer, Rachel Story, Michael S Clarke, Timothy Walls, Vivian Snyder, Briana C Gleason, Antoinette B Thomas, Thomas Cibull
JournalJournal of cutaneous pathology (J Cutan Pathol) Vol. 42 Issue 5 Pg. 329-32 (May 2015) ISSN: 1600-0560 [Electronic] United States
PMID25726718 (Publication Type: Journal Article)
Copyright© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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