The coincidence of Hashimoto thyroiditis (HT) and chronic idiopathic urtica
ria (CIU) is a commonly observed phenomenon in western New York. Previous l
iterature suggested that there may be a direct relationship between them. W
e undertook these studies to determine whether humoral or cell-mediated mec
hanisms might link HT and CIU.
Skin biopsies from patients with CIU, with or without HT, were indistinguis
hable by light microscopy. No immune complex deposition was observed, altho
ugh only the skin from patients with CIU and HT contained perivascular fibr
in deposits. Similarly, inummohistochemical studies evaluating cellular exp
ression of CD3, CD4, CD8, CD20, and CD68 failed to differentiate between CI
U with or without HT. Analysis of VG restriction in thyroid tissue of patie
nts with HT and the skin of patients with CIU and HT by in situ polymerase
chain reaction failed to reveal any oligoclonal T-lymphocyte subpopulations
. In contrast, only patients with CIU and HT had anti-Fc epsilon RI antibod
ies in their sera that could induce degranulation of normal basophils. Some
sera from patients with CIU and HT caused degranulation of normal basophil
s in the absence of anti-FceRI. The factor causing basophil degranulation i
n these sera was not determined. Patients with CIU and HT failed to improve
clinically with thyroid replacement therapy. All CIU patients were equally
well managed with symptomatic therapies.
In conclusion, HT likely represents a marker of other autoimmunity, rather
than being a direct causative agent in CIU. Management of CIU, with or with
out HT and with or without anti-FceRI antibodies, should be the same. Futur
e studies will have to examine whether cell-mediated responses participate
in CIU, especially in association with HT.