TY - JOUR
T1 - The possible contribution of anti-Gal to Graves' disease
AU - Fullmer, Joseph
AU - Lindall, Arnold
AU - Bahn, Rebecca
AU - Mariash, Cary N.
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2005/11
Y1 - 2005/11
N2 - Anti-Gal is a natural antibody specific for the α-galactosyl epitope. Previous studies suggested that Graves' disease (GD) patients had elevated anti-Gal titers compared to normal controls, but titers returned to normal after treatment. We developed an anti-Gal enzyme-linked immunosorbent assay (ELISA) using the property of anti-Gal to bind tightly to mouse laminin. We found no significant correlations between anti-Gal and thyroid-stimulating immunoglobulin (TSI) or free thyroxine (T4) in untreated hyperthyroid GD patients (n = 15) without clinical ophthalmopathy or euthyroid, previously treated GD patients with ophthalmopathy. There was a significant regression between TSI and free T4 in the hyperthyroid patients (p < 0.01). Addition of total anti-Gal antibody to the regression showed a trend toward improved correlation (p = 0.15 for improved correlation relative to TSI and free T 4 alone), suggesting it may stimulate GD thyroid tissue. However, in contrast to previous studies we found hyperthyroid patients (n = 20) had lower levels of anti-Gal immunoglobulin G (IgG) (18.4 ± 4.0 vs. 41.8 ± 8.9) than normals (n = 36 p < 0.05). Interestingly, hyperthyroid patients without clinical ophthalmopathy tended to have lower IgG anti-Gal levels than euthyroid patients with ophthalmopathy (p = 0.1). Hyperthyroidism significantly lowers anti-Gal, but the possible increase of anti-Gal in patients with ophthalmopathy suggests anti-Gal may play a role in ophthalmopathy, or may reflect the euthryoid status of these patients. This trend needs further study.
AB - Anti-Gal is a natural antibody specific for the α-galactosyl epitope. Previous studies suggested that Graves' disease (GD) patients had elevated anti-Gal titers compared to normal controls, but titers returned to normal after treatment. We developed an anti-Gal enzyme-linked immunosorbent assay (ELISA) using the property of anti-Gal to bind tightly to mouse laminin. We found no significant correlations between anti-Gal and thyroid-stimulating immunoglobulin (TSI) or free thyroxine (T4) in untreated hyperthyroid GD patients (n = 15) without clinical ophthalmopathy or euthyroid, previously treated GD patients with ophthalmopathy. There was a significant regression between TSI and free T4 in the hyperthyroid patients (p < 0.01). Addition of total anti-Gal antibody to the regression showed a trend toward improved correlation (p = 0.15 for improved correlation relative to TSI and free T 4 alone), suggesting it may stimulate GD thyroid tissue. However, in contrast to previous studies we found hyperthyroid patients (n = 20) had lower levels of anti-Gal immunoglobulin G (IgG) (18.4 ± 4.0 vs. 41.8 ± 8.9) than normals (n = 36 p < 0.05). Interestingly, hyperthyroid patients without clinical ophthalmopathy tended to have lower IgG anti-Gal levels than euthyroid patients with ophthalmopathy (p = 0.1). Hyperthyroidism significantly lowers anti-Gal, but the possible increase of anti-Gal in patients with ophthalmopathy suggests anti-Gal may play a role in ophthalmopathy, or may reflect the euthryoid status of these patients. This trend needs further study.
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U2 - 10.1089/thy.2005.15.1239
DO - 10.1089/thy.2005.15.1239
M3 - Article
C2 - 16356086
AN - SCOPUS:29244489054
SN - 1050-7256
VL - 15
SP - 1239
EP - 1243
JO - Thyroid
JF - Thyroid
IS - 11
ER -