Advanced glycation end-product (AGE)-damaged IgG occurs as a result of hyperglycemia
and/or oxidative stress. Autoantibodies to IgG-AGE were previously demonstrated in patients …

Hyperglycaemia and/or oxidative stress can cause IgG to be modified by advanced glycation
end products (AGE). Three patients with aggressive rheumatoid arthritis (RA) and vasculitis …

Objective To determine the association of serum IgG advanced glycation endproducts (AGE)
and IgM anti-IgG-AGE antibodies with clinical measurements of rheumatoid arthritis (RA) …

Advanced glycation end-products (AGE) play a role in diabetes complications and in RA. An
autoantibody to IgG-AGE has been shown to correlate with RA disease activity. Thus we …

Several tribes of North American Indians are known to have poor glucose control and are at
a high risk of developing type 2 diabetes. Similarly some tribes also exhibit RA at a high …

Incubation of proteins with glucose lead to their non-enzymatic glycation ultimately resulting
in the formation of advanced glycation end products (AGEs) in vivo. AGEs alter unique three …

AIMS: To study the immunogenicity of advanced glycation end product (AGE) modified IgG
(AGE-IgG) in experimental animals. MAIN METHODS: Human IgG was subjected to in vitro …

The role of advanced glycation end products (AGEs)–damaged immunoglobulin G (AGE-
IgG) in type 1 diabetes has been investigated in the present study. IgG was isolated from the …

Objectives Generation of advanced glycation end products (AGE) is an inevitable process in
vivo and can be accelerated under pathologic conditions such as oxidative stress, eg in …

Background Levels of pentosidine (representative of advanced glycation end-products) in
sera of patients with rheumatoid arthritis are increased when compared with sera of other …