Accumulation of advanced glycation endproducts in patients with systemic lupus erythematosus

Abstract

AGEs are increased in SLE compared with controls. Our findings indicate that AGE accumulation is associated with disease duration and might contribute to the development of accelerated atherosclerosis in SLE and, therefore, could be used for assessment of risk for long-term vascular complications.

Is Small Artery Elasticity Decreased Prior to Intima-Media Thickening in Patients with Longstanding Rheumatoid Arthritis?

“…Hypertension was defined as systolic BP > 140 mm Hg and/or diastolic BP > 90 mm Hg and/or current use of antihypertensive drugs 30,31 . Dyslipidemia was defined as plasma cholesterol > 6.21 mmol/l (240 mg/dl), plasma low-density lipoprotein (LDL) cholesterol > 3.36 mmol/l (130 mg/dl), plasma triglycerides > 2.26 mmol/l (300 mg/dl), or current use of lipid-lowering drugs 30,32 .…”

Skin autofluorescence as proxy of tissue AGE accumulation is dissociated from SCORE cardiovascular risk score, and remains so after 3 years

“…In the context of the very prolonged intervention effects in The Diabetes Control and Complications Trial, and Epidemiology of Diabetes Interventions and Complications Follow-up Study (DCCT-EDIC) and UK Prospective Diabetes Study (UKPDS) studies, AGE have been proposed to be the prime candidate as carrier of (glyco)metabolic memory in type 1 and type 2 diabetes, and in other conditions [10,11]. Tissue AGE and SAF levels are also associated with and predictive for cardiovascular and microvascular complications in type 1 diabetes and autoimmune disease [12][13][14]. Skin AF levels have been confirmed to be strong, independent predictors for cardiovascular disease (CVD) and mortality in intermediate [chronic kidney disease (CKD) III] and later stages of renal failure including hemodialysis, peritoneal dialysis and renal transplant patients [2,15,16].…”

Glycated-H2A histone is better bound by serum anti-DNA autoantibodies in SLE patients: Glycated-histones as likely trigger for SLE?

“…Therefore, under oxidative stress and similar conditions the cell nucleus may be a likely site for histone glycation [8]. The hyperchromicity observed in deoxyribose-modified-H2A samples at 278 nm could be due to changes in the microenvironment of UV absorbing amino acid residues as a consequence of glycation of lysyl/arginyl residues.…”

“…Despite this knowledge, it is still a challenge to fully understand the etiopathogenesis of SLE [7]. Recent studies have highlighted the importance of advanced glycation end products (AGEs) for better understanding of SLE [8]. Now the question arises whether these AGEs are hallmark of the disease or play a role in initiating signal transduction which alters genetic and cellular function.…”

“…There is much evidence which points towards role of AGEs in both the conditions. In SLE, AGEs generate as a result of chronic oxidative stress [8]. Hence, a vicious cycle results in inflammation, AGEs formation which may result in persistence of autoantigens, and autoantibodies against nuclear components and immune complexes in SLE.…”