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Women Suffering from Systemic Lupus Erythematosus Are Characterized by Low Blood Levels of α-dicarbonyl Compounds

Overview
Journal Arch Med Sci
Specialty General Medicine
Date 2024 Jul 25
PMID 39050180
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Abstract

Introduction: Systemic lupus erythematosus (SLE) is a chronic, autoimmune disease, often characterised by severe course and unclear etiopathogenesis. The reaction of protein glycoxidation, also known as glycation, may be linked to etiopathogenesis of SLE. Advanced glycation end-products (AGEs) exhibit cytotoxic properties, affect cellular signalling, impair functions of extracellular proteins, and may act as neoepitopes. Glucosone (GS), glyoxal (GO), and methylglyoxal (MGO) are examples of α-dicarbonyl compounds (α-DCs) partaking in glycoxidation. The study aimed to evaluate concentrations of these three compounds in blood serum of SLE patients, and to compare the results with healthy individuals.

Material And Methods: 31 women suffering from SLE and 26 healthy individuals were included in the study. High-performance liquid chromatography with fluorescence detection was applied to evaluate concentrations of α-DCs in their serum samples. Correlations between the results and parameters such as disease duration time, age, glomerular filtration rate (GFR), Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K), and creatinine were analysed.

Results: The SLE patients exhibited lower concentrations of glucosone, glyoxal, and methylglyoxal than the control group. Analysis of correlations showed a difference between the examined groups.

Conclusions: In women suffering from SLE the course of α-DCs metabolism is altered. SLE patients are characterised by low serum levels of α-DCs. We hypothesise that either hindered proteasomal degradation or fast consumption of α-DCs in oxidative conditions may cause the observed low concentration of these compounds.

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Low Serum Methylglyoxal Levels Correlate with Psoriasis Severity and Inflammatory Response Indices.

Damasiewicz-Bodzek A, Nowak A, Maciejczyk M, Waligora S, Przywara-Chowaniec B Pathophysiology. 2025; 32(1).

PMID: 39982364 PMC: 11843881. DOI: 10.3390/pathophysiology32010008.

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