Chronic inflammation and low-dose glucocorticoid effects on glucose metabolism in premenopausal females with rheumatoid arthritis free of conventional metabolic risk factors
Language English Country Czech Republic Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
23173679
DOI
10.33549/physiolres.932359
PII: 932359
Knihovny.cz E-resources
- MeSH
- Analysis of Variance MeSH
- Biomarkers blood MeSH
- C-Reactive Protein metabolism MeSH
- Time Factors MeSH
- Adult MeSH
- Glucocorticoids administration & dosage adverse effects MeSH
- Glucose Tolerance Test MeSH
- Interleukin-6 blood MeSH
- Insulin blood MeSH
- Insulin Resistance MeSH
- Blood Glucose drug effects metabolism MeSH
- Fatty Acids, Nonesterified blood MeSH
- Humans MeSH
- Linear Models MeSH
- Inflammation Mediators blood MeSH
- Young Adult MeSH
- Prednisone administration & dosage adverse effects MeSH
- Premenopause MeSH
- Arthritis, Rheumatoid blood diagnosis drug therapy MeSH
- Case-Control Studies MeSH
- Tumor Necrosis Factor-alpha blood MeSH
- Treatment Outcome MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Young Adult MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Biomarkers MeSH
- C-Reactive Protein MeSH
- Glucocorticoids MeSH
- IL6 protein, human MeSH Browser
- Interleukin-6 MeSH
- Insulin MeSH
- Blood Glucose MeSH
- Fatty Acids, Nonesterified MeSH
- Inflammation Mediators MeSH
- Prednisone MeSH
- Tumor Necrosis Factor-alpha MeSH
Chronic systemic inflammation is associated with increased cardiovascular mortality in patients with rheumatoid arthritis (RA). The aim of our study was to investigate association of glucose metabolism and inflammatory markers in a group of patients with rheumatoid arthritis free of other metabolic risk factors. Twenty-two premenopausal RA females (11 patients on low-dose GC (<8.5 mg/day of prednisone or equivalent), 11 patients without glucocorticoid therapy) and 15 age- and BMI-matched healthy females underwent the oral glucose tolerance test. The insulin sensitivity indices according Matsuda (ISI(MAT)) and Cederholm (ISI(CED)) as well as HOMA2 %S were calculated. Cytokines, lipid profile, non-esterified fatty acids (NEFA) and plasminogen activator inhibitor-1 (PAI-1) were measured in baseline blood samples. Despite elevated interleukin IL-6 and TNF alpha, glucose, insulin and C-peptide responses to oral glucose load as well as ISI(MAT), ISI(CED), PAI-1 and NEFA were comparable in both RA groups and healthy controls. HOMA2 %S correlated with disease activity. In conclusions, low-dose glucocorticoid treatment does not lead to glucose metabolism impairment in RA patients without other metabolic risk factors. Increased cardiovascular mortality and morbidity is probably due to a direct effect of systemic inflammation on myocardium and/or blood vessels.
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