title: Chronic inflammation and low-dose glucocorticoid effects on glucose metabolism in premenopausal females with rheumatoid arthritis free of conventional metabolic risk factors.
abstract: 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.
authors.affiliation: Laboratory of Human Endocrinology, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovak Republic. adela.penesova@savba.sk
authors.forename: A
authors.initials: A
authors.lastname: Penesová
authors.forename: Z
authors.initials: Z
authors.lastname: Rádiková
authors.forename: M
authors.initials: M
authors.lastname: Vlček
authors.forename: J
authors.initials: J
authors.lastname: Kerlik
authors.forename: J
authors.initials: J
authors.lastname: Lukáč
authors.forename: J
authors.initials: J
authors.lastname: Rovenský
authors.forename: R
authors.initials: R
authors.lastname: Imrich
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000175:diagnosis / Q000188:drug therapy*; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000187:drug effects* / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage* / Q000009:adverse effects; D005951:Glucose Tolerance Test; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000097:blood; D016014:Linear Models; D011241:Prednisone / Q000008:administration & dosage* / Q000009:adverse effects; D017697:Premenopause; D013997:Time Factors; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D055815:Young Adult
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D005938:Glucocorticoids; C508600:IL6 protein, human; D018836:Inflammation Mediators; D007328:Insulin; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D011241:Prednisone