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AB0323 Carbohydrate metabolism and glucocorticoid therapy in patients with systemic inflammatory diseases
  1. G Nurullina
  1. Kazan Medical State University, Kazan, Russian Federation

Abstract

Background Glucocorticoid therapy (GCT) is one of the risk factors of carbohydrate metabolism disorders (CMD) in patents with systemic inflammatory diseases. CMD development is a concern not only with long-term therapy, but also during intensive short-term GC administration, which can lead to different CMDs, including impaired glucose tolerance (IGT) and diabetes mellitus (DM).

Objectives to evaluate the prevalence of CMD after long-term and intensive GC treatment (GCT) in patients with systemic lupus erythematosus (SLE), systemic vasculitis (SV) and chronic glomerulonephritis (CGN).

Methods Ninety eight patients with systemic inflammatory diseases were included (SLE - 53, SV – 35), among them 68 received GC pulse-therapy (GCPT) (1 series of 3 sessions), and 30 – oral GCT (OGCT). All patients underwent standard clinical and laboratory evaluation, oral glucose tolerance test (OGTT), evaluation of C-peptide, HOMA-IR and HOMA-islet indices.

Results CMDs developed less often in patients receiving GCPT compared to long-term OGCT (p=0.035). In patients receiving OGCT the most prevalent CMDs were IGT and DM – in 9 (30.0%) and 8 (26.7%) patients respectively, which was significantly higher compared to patients in GCPT group – 7 (10.3%) and 6 (8.8%) respectively (p=0.038 and p=0.049). Baseline C-peptide was elevated in patients who developed IGT after a course of GCPT (850 pmol/l before GCPT, 4099 pmol/l 4–6 hours after GCPT and 1904 pmol/l after a 3-days course of GCPT) or DM (1050 pmol/l, 3170 pmol/l and 1796 pmol/l before GCPT, at peak blood glucose level and after a 3-days course of GCPT, respectively) (p<0.05). C-peptide remained normal in the absence of CMD and in IGT patients.

Baseline HOMA-IR index was elevated in patients with IGT (4.52, 17.47, 9.67 before GCPT, at peak blood glucose level and after a 3-days course of GCPT, respectively) and DM (5.04, 15.2, 10.4 respectively) (p<0.05), and normal in patients without CMD (2.2, 5.84 and 4.01 respectively) and patients with impaired fasting glucose (IFG) (2.46, 7.08 and 5.46).

HOMA-islet index analysis revealed that in the absence of CMD and at earlier stages of CMDs (IFG, IGT) insulin resistance is compensated via an increase of β-cell secretory activity. In DM patients there is a trend towards decreased β-cell secretory activity, which is associated with a significant decrease of HOMA-islet index to 64,6 at peak blood glucose levels after GCPT compared to baseline level (170) (p<0.05). C-peptide, HOMA-IR and HOMA-islet index levels in OGCT patients demonstrated same trend as in GCPT patients. Significant differences were observed in patients with IGT and DM before and after oral glucose tolerance test (OGTT) on C-peptide (1042 pmol/l vs. 1978 pmol/l in IGT; 1306 pmol/l vs. 2286 pmol/l in DM) and HOMA-IR (4.53 vs. 9.81 in IGT; 5.6 vs. 11.27 in DM patients), whereas in patients without CMD and in patients with IFG, C-peptide before OGTT was 489 pmol/l vs. 743 pmol/l, after - 1295 pmol/l vs. 1488 pmol/l, HOMA-IR – 2.59 vs. 2.88 before OGTT and 2.88 vs. 5.85 after the test in the absence of CMD and in IFG patients, respectively. A significant decrease of β–cell function was observed in DM patients, reflected by a decrease of HOMA-islet after OGTT compared to baseline (147 vs. 78.4).

Conclusions GCT leads to IGT and DM in patients with increased IR both during GCPT and long-term OGCT. Long-term OGCT is associated with more CMDs compared to GCPT.

Disclosure of Interest None declared

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