Background Diabetogenic effect limits the use of glucocorticoids (GC), especially in patients with diabetes risk factors. At present HOMA index is widely used for the evaluation of insulin resistance (IR) and β-cell function. HOMA-IR index increase is an indirect measure of IR progression and cardiovascular risk elevation.
Objectives To evaluate the role of modified HOMA-IR and HOMA-islet indices in different carbohydrate metabolism disorders (CMD) during oral (OGCT) and PULSE (GCPT) glucocorticoid therapy (GCT).
Methods A prospective study including 118 patients with systemic lupus erythematosus (SLE) (n=63) and systemic vasculitis (SV) (n=55) was performed. Seventy one patients received GCPT (i.v. infusion of 10–15 mg/kg of prednisolone with 250 ml of normal saline per day, for 3 consecutive days (1 course of 3 sessions); course dose was 1800–3000 mg; 47 patients received oral GC 15–30 mg/day. HOMA-IR index and β-cell function (HOMA-islet index) were calculated as follows: Homa-IR =1.5 + fasting blood glucose (mmol/l) x fasting C-peptide level (pmol/l) /2800. HOMA-islet =0.27 x fasting C-peptide level (pmol/l)/(fasting blood glucose (mmol/l) – 3,5).
Results GCPT was associated with less CMD compared to OGCT. Impaired fasting glucose (IFG) was observed in 7 (9.9%) and 9 (19.1%), impaired glucose tolerance (IGT) – in 9 (12.7%) and 14 (29.8%) and diabetes mellitus (DM) – in 9 (12.7%) and 13 (27.7%) patients in GCPT and OGCT groups, respectively. There was a significant decrease of HOMA-islet during glycemic peak in DM patients from 13.96 to 6.17 after GCPT (p<0.05), compared to insignificant changes in other groups. Decrease of HOMA-islet index reflects a disturbance of overall functional activity of β-cells in DM patients. After a course of GCPT HOMA-islet index was significantly lower in DM patients compared to patients with no CMD (11.8 vs. 15.4), as GCPT is associated with a decrease of β-cell function which does not return to baseline as a consequence of β-cell reserve depletion. No rapid decrease of β–cell function was observed in OGCT group, instead there was a compensatory increase, which was insufficient to maintain normoglycia because of high insulin resistance. C-peptide, HOMA-IR and HOMA-islet levels in OGCT patients demonstrated the 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 index after OGTT compared to baseline (147 vs. 78.4).
Conclusions Evaluation of blood glucose level, which was normal in all included patients, and isolated C-peptide evaluation are insufficient for the evaluation of carbohydrate metabolism before GCPT and long-term OGCT. The evaluation of modified HOMAA-IR and HOMA-islet indices before the start of intensive GC treatment and during OGCT may improve early detection of risk groups for serious CMDs – IGT and DM.
Disclosure of Interest None declared