<h3>Background</h3> HOMA-IR index is widely used in current clinical practice for the evaluation of insulin resistance (IR). Elevation of HOMA-IR index is an indirect marker of IR progression. <h3>Objectives</h3> To evaluate the role of modified HOMA-IR index in patients with rheumatic diseases receiving glucocorticoid (GC) therapy. <h3>Methods</h3> The study included 98 patients with rheumatic diseases, including systemic lupus erythematosus (SLE) - 53 patients and systemic vasculitis (SV) – 45 patients. The first group included 52 patients receiving GC pulse-therapy (GC-PT) (prednisolone 10–15 mg/kg a day i/v, on 3 consecutive days), the second group included 46 patients receiving oral prednisolone 15–30 mg/day. The first group included 31 (59.6%) women and 21 (40.4%) men aged 18–69 years. Control group included 27 (58.7%) women and 19 (41.3%) men aged 19–63 years. All patients underwent standard clinical evaluation and an oral glucose tolerance test (OGTT): patients receiving GC-PT underwent OGTT 72 hours after the end of PT course, patients receiving oral GC – during the time of inpatient treatment. According to OGTT results patients were divided into 4 groups: no carbohydrate metabolism disturbance (CMD), impaired fasting glucose (IFG), impaired glucose tolerance (IGT) and diabetes mellitus (DM). IR calculation according to HOMA-IR index was performed according to a formula proposed by X. Li et al. (2004): Homa-IR =1,5 + fasting blood glucose (mmol/l) x fasting C-peptide level (pmol/l) /2800. <h3>Results</h3> CMD developed in 10 (33.3%) patients in SLE group receiving GC-PT, compared to 18 (81.8%) patients receiving oral GC (p=0.002). In SV patients CMD was more prevalent in those receiving oral GC compared to GC-PT (4 (19.1%) vs. 19 (79.2%) patients, respectively (p=0.035). HOMA-IR index, reflecting the degree of IR, was elevated in patients with IGT and DM at baseline, during maximal blood glucose level and after GC-PT, compared to patients without CMD and IFG (p<0.05). IR was more pronounced in patients receiving oral GC and IGT and DM after OGTT (p<0.05), which demonstrates that a more pronounced IR during GC therapy predisposes to the development of more pronounced CMD. <h3>Conclusions</h3> GC therapy results in the development of IGT and DM in patients with elevated IR after GC-PT or prolonged oral GC treatment. CMD is more prevalent among patients receiving prolonged oral GC therapy. <h3>Disclosure of Interest</h3> None declared
