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AB0409 Modified Homa-Ir Index in Patients with Rheumatic Diseases Receiving Glucocorticoid Therapy
  1. G. Nurullina,
  2. F. Valeeva
  1. Kazan Medical State University, Kazan, Russian Federation

Abstract

Background 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.

Objectives To evaluate the role of modified HOMA-IR index in patients with rheumatic diseases receiving glucocorticoid (GC) therapy.

Methods 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.

Results 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.

Conclusions 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.

Disclosure of Interest None declared

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