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Effects of insulin glulisine as mono‐ or add‐on therapy in patients with type 2 diabetes mellitus
Author(s) -
Kawamori R.,
Iwamoto Y.,
Kadowaki T.,
Iwasaki M.,
Kim S.W.,
Woo J.T.,
Baik S.H.,
Yoon K.H.
Publication year - 2009
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2009.01088.x
Subject(s) - biguanide , medicine , postprandial , clinical endpoint , diabetes mellitus , type 2 diabetes mellitus , regimen , insulin , randomized controlled trial , population , type 2 diabetes , glycemic , metformin , gastroenterology , endocrinology , environmental health
Aim: To evaluate the safety and efficacy of insulin glulisine (glulisine) with and without oral antidiabetic drugs (OAD; sulphonylurea or sulphonylurea + biguanide) relative to that of OAD alone in Japanese and Korean patients with inadequately controlled type 2 diabetes mellitus (T2DM). Methods: In an open, randomized, parallel‐group, comparative, controlled trial, 387 patients were randomized and treated with glulisine + OAD (n = 130), glulisine monotherapy (n = 127) or OAD only (n = 130) for 16 weeks. Glulisine was self‐injected subcutaneously three times daily (0–15 minutes before meals) at a starting dose of ≥0.2 U/kg/day. Patients titrated the glulisine dose to achieve a 2‐h postprandial plasma glucose (2h‐PPG) level of 7.1–9.5 mmol/l (128–172 mg/dl) by administering at least one additional unit at each appropriate meal time if the 2h‐PPG level was > 9.5 and < 11.1 mmol/l (> 172 and < 200 mg/dl) and by administering at least two additional units if the 2h‐PPG level was ≥ 11.1 mmol/l (≥ 200 mg/dl). Therapy with OAD was continued at the stable baseline regimen. The primary efficacy endpoint was change in haemoglobin A 1c (HbA 1c ) from baseline to endpoint in the intention‐to‐treat population. Results: At baseline, therapy with OAD was a sulphonylurea only and a sulphonylurea + a biguanide in approximately 24 and 76% of patients respectively. Both glulisine groups had larger reductions in adjusted mean HbA 1c than the OAD‐only group (glulisine + OAD, −2.07%; glulisine monotherapy, −1.25%; OAD only, −0.61%). Superiority of glulisine + OAD and glulisine monotherapy vs. OAD only was shown by differences in adjusted mean HbA 1c change from baseline values of −1.46% (p < 0.0001) and −0.64% (p < 0.0001) respectively. Both glulisine groups had better 2h‐PPG control than the OAD‐only group. Mean daily glulisine doses increased from baseline to endpoint (glulisine + OAD, 13.3–22.5 U; glulisine monotherapy, 14.2–38.0 U). The rate of all symptomatic hypoglycaemia events per patient‐year in the entire treatment phase was 11.9 in the glulisine + OAD group, 8.8 in the glulisine monotherapy group and 1.7 in the OAD‐only group. There was only one event of severe hypoglycaemia, which occurred in the glulisine + OAD group. Efficacy and safety were similar in Japanese and Korean subpopulations. Conclusions: Both glulisine + OAD and glulisine monotherapy were well tolerated and effective for Japanese and Korean patients with T2DM mellitus inadequately controlled by OAD therapy alone.