혈당 조절이 되지 않는 제2형 당뇨병환자에서 로지글리타존과 메트포르민 병합요법의 유효성 = The Efficacy of Fixed Dose Rosiglitazone and Metformin Combination Therapy in Poorly Controlled Subjects with Type 2 Diabetes Mellitus

다국어 초록 (Multilingual Abstract)

Background: Obese type 2 diabetic subjects are recently increasing in Korea, indicating the importance of
insulin resistance rather than insulin secretory defects in the pathophysioloy of type 2 diabetes. The purpose
of this study is to evaluate the safety and efficacy of fixed dose rosiglitazone/metformin combination therapy
in poorly controlled subjects with type 2 diabetes mellitus.
Methods: 12 type 2 diabetic subjects who had a HbA1c > 11% or fasting plasma glucose > 15 mmol/L were
included. After a 2 week screening period, the subjected took the fixed does rosiglitazone/metformin for 24
weeks. The treatment with rosiglitazone/metformin began at week 0 with an initial dose of 4 mg/1000 mg
and, unless tolerability issues arose, subjects would be increased to 6 mg/1500 mg at week 4 and at week
8 to the maximum dose of 8 mg/2000 mg. The primary object of this study was to characterize the
magnitude of HbA1c reduction from baseline after 24 weeks of rosiglitazone and metformin treatment in
poorly controlled type 2 diabetics.
Results: The mean age of the subjects was 48.9 ± 10.6 years old, body mass index was 25.0 ± 3.5 kg/m2,
HbA1c was 12.0 ± 1.0%, and fasting plasma glucose was 16.3 ± 3.1 mmol/L. HbA1c was reduced to 7.54
± 1.45% and fasting plasma glucose reduced to 7.96 ± 2.38 mmol/L at week 24. The proportion of HbA1c
responder who showed the reduction from baseline of ≥ 0.7% or HbA1c < 7% was 11 among 12 subjects
(91.7%). 41% of the subjects (5 among 12 subjects) achieved HbA1c level < 7.0% and 75% (9 among 12
subjects) achieved HbA1c level < 8.0%.
Conclusions: In this study, rosiglitazone and metformin combination therapy was effective in glycemic
control in poorly controlled subjects with type 2 diabetes mellitus. (KOREAN DIABETES J 32:506-512, 2008)

다국어 초록 (Multilingual Abstract)

Background: Obese type 2 diabetic subjects are recently increasing in Korea, indicating the importance of
insulin resistance rather than insulin secretory defects in the pathophysioloy of type 2 diabetes. The purpose
of this study is to evaluate the safety and efficacy of fixed dose rosiglitazone/metformin combination therapy
in poorly controlled subjects with type 2 diabetes mellitus.
Methods: 12 type 2 diabetic subjects who had a HbA1c > 11% or fasting plasma glucose > 15 mmol/L were
included. After a 2 week screening period, the subjected took the fixed does rosiglitazone/metformin for 24
weeks. The treatment with rosiglitazone/metformin began at week 0 with an initial dose of 4 mg/1000 mg
and, unless tolerability issues arose, subjects would be increased to 6 mg/1500 mg at week 4 and at week
8 to the maximum dose of 8 mg/2000 mg. The primary object of this study was to characterize the
magnitude of HbA1c reduction from baseline after 24 weeks of rosiglitazone and metformin treatment in
poorly controlled type 2 diabetics.
Results: The mean age of the subjects was 48.9 ± 10.6 years old, body mass index was 25.0 ± 3.5 kg/m2,
HbA1c was 12.0 ± 1.0%, and fasting plasma glucose was 16.3 ± 3.1 mmol/L. HbA1c was reduced to 7.54
± 1.45% and fasting plasma glucose reduced to 7.96 ± 2.38 mmol/L at week 24. The proportion of HbA1c
responder who showed the reduction from baseline of ≥ 0.7% or HbA1c < 7% was 11 among 12 subjects
(91.7%). 41% of the subjects (5 among 12 subjects) achieved HbA1c level < 7.0% and 75% (9 among 12
subjects) achieved HbA1c level < 8.0%.
Conclusions: In this study, rosiglitazone and metformin combination therapy was effective in glycemic
control in poorly controlled subjects with type 2 diabetes mellitus. (KOREAN DIABETES J 32:506-512, 2008)

참고문헌 (Reference)

1 김상아, "우리나라 당뇨병의 유병률과 관리 상태" 대한내과학회 68 (68): 10-17, 2005

2 Baily CJ, "Treating insulin resistance in type 2 diabetes with metformin and thiazolidinediones" 7 : 675-691, 2005

3 Diamant M, "Thiazolidinediones in type 2 diabetes mellitus: current clinical evidence" 63 : 1373-1405, 2003

4 Yoon KH, "Selective beta-cell loss and alpha-cell expansion in patients with type 2 diabetes mellitus in Korea" 88 : 2300-2308, 2003

5 Home PD, "Rosiglitazone evaluated for cardiovascular outcomesan interim analysis" 357 : 28-38, 2007

6 Park JY, "Past and current obesity in Koreans with non-insulin-dependent diabetes mellitus" 35 : 49-56, 1997

7 Nathan DM, "Management of hyperglycemia in type 2 diabetes: A consensus algorithm for the initiation and adjustment of therapy: a consensus statement from the American Diabetes Association and the European Association for the Study of Diabetes" 29 : 1963-1972, 2006

8 UK Prospective Diabetes Study (UKPDS) Group, "Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33)" 352 : 837-853, 1998

9 Ginsberg HN, "Insulin resistance and cardiovascular disease" 106 : 453-458, 2000

10 Turner RC, "Glycemic control with diet, sulfonylurea, metformin, or insulin in patients with type 2 diabetes mellitus: progressive requirement for multiple therapies (UKPDS 49)" 281 : 2005-2012, 1999

11 Nissen SE, "Effect of rosiglitazone on the risk of myocardial infarction and death from cardiovascular causes" 356 : 2457-2471, 2007

12 Miyazaki Y, "Effect of rosiglitazone on glucose and nonesterified fatty acid metabolism in Type II diabetic patients" 44 : 2210-2219, 2001

13 Fonseca V, "Effect of metformin and rosiglitazone combination therapy in patients with type 2 diabetes mellitus: a randomized controlled trial" 283 : 1695-1702, 2000

14 Grundy SM, "Diabetes and cardiovascular disease" 100 : 1134-1146, 1999

15 Kim DJ, "Clinical characteristics of Korean type 2 diabetic patients in 2005" 77S-S257, 2007

16 Jones TA, "Addition of rosiglitazone to metformin is most effective in obese, insulin-resistant patients with type 2 diabetes" 5 : 163-170, 2003

17 Kahn SE, "ADOPT Study Group: Glycemic durability of rosiglitazone, metformin, or glyburide monotherapy" 355 : 2427-2443, 2006