Optimization of insulin therapy in patients with Type 2 diabetes mellitus: beyond basal insulin.
Summary of "Optimization of insulin therapy in patients with Type 2 diabetes mellitus: beyond basal insulin."
Aims:  To describe patients with Type 2 diabetes mellitus treated with basal insulin, with or without oral antidiabetics in UK primary care, and evaluate insulin treatment patterns and factors explaining changes in therapy. Methods:  Retrospective analysis of patients with Type 2 diabetes within The Health Improvement Network UK primary care database. Patients receiving basal insulin between January and June 2006 were followed until July 2009. Results:  Analysis included 3185 patients, mean age 65.6 years [standard deviation (SD) 12.4], 50.9% men, median diabetes duration 9.6 years, median basal insulin use 1.3 years, 86.5% had received oral antidiabetics in the previous 12 months. Mean follow-up was 2.9 years (SD 1.0), 59.8% patients maintained basal insulin throughout follow-up with a mean HbA(1C) of 69 mmol/mol (SD 19 8.4%, SD 1.7) at baseline and 65 mmol/mol (SD 17; 8.1%, SD 1.6) during follow-up. During follow-up, 6.9% of patients discontinued, 19.3% intensified with and 14.1% switched to prandial or premixed insulin. Patients who intensified (prandial) had a mean HbA(1c) of 77 mmol/mol (SD 18; 9.2%, SD 1.6) before change and a mean HbA(1c) of 71 mmol/mol (SD 21; 8.6%, SD 2.0) at the end of the study. Those switching to premixed insulin had mean a HbA(1c) of 80 mmol/mol (SD 18; 9.5%, SD 1.7) before change and a HbA(1c) of 69 mmol/mol (SD 17; 8.5%, SD 1.5) at the end of the study. Increasing HbA(1c) and longer diabetes duration explained intensification and switch. Conclusions:  The majority of patients had HbA(1c) above the 53 mmol/mol (< 7%) target at baseline and post-intensification/switch. The HbA(1c) levels were reduced by intensification/switch suggesting that insulin changes did have some impact. Most patients did not change insulin treatment despite having higher than recommended HbA(1c) levels. Reasons for not changing treatment in face of unsatisfactory clinical outcomes are unclear. Further research is warranted to explore barriers towards therapy change. © 2012 The Authors. Diabetic Medicine © 2012 Diabetes UK.
Affiliation
Cegedim Strategic Data Medical Research Ltd, London Lilly UK, Erl Wood Manor, Windlesham, UK Lilly USA, Indianapolis, IN, USA Lilly Hungary, Budapest, Hungary.
Journal Details
This article was published in the following journal.
Name: Diabetic medicine : a journal of the British Diabetic Association
ISSN: 1464-5491
Pages:
Links
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22268988
- DOI: http://dx.doi.org/10.1111/j.1464-5491.2012.03586.x
Medical and Biotech [MESH] Definitions
Diabetes Mellitus, Type 2
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.
Diabetes Mellitus, Type 1
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.
Insulin
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
Prediabetic State
The time period before the development of symptomatic diabetes. For example, certain risk factors can be observed in subjects who subsequently develop INSULIN RESISTANCE as in type 2 diabetes (DIABETES MELLITUS, TYPE 2).
Rats, Inbred Bb
A strain of Rattus norvegicus which is a model for spontaneous insulin-dependent diabetes mellitus (DIABETES MELLITUS, INSULIN-DEPENDENT).
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