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Clinical inertia with regard to intensifying therapy in people with type 2 diabetes treated with basal insulin

AIM: To investigate whether clinical inertia, the failure to intensify treatment regimens when required, exists in people with type 2 diabetes treated with basal insulin. METHODS: This was a retrospective cohort study involving patients with type 2 diabetes in the UK Clinical Practice Research Datal...

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Autores principales: Khunti, K., Nikolajsen, A., Thorsted, B. L., Andersen, M., Davies, M. J., Paul, S. K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5067688/
https://www.ncbi.nlm.nih.gov/pubmed/26743666
http://dx.doi.org/10.1111/dom.12626
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author Khunti, K.
Nikolajsen, A.
Thorsted, B. L.
Andersen, M.
Davies, M. J.
Paul, S. K.
author_facet Khunti, K.
Nikolajsen, A.
Thorsted, B. L.
Andersen, M.
Davies, M. J.
Paul, S. K.
author_sort Khunti, K.
collection PubMed
description AIM: To investigate whether clinical inertia, the failure to intensify treatment regimens when required, exists in people with type 2 diabetes treated with basal insulin. METHODS: This was a retrospective cohort study involving patients with type 2 diabetes in the UK Clinical Practice Research Datalink database between January 2004 and December 2011, with follow‐up until December 2013. RESULTS: A total of 11 696 patients were included in the analysis. Among all patients, 36.5% had their treatment intensified during the study period; of these, the treatment of 50.0, 42.5 and 7.4% was intensified with bolus or premix insulin or glucagon‐like peptide‐1 receptor agonists, respectively. The median time from initiation of basal insulin to treatment intensification was 4.3 years [95% confidence interval (CI) 4.1, 4.6]. Among patients clinically eligible for treatment intensification [glycated haemoglobin (HbA1c) ≥7.5% (58 mmol/mol)], 30.9% had their treatment regimen intensified. The median time to intensification in this group was 3.7 years (95% CI 3.4, 4.0). Increasing age, duration of diabetes, oral antihyperglycaemic agent usage and Charlson comorbidity index score were associated with a significant delay in the time to intensification (p < 0.05). Among patients with HbA1c ≥7.5% (58 mmol/mol), 32.1% stopped basal insulin therapy. CONCLUSIONS: Strategies should be developed to increase the number of patients undergoing therapy intensification and to reduce the delay in intensifying therapy for suitable patients on basal insulin. Initiatives to support patients continuing on insulin are also required.
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spelling pubmed-50676882016-11-01 Clinical inertia with regard to intensifying therapy in people with type 2 diabetes treated with basal insulin Khunti, K. Nikolajsen, A. Thorsted, B. L. Andersen, M. Davies, M. J. Paul, S. K. Diabetes Obes Metab Original Articles AIM: To investigate whether clinical inertia, the failure to intensify treatment regimens when required, exists in people with type 2 diabetes treated with basal insulin. METHODS: This was a retrospective cohort study involving patients with type 2 diabetes in the UK Clinical Practice Research Datalink database between January 2004 and December 2011, with follow‐up until December 2013. RESULTS: A total of 11 696 patients were included in the analysis. Among all patients, 36.5% had their treatment intensified during the study period; of these, the treatment of 50.0, 42.5 and 7.4% was intensified with bolus or premix insulin or glucagon‐like peptide‐1 receptor agonists, respectively. The median time from initiation of basal insulin to treatment intensification was 4.3 years [95% confidence interval (CI) 4.1, 4.6]. Among patients clinically eligible for treatment intensification [glycated haemoglobin (HbA1c) ≥7.5% (58 mmol/mol)], 30.9% had their treatment regimen intensified. The median time to intensification in this group was 3.7 years (95% CI 3.4, 4.0). Increasing age, duration of diabetes, oral antihyperglycaemic agent usage and Charlson comorbidity index score were associated with a significant delay in the time to intensification (p < 0.05). Among patients with HbA1c ≥7.5% (58 mmol/mol), 32.1% stopped basal insulin therapy. CONCLUSIONS: Strategies should be developed to increase the number of patients undergoing therapy intensification and to reduce the delay in intensifying therapy for suitable patients on basal insulin. Initiatives to support patients continuing on insulin are also required. Blackwell Publishing Ltd 2016-02-09 2016-04 /pmc/articles/PMC5067688/ /pubmed/26743666 http://dx.doi.org/10.1111/dom.12626 Text en © 2016 The Authors. Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs (http://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Khunti, K.
Nikolajsen, A.
Thorsted, B. L.
Andersen, M.
Davies, M. J.
Paul, S. K.
Clinical inertia with regard to intensifying therapy in people with type 2 diabetes treated with basal insulin
title Clinical inertia with regard to intensifying therapy in people with type 2 diabetes treated with basal insulin
title_full Clinical inertia with regard to intensifying therapy in people with type 2 diabetes treated with basal insulin
title_fullStr Clinical inertia with regard to intensifying therapy in people with type 2 diabetes treated with basal insulin
title_full_unstemmed Clinical inertia with regard to intensifying therapy in people with type 2 diabetes treated with basal insulin
title_short Clinical inertia with regard to intensifying therapy in people with type 2 diabetes treated with basal insulin
title_sort clinical inertia with regard to intensifying therapy in people with type 2 diabetes treated with basal insulin
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5067688/
https://www.ncbi.nlm.nih.gov/pubmed/26743666
http://dx.doi.org/10.1111/dom.12626
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