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Direct head‐to‐head comparison of glycaemic durability of dipeptidyl peptidase‐4 inhibitors and sulphonylureas in patients with type 2 diabetes mellitus: A meta‐analysis of long‐term randomized controlled trials

We performed a meta‐analysis of randomized controlled trials (RCTs) to compare the long‐term glycaemic durability of dipeptidyl‐peptidase 4 (DPP‐4) inhibitors vs that of sulphonylureas (SUs) in patients with type 2 diabetes mellitus (T2DM), in terms of the changes in glycated haemoglobin (HbA1c) lev...

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Detalles Bibliográficos
Autores principales: Chen, Kang, Kang, Deying, Yu, Miao, Zhang, Ruya, Zhang, Ye, Chen, Guojuan, Mu, Yiming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5873267/
https://www.ncbi.nlm.nih.gov/pubmed/29095568
http://dx.doi.org/10.1111/dom.13147
Descripción
Sumario:We performed a meta‐analysis of randomized controlled trials (RCTs) to compare the long‐term glycaemic durability of dipeptidyl‐peptidase 4 (DPP‐4) inhibitors vs that of sulphonylureas (SUs) in patients with type 2 diabetes mellitus (T2DM), in terms of the changes in glycated haemoglobin (HbA1c) levels from an intermediate time point (26 or 52 weeks) to 104 weeks of treatment. The Medline (PubMed), Embase (Ovid), and CENTER (Cochrane Library) databases were searched for relevant RCTs. Eight RCTs were included. Compared with SUs, DPP‐4 inhibitors were associated with significantly smaller increases in the HbA1c level from 24 to 28 weeks to 104 weeks (mean difference [MD]: −0.16%, 95% confidence interval [CI]: −0.21 to −0.11; P < .001) and from 52 weeks to 104 weeks (MD −0.06%, 95% CI −0.10 to −0.02; P = .001). No significant heterogeneities were detected among the included comparisons (I(2) = 0%). These results suggest that long‐term treatment with DPP‐4 inhibitors confers better durability of glycaemic response than treatment with SUs in patients with T2DM, which may indicate that DPP‐4 inhibitors better preserve islet β‐cell function compared with SUs.