PMID- 21635988
OWN - NLM
STAT- MEDLINE
DCOM- 20110923
LR  - 20221207
IS  - 1879-114X (Electronic)
IS  - 0149-2918 (Linking)
VI  - 33
IP  - 4
DP  - 2011 Apr
TI  - Evaluating treatment algorithms for the management of patients with type 2 
      diabetes mellitus: a perspective on the definition of treatment success.
PG  - 408-24
LID - 10.1016/j.clinthera.2011.04.008 [doi]
AB  - BACKGROUND: Traditional treatment of type 2 diabetes mellitus (T2DM) has focused 
      on correcting hyperglycemia. However, T2DM is often accompanied by other 
      conditions and risk factors, including hypertension, overweight/obesity, and 
      dyslipidemia, that affect morbidity and mortality. A broader view toward treating 
      the array of physiologic derangements may provide significant long-term outcomes 
      benefits. OBJECTIVE: This perspective paper reviews recent data regarding the 
      pathophysiology of T2DM, evaluates current treatment recommendations/algorithms, 
      and discusses potential risks and benefits associated with the various 
      therapeutic options and their combinations. METHODS: Information was obtained by 
      a search of the PubMed and Embase databases using the key words type 2 diabetes 
      mellitus, glycosylated hemoglobin, pathophysiology of type 2 diabetes, glycemic 
      control, antidiabetes therapy, multifactorial therapy, and treatment algorithms 
      for the period of 1985 to 2010. A representative number of relevant articles 
      dealing with these topics was then selected for review. RESULTS: Three recently 
      proposed treatment algorithms, the American Diabetes Association/European 
      Association for the Study of Diabetes less well-validated algorithm, the American 
      Association of Clinical Endocrinologists/American College of Endocrinology 
      algorithm, and the DeFronzo algorithm, were compared and contrasted. Metformin is 
      usually the first oral agent to be used when not contraindicated because of its 
      ability to suppress hepatic glucose production. Some recommended agents, such as 
      sulfonylureas, drive beta-cell failure even as they improve glycosylated hemoglobin. 
      Others, such as glucagon-like peptide-1 (GLP-1) receptor agonists and 
      thiazolidinediones, support and enhance beta-cell function. Also, some agents 
      predispose to weight gain (eg, sulfonylureas and insulin), whereas others are 
      weight neutral (eg, dipeptidyl-peptidase-4 inhibitors) or result in weight loss 
      (eg, GLP-1 receptor agonists, pramlintide). Finally, the impact of these agents 
      on associated cardiovascular risk factors is varied. Agents that improve glycemic 
      control while favorably affecting blood lipid levels and/or systemic blood 
      pressure may lead to improvements in morbidity and mortality. Attention to the 
      mechanisms of action and associated consequences of the numerous pharmacologic 
      treatment choices may provide clinicians a better selection of agents in treating 
      patients with T2DM. CONCLUSIONS: Physicians should evaluate the array of 
      treatment options available for patients with T2DM. An aggressive regimen 
      including metformin, a thiazolidinedione, and a GLP-1 receptor agonist may 
      improve insulin sensitivity and enhance beta-cell function. Addressing the 
      pathophysiologic defects associated with T2DM, as well as the various associated 
      cardiovascular risk factors, with combination therapy may slow the natural 
      progression of the disease and development of its associated complications.
CI  - Copyright (c) 2011 Elsevier HS Journals, Inc. All rights reserved.
FAU - Aguilar, Richard B
AU  - Aguilar RB
AD  - Diabetes Nation LLC, Sisters, OR 97708, USA. fovalle@uab.edu
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Clin Ther
JT  - Clinical therapeutics
JID - 7706726
RN  - 0 (Blood Glucose)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (Hypoglycemic Agents)
SB  - IM
MH  - Algorithms
MH  - Blood Glucose/drug effects
MH  - Cardiovascular Diseases/etiology/*prevention & control
MH  - Diabetes Mellitus, Type 2/*drug therapy/physiopathology
MH  - Drug Therapy, Combination
MH  - Glycated Hemoglobin/metabolism
MH  - Humans
MH  - Hypoglycemic Agents/administration & dosage/adverse effects/*therapeutic use
MH  - Insulin Resistance
MH  - Risk Factors
EDAT- 2011/06/04 06:00
MHDA- 2011/09/29 06:00
CRDT- 2011/06/04 06:00
PHST- 2011/04/08 00:00 [accepted]
PHST- 2011/06/04 06:00 [entrez]
PHST- 2011/06/04 06:00 [pubmed]
PHST- 2011/09/29 06:00 [medline]
AID - S0149-2918(11)00191-3 [pii]
AID - 10.1016/j.clinthera.2011.04.008 [doi]
PST - ppublish
SO  - Clin Ther. 2011 Apr;33(4):408-24. doi: 10.1016/j.clinthera.2011.04.008.