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The ACP and its Latest Guidelines on Type 2 Diabetes Mellitus: A View from the Trenches

By Charles F. Shaefer, Jr, MD | February 17, 2012
Dr Shaefer is Assistant Clinical Professor of Medicine at the Georgia Health Sciences University in Augusta.

The American College of Physicians (ACP) has recently published its updated guidelines for type 2 diabetes (T2DM) management, the first since 2007.1 While touted as "new," these guidelines offer no real breakthroughs in understanding. In some ways they are in subtle conflict with well accepted, current recommendations by the AACE/ACE2 and ADA/EASD.3 The real value of this new ACP release may be that it calls upon clinicians to pause and actively consider what advice is currently being offered for "best practice" in diabetes care.

Lifestyle changes are likely to fail. The ACP guidelines—derived from review of literature between 1966 and April, 2010—call for addition of drug therapy only after lifestyle interventions have been tried and fail to achieve glycemic control. While properly emphasizing the value of lifestyle change (diet, exercise, and weight management should always be initiated at diagnosis), the ACP strategy ignores the established fact that such therapy alone is far more likely to fail than succeed.4 Also, in the hands of most clinicians, such a strategy is the first step down a road to clinical inertia. Studies show that often patients are left in the "lifestyle only" mode while the hemoglobin A1C (A1C) remains significantly elevated for years.5 Concerns about the lack of appropriately aggressive therapy have led the ADA/EASD and AACE/ACE to recommend initiation of metformin(Drug information on metformin), the drug primarily called for by the ACP guidelines, concomitantly with lifestyle modification at the time of diagnosis, and not at an indefinite later time when lifestyle change fails to sustain glycemic control.

(MORE: Spotting Signs of Diabetes)

Initial monotherapy vs combination therapy. The ACP guidelines specifically call for monotherapy at drug initiation for most patients. While this recommendation is in line with the ADA/EASD path that initiates drug therapy with metfomin as monotherapy, it is at distinct odds with the AACE/ACE guidelines which call for initial multi-drug oral combination therapy for treatment-naive patients who have  an A1C > 7.5%.2 Our current understanding is that deterioration of glycemic control stems from a combination of multiple pathophysiologic problems (ie, DeFronzo's "ominous octet," see below).6 Thus, it is quite sensible to use multiple drugs at the outset of therapy to affect as many of these defects as early as possible, to help control hyperglycemia, preserve beta cell competence, and prevent rises in the A1C.  The alternative—a "treat to failure" step therapy approach—introduces one oral drug after another as the predecessor fails to control hyperglycemia while the A1C is often left above target for a prolonged time.5

Advancing therapy. The ACP’s call for the addition of a second drug, in fact any second drug (with some considerations), after failure to meet A1C goals with metformin, is consistent with all existing guidelines. What is not conveyed by the ACP guidelines is a proper sense of timing and urgency to get this second drug on board. Despite results from seminal trials including UKPDS,7 DCCT,8 and many others that link a reduction in microvascular complications and an overall reduction in annualized cost of care9 to A1C control, the ACP guidelines are somewhat vague about how urgently the clinician should  advance therapy. In contrast, the ADA/EASD and AACE/ACE guidelines are abundantly clear about the need to advance therapy every 2 to 3 months if the current regimen is not achieving the stated A1C goal. Clinical inertia is a very real issue in diabetes management and the ACP guidelines fall short of addressing this point.

In my opinion, the disparity between the ADA/EASD, AACE/ACE and ACP guidelines arises from 2 areas: consideration of a data set spanning nearly 50 years in the ACP compilation and the ACP reliance on strict evidence-based medicine criteria. The ACP guidelines are based on consideration of a wealth of studies—in some cases nearly 50 years old. While insulin, some sulfonylureas, and metformin date back that far, the other 8 classes of antidiabetic drugs have only recently appeared on the scene and may be under represented in the data set considered. Diabetes therapeutics may be one of the most rapidly evolving areas in medicine. To look back nearly 50 years for guidance may be looking in the wrong direction.

Also, I completely agree that we should be validating our therapies against strong evidence-based criteria. However, if we withhold therapies (or wait before we make reasonable, well thought out treatment recommendations) until extensive clinical data are gathered to provide evidence-based validation, many people will be denied safe and beneficial treatments in the swiftly changing therapeutic area of diabetes care.

In my view, the ADA/EASD and AACE/ACE guidelines are forward-looking sets of advice on how to best incorporate all the therapeutic tools we currently have on hand to manage the complexities of T2DM. The ACP guidelines represent something of a retrospective look at what has been proven to work in the past, with little consideration of what has not worked (eg, clinical inertia) and no real guidance about how to best use the newer tools at hand (eg, DPP-4 inhibitors, GLP-1 mimetics, and more aggressive insulin approaches).

And finally, lost in the ACP document is the sense of urgency every clinician should feel about managing the expanding epidemic of T2DM.

The Ominous Octet6
Islet beta cells           Impaired insulin secretion
Islet alpha cells         Increased glucagon(Drug information on glucagon) secretion
Liver                         Increased hepatic glucose production
Brain                         Neurotransmitter dysfunction
Muscle tissue            Decreased glucose uptake
Kidneys                     Increased glucose reabsorption
Adipose tissue           Increased lypolysis
Gut                            Decreased incretin effect 
 

 

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References
1. Qaseem A, Humphrey LL, Sweet DE, et al. Oral Pharmacologic Treatment of Type 2 Diabetes Mellitus: A Clinical Practice Guideline from the American College of Physicians. Ann Int Med 2012; 156:218-232.
2. Rodbard HW, Jellinger PS, Davidson, et al. Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology Consensus Panel on Type 2 Diabetes Mellitus: An Algorithm for Glycemic Control. Endocrine Practice 2009; 15:540-559.
3. Nathan DM, Buse JB, Davidson MD, et al. ADA/EASD Medical Management of Hyperglycemia in Type 2 Diabetes: A Consensus Algorithm for the Initiation and Adjustment of Therapy: A consensus statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 2009; 32:193-203.
4. Nathan DM, Buse JB, Davidson MD, et al. ADA/EASD Medical Management of Hyperglycemia in Type 2 Diabetes: A Consensus Algorithm for the Initiation and Adjustment of Therapy: A consensus statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 2006; 29:1963-1972.
5. Brown JB, Nichols GA, Perry A. The burden of treatment failure in type 2 diabetes. Diabetes Care 2004;27:1535-1544.
6. DeFronzo R. Banting lecture. "The Ominous Octet" at ADA 68th Scientific Sessions 2008, San Francisco, California.
7. Stratton IM, Adler AI, Neil HA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. Brit Med J. 2000;321:405-412.
8. The Diabetes Control and Complications Trial Group. The effect of intensive treatment of diabetes on the development and progression of long term complications in insulin dependent diabetes mellitus. N Engl J Med. 1993;329:977-980.
9. Stephens JM, Botteman MF, Hay JW. Economic impact of antidiabetic medications and glycemic control on managed care organizations: a review of the literature. J Manag Care Pharm. 2006;12:130-142.


 
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