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Diabetes Care 30:192-193, 2007
DOI: 10.2337/dc06-1858
© 2007 by the American Diabetes Association
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Letters: Comments and Responses

Management of Hyperglycemia in Type 2 Diabetes: A Consensus Algorithm for the Initiation and Adjustment of Therapy: A Consensus Statement From the American Diabetes Association and the European Association for the Study of Diabetes

Response to Nathan et al.

Christopher G. Parkin, MS1 and Jaime A. Davidson, MD, FACP, FACE2

1 CGParkin Communications, Carmel, Indiana
2 Medical City Dallas Hospital, University of Texas Southwestern Medical School, Dallas, Texas.

Address correspondence to Christopher G. Parkin, MS, CGParkin Communications, 11360 Royal Ct., Carmel, IN 46032. E-mail: cgparkin{at}aol.com

We applaud the efforts of those who developed the American Diabetes Association/European Association for the Study of Diabetes algorithm for managing type 2 diabetes (1). Although the algorithm provides a comprehensive assessment of the clinical utility of various medications, the authors’ strong focus on A1C as a measure of glycemic control may lead to inadequate management of glycemia because it fails to consider important issues relevant to diabetes pathophysiology and outcomes.

First, the algorithm assumes that patients have only recently developed type 2 diabetes and that the A1C is only slightly elevated. The majority of type 2 diabetes is diagnosed 9–12 years after it develops (2). Further, the algorithm suggests that individuals should first be started on lifestyle modification and metformin and then evaluated at 3 months regardless of current A1C. This initial therapy is inappropriate for patients with an A1C >10% because the average lowering capacity of metformin at a 2,000-mg dose is ~2%. In addition, not all patients are responders or candidates for that specific therapy (as with most medications). Early and aggressive intervention improves outcomes; however, the algorithm neither promotes nor supports early, aggressive management.

Second, although the authors focus on an A1C <7% as the goal, the contribution of postprandial glucose (PPG) to A1C is ignored. Monnier et al. (3) showed that PPG is the primary contributor to glycemia when A1C levels are <7.3% and very similar to fasting at levels of 8.4%. Earlier studies (4,5) showed fasting plasma glucose to be an inexact measure of glycemic control relative to A1C. Why, then, should we recommend that clinicians and patients rely on fasting plasma glucose measures to guide daily diabetes management?

Third, there is a strong link between postchallenge/PPG excursions and macrovascular disease independent of A1C levels (6,7). Monnier et al. (8) showed that glucose fluctuations during postprandial periods exhibited a more specific triggering effect on oxidative stress than chronic sustained hyperglycemia. Further, reducing glycemic excursions is causally associated with carotid intima-media thickness, a validated surrogate cardiovascular end point (7).

Assessing the benefit of a given therapy cannot be based solely on cost and efficacy in lowering glucose. The STOP-NIDDM (9) study showed a clear association between treatment with acarbose and a significant reduction in cardiovascular disease and hypertension. Use of rapid insulin reduces hypoglycemia (10). Newer medications, such as pramlintide and exenatide, have demonstrated improved PPG control and significant weight loss (11,12).

The mission of the American Diabetes Association is "to prevent and cure diabetes and to improve the lives of all people affected by diabetes" (13). Is it prudent to ignore or diminish the value and clinical utility of these medications simply because they do not meet subjective criteria regarding cost versus A1C-lowering effects? Exenatide, in combination with metformin, could be used earlier to get more patients to target and avoid costly long-term complications. We must remember that the highest cost in diabetes is not the medications; rather, it is the complications that result from not achieving good diabetes control.

The algorithm is substantially incomplete in communicating the necessity for early, aggressive management using treatment modalities that address all glycemic abnormalities. We strongly urge the authors to reevaluate their focus on A1C and expand the algorithm to include strategies to manage postprandial hyperglycemia, which is clearly required to achieve normal metabolic control.

Footnotes

C.G.P. has received consulting fees from Abbott Diabetes Care, Bayer Diagnostics, Eli Lilly, EMD Pharmaceuticals, Roche Diagnostics, and Sanofi- Aventis Pharmaceuticals.

References

  1. Nathan DM, Buse JB, Davidson MB, Heine RJ, Holman RR, Sherwin R, Zinman B: Management of hyperglycemia in type 2 diabetes: a consensus algorithm for the initiation and adjustment of therapy: a consensus statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care 29:1963–1972, 2006[Free Full Text]
  2. Harris MI, Klein R, Welborn TA, Knuiman MW: Onset of NIDDM occurs at least 4–7 yr before clinical diagnosis. Diabetes Care 15:815–819, 1992[Abstract]
  3. Monnier L, Lapinski H, Colette C: Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of type 2 diabetic patients: variations with increasing levels of HbA1c. Diabetes Care 26:881–885, 2003[Abstract/Free Full Text]
  4. Avignon A, Radauceanu A, Monnier L: Nonfasting plasma glucose is a better marker of diabetic control than fasting plasma glucose in type 2 diabetes. Diabetes Care 20:1822–1826, 1997[Abstract]
  5. Bouma M, Dekker JH, de Sonnaville JJ, van der Does FE, de Vries H, Kriegsman DM, Kostense PJ, Heine RJ, van Eijk JT: How valid is fasting plasma glucose as a parameter of glycemic control in non–insulin-using patients with type 2 diabetes? Diabetes Care 22:904–907, 1999[Abstract]
  6. Ceriello A, Quagliaro L, Piconi L, Assaloni R, Da Ros R, Maier A, Esposito K, Guigliano D: Effect of postprandial hypertriglyceridemia and hyperglycemia on circulating adhesion molecules and oxidative stress generation and the possible role of simvastatin treatment. Diabetes 53:701–710, 2004[Abstract/Free Full Text]
  7. Esposito K, Giugliano D, Nappo F, Marfella R: Regression of carotid atherosclerosis by control of postprandial hyperglycemia in type 2 diabetes mellitus. Circulation 110:214–219, 2004[Abstract/Free Full Text]
  8. Monnier L, Mas E, Ginet C, Michel F, Villon L, Christol JP, Colette C: Activation of oxidative stress by acute glucose fluctuations compared with sustained chronic hyperglycemia in patients with type 2 diabetes. JAMA 295:1681–1687, 2006[Abstract/Free Full Text]
  9. Chiasson JL, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M: Acarbose treatment and the risk of cardiovascular disease and hypertension in patients with impaired glucose tolerance: the STOP-NIDDM trial. JAMA 290:486–494, 2003[Abstract/Free Full Text]
  10. Anderson JH Jr, Brunelle RL, Keohane P, Koivisto VA, Trautmann ME, Vignati L, DiMarchi R, the Multicenter Insulin Lispro Study Group: Mealtime treatment with insulin analog improves postprandial hyperglycemia and hypoglycemia in patients with non-insulin-dependent diabetes mellitus. Arch Intern Med 157:1249–1255, 1997[Abstract]
  11. Hollander P, Maggs DG, Ruggles JA, Fineman M, Shen L, Kolterman OG, Weyer C: Effect of pramlintide on weight in overweight and obese insulin-treated type 2 diabetes patients. Obes Res 12:661–668, 2004[Medline]
  12. Buse JB, Henry RR, Han J, Kim DD, Fineman MS, Baron AD, the Exenatide-113 Clinical Study Group: Effects of exenatide (exendin-4) on glycemic control over 30 weeks in sulfonylurea-treated patients with type 2 diabetes. Diabetes Care 27:2628–2635, 2004[Abstract/Free Full Text]
  13. American Diabetes Association: About us: American Diabetes Association, 2006. Alexandria, VA, American Diabetes Association. Available from http://www.diabetes.org/aboutus.jsp?WTLPromo=HEADER_aboutus&vms=215774926324. Accessed 23 July 2006

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D. M. Nathan and On Behalf of the ADA/DASD Consensus Group
Management of Hyperglycemia in Type 2 Diabetes: A Consensus Algorithm for the Initiation and Adjustment of Therapy: A Consensus Statement From the American Diabetes Association and the European Association for the Study of Diabetes: Response to Cryer, Porta and Trento, and Parkin and Davidson
Diabetes Care, January 1, 2007; 30(1): 194 - 196.
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