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Glucose Lowering to Control Macrovascular Disease in Type 2 DiabetesTreating the Wrong Surrogate End Point?
Mark O. Goodarzi, MD, PhD;
Bruce M. Psaty, MD, PhD
JAMA. 2008;300(17):2051-2053.
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In the 1920s, the use of insulin to treat type 1 diabetes was lifesaving for children in diabetic ketoacidosis. Among the surviving patients with diabetes, the microvascular and macrovascular disease complications proved to be nonetheless devastating. The treatment of type 1 diabetes was revolutionized by the discovery that intensive glycemic control could prevent or delay the development of the microvascular complications of retinopathy, neuropathy, and nephropathy. Indeed, for patients with type 1 diabetes, aggressive insulin treatment also reduced the long-term risk of cardiovascular disease.1
Therapeutic enthusiasm for intensive treatment expanded to include patients with type 2 diabetes, who typically have insulin resistance rather than the absence of insulin production characteristic of type 1 diabetes. Elevated glucose levels in patients with type 2 diabetes, like the high white blood cell counts in patients with bacterial pneumonia, are a consequence of insulin . . . [Full Text of this Article]
Author Affiliations: Division of Endocrinology, Diabetes and Metabolism, Medical Genetics Institute, Cedars-Sinai Medical Center, and Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California (Dr Goodarzi); and Cardiovascular Health Research Unit, Departments of Medicine, Epidemiology, and Health Services, University of Washington, and Center for Health Studies, Group Health, Seattle, Washington (Dr Psaty).
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