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Clinical Chemistry 51: 1354-1357, 2005; 10.1373/clinchem.2005.053587
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(Clinical Chemistry. 2005;51:1354-1357.)
© 2005 American Association for Clinical Chemistry, Inc.

Point/Counterpoint

Counterpoint: Just Being Alive Is Not Good Enough

Gerald Reaven

Division of Cardiovascular Medicine, Falk CVRC, Stanford University School of Medicine, 300 Pasteur Dr., Stanford, CA 94305. Fax 650-725-1599; e-mail greaven@cvmed.stanford.edu.

The first 300 words of the full text of this article appear below.


   Introduction
 
Although Dr. Scott Grundy assures us that the Adult Treatment Panel III (ATP III) version of the metabolic syndrome is still alive (1), the real question is whether its continued existence provides us with any useful informa-tion. Just being alive is not enough, for as Sportin’ Life points out in Gershwin’s Porgy and Bess, "Methuselah lived 900 years, but who calls it living, when no gal will give in, to him that’s 900 years."


   Does Diagnosing the Metabolic Syndrome Have Clinical Utility?
 
Before addressing the substance of Dr. Grundy’s comments, I must defend myself against his charge that I have limited my critical comments to the ATP III version of the metabolic syndrome. I am not xenophobic, and in a recent editorial addressed what I perceived to be the drawbacks of both the ATP and WHO versions of the metabolic syndrome (2). The most obvious problem for me is the notion that making a positive diagnosis of the metabolic syndrome, compared with a negative one, helps guide clinical decisions. For example, WHO criteria would not lead to a diagnosis of the metabolic syndrome in an apparently healthy, normotensive man, body mass index of 27.8 kg/m2, with fasting plasma glucose and triglyceride (TG) concentrations of 111 mg/dL (6.16 mmol/L) and 185 mg/dL (2.09 mmol/L), respectively, if he had a HDL-cholesterol (HDL-C) concentration of 37 mg/dL (0.96 mmol/L). By implication, this person would not be at increased risk of cardiovascular disease (CVD). On the other hand, given essentially identical findings, another man, with a HDL-C concentration of 33 mg/dL (0.85 mmol/L), has the metabolic syndrome by WHO criteria and is, by definition, at increased CVD risk. Is the CVD risk any different in these 2 men? Would not the clinical approach be similar in both? More of this later, but suffice it to say . . . [Full Text of this Article]


   Has the Introduction of Criteria for Diagnosing the Metabolic Syndrome Stimulated Basic, Clinical, or Epidemiologic Research?
 

   Does the ATP III Definition of the Metabolic Syndrome Have Any Redeeming Virtues?
 





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