HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Vaccaro, O. Articles by Riccardi, G. Search for Related Content PubMed PubMed Citation Articles by Vaccaro, O. Articles by Riccardi, G. Social Bookmarking                What's this?

Changing the Definition of Impaired Fasting Glucose

Impact on the classification of individuals and risk definition

Department of Clinical and Experimental Medicine, University of Naples Federico II, Naples, Italy

Address correspondence and reprint requests to Olga Vaccaro, MD, Department of Clinical and Experimental Medicine, University of Naples Federico II, Via S Pansini 5, 80131 Napoli, Italy. E-mail ovaccaro{at}unina.it

	ABSTRACT

TOP ABSTRACT INTRODUCTION RESEARCH DESIGN AND METHODS RESULTS CONCLUSIONS References

 
OBJECTIVE—This study evaluates the impact of lowering the diagnostic threshold for impaired fasting glucose (IFG) from 6.1 to 5.6 mmol/l as proposed by the American Diabetes Association (ADA) on the prevalence of the condition, classification of individuals, and risk definition.

RESEARCH DESIGN AND METHODS—A total of 1,285 employees of the Italian Telephone Company aged 35–59 years without known diabetes underwent an oral glucose tolerance test (OGTT). BMI, serum cholesterol, triglycerides, and blood pressure were measured. Medication use was recorded.

RESULTS—With the new ADA criterion, the proportion of people diagnosed with IFG increased from 3.2 to 9.7%. The newly proposed IFG category identified 41% of all subjects with impaired glucose tolerance (IGT) compared with 16.2% identified with the use of the World Health Organization criterion for IFG; the improvement in accuracy has been achieved at the cost of classifying more previously "normal" subjects as having IFG (from 2.3 to 7.3%). Both IFG and IGT were associated with an unfavorable risk profile for diabetes and cardiovascular disease, with a higher estimated risk for IGT than IFG.

CONCLUSIONS—Even with the revised diagnostic criterion, IFG and IGT identify distinct groups that have a different background risk. The cost/benefit of preventive measures tested in people with IGT may not apply to the new IFG category.

Abbreviations: ADA, American Diabetes Association • CVD, cardiovascular disease • IFG, impaired fasting glucose • IGT, impaired glucose tolerance • OGTT, oral glucose tolerance test • WHO, World Health Organization

	INTRODUCTION

TOP ABSTRACT INTRODUCTION RESEARCH DESIGN AND METHODS RESULTS CONCLUSIONS References

 
The American Diabetes Association (ADA) Expert Committee on the Diagnosis and Classification of Diabetes Mellitus has recommended lowering the diagnostic threshold of impaired fasting glucose (IFG) from 6.1 to 5.6 mmol/l (1). The advantages of this change as reported by the committee (1) have been questioned (2,3). Impaired glucose tolerance (IGT) and IFG, as defined by the World Health Organization (WHO) (4), differ in various aspects: IGT is more prevalent than IFG, and postchallenge hyperglycemia is more closely associated with a risk of developing diabetes and cardiovascular disease (CVD) (5–7) than fasting hyperglycemia. Lowering the diagnostic glucose threshold for IFG to 5.6 mmol/l would supposedly result in a similar prevalence of IFG and IGT and increase the concordance between the two groups with respect to risk definition (1). Application of the lower diagnostic threshold would increase the prevalence of IFG, and this has indeed been demonstrated in various, mostly nonwhite populations (3,8). To what extent this would also enhance alignment between IFG and IGT in the classification of individuals and, more importantly, in the definition of risk for diabetes and CVD is less clear and is relevant for the implementation of preventive strategies.

The present analysis was undertaken to evaluate to what extent lowering the IFG diagnostic threshold would increase the concordance between the IFG and IGT categories with regard to classification of individuals, cardiovascular risk, and risk of progression to diabetes in an Italian population of white adults.

	RESEARCH DESIGN AND METHODS

TOP ABSTRACT INTRODUCTION RESEARCH DESIGN AND METHODS RESULTS CONCLUSIONS References

 
Our analysis was conducted with data obtained in a survey of employees of the Italian Telephone Company who resided in the province of Naples (6). All employees aged 35–59 years (n = 1,372) were eligible for this company-sponsored screening program for cardiovascular risk factors, and 95% of the target population was examined. Subjects were examined at their workplace by trained observers according to a standard protocol. The company allowed free time for the examination. Medical records were strictly confidential. In all, 44 subjects reported diabetes or hypoglycemic medication use and were not included in our analysis. A total of 1,245 male and female subjects without self-reported diabetes underwent a 75-g oral glucose tolerance test (OGTT); glucose was measured at fasting and 2-h postload on venous whole blood. The WHO (4) conversion tables were used to correct for differences in glucose measurements between plasma and venous whole blood. Fasting serum cholesterol and triglycerides were also measured by standard methods. Supine blood pressure was measured after a 5-min rest according to a standard protocol, and the average of two measurements taken at a 2-min interval was used in the analyses. Information on use of medication was collected.

Data are reported as means or percentages together with 95% CIs. Between-group differences were tested by unpaired t test or ² test as appropriate. Statistical significance was set at P < 0.05, two sided, after correction for multiple comparisons by the Bonferroni method (IFG or IGT vs. normoglycemia).

	RESULTS

TOP ABSTRACT INTRODUCTION RESEARCH DESIGN AND METHODS RESULTS CONCLUSIONS References

 
Complete datasets were available for 1,177 individuals without previously known diabetes. According to the WHO 1999 criterion, 38 people (3.2% of participants) had IFG; among these, 13 (34%) had abnormal postload glucose (11 IGT and 2 diabetes). With the ADA 2003 criterion, 114 people (9.7% of participants) were diagnosed with IFG, 34 (29.8%) of whom also had abnormal postload glucose (28 IGT and 6 diabetes). The newly proposed IFG category identified 41% of all IGT subjects compared with 16.2% identified by the WHO criterion. Furthermore, 43.7% of those with diabetes by OGTT were previously classified "normal," but now only 18.7% are so classified (Table 1). The improvement in accuracy was achieved at the cost of classifying more previous "normal" subjects as having IGT (from 2.3 to 7.3%). Thus, a lower diagnostic threshold for IFG captured more individuals with postload glucose abnormalities. However, nearly 50% of all cases of IGT still remained undetected. Moreover, of the 76 additional subjects diagnosed with IFG with the new criterion, only 21 had a positive OGTT in this population (Table 1).

	CONCLUSIONS

TOP ABSTRACT INTRODUCTION RESEARCH DESIGN AND METHODS RESULTS CONCLUSIONS References

IFG and IGT are not diseases per se and are totally asymptomatic. Nonetheless, we cannot exclude that by surveying a group of active workers who may be healthier than the general population, we may have underestimated the impact of lowering the IFG diagnostic threshold on the prevalence of these conditions and their associated background risk. Furthermore, we only examined people aged 35–59 years. The truncated age distribution and the relatively small sample size precluded analysis by age, sex, and BMI. Hence, it remains to be established if and how these factors interact with the new definition of IFG in the classification of people. Notwithstanding these limitations, the prevalence figures for IFG obtained in our study coincide with those reported in population-based studies (3,8) and the relation of obesity and age with glucose regulation status was confirmed, thereby providing internal and external support to the results.

Both IFG and IGT were associated with an unfavorable risk profile for diabetes and CVD. More than 80% of both groups had BMI, blood pressure, or plasma lipid levels above optimal values. Moreover, the percentage of people with three or more risk factors (obesity, hypertension, dyslipidemia, or older age), and hence with a high risk of developing diabetes or CVD according to validated risk scores and population-based studies on the effectiveness of screening procedures (9–12), was significantly higher in the IGT group than in normoglycemic individuals. This was not always the case in subjects with IFG. These results suggest that people with IGT have a higher estimated risk and are in line with data on the incidence of diabetes and CVD in people with IFG reported in two recent prospective studies conducted using the ADA 2003 diagnostic criterion: one in Singapore on a population of Asian ethnicity (62% Chinese, 21% Malay, 15% Asian Indians) and the other in a relatively small group of middle-aged residents of Baltimore, Maryland (13,14).

The metabolic abnormalities of the postprandial phase are more relevant risk markers than previously thought (15,16), and the benefits of preventive strategies tested in people with IGT may be partly due to the correction of postprandial hyperglycemia (17). Even though OGTT is nonphysiological and postchallenge glucose is not the same as glucose after a mixed meal, it can be a better proxy than IFG for the hyperglycemic spikes occurring in the postprandial phase in nondiabetic people (18). Performing OGTT in people with fasting glucose of 5.7–6.9 mmol/l, as recommended by the Canadian Diabetes Association, would help with risk stratification and targeting of intervention in people with IFG, particularly when other risk factors for diabetes or IGT are present (9,19).

In conclusion, a better understanding of the prognostic significance of IFG is relevant for the implementation of preventive strategies and the evaluation of the cost/benefit balance of labeling three times more people with IFG. Based on the evidence available, it is not obvious that the benefits of preventive measures tested in people with IGT will apply, at least quantitatively, in people with IFG defined by the ADA 2003 criterion.

	Footnotes

 
A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

Received for publication October 15, 2004. Accepted for publication April 6, 2005.

	References

TOP ABSTRACT INTRODUCTION RESEARCH DESIGN AND METHODS RESULTS CONCLUSIONS References

 

1. Genuth S, Alberti KG, Bennett P, Buse J, Defronzo R, Kahn R, Kitzmiller J, Knowler WC, Lebovitz H, Lernmark A, Nathan D, Palmer J, Rizza R, Saudek C, Shaw J, Steffes M, Stern M, Tuomilehto J, Zimmet P, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: Follow-up report on the diagnosis of diabetes mellitus. Diabetes Care 26:3160–3167, 2003[Free Full Text]
   
2. Davidson MB, Landsman PB, Alexander CM: Lowering the criterion for impaired fasting glucose will not provide clinical benefits. Diabetes Care 26:3229–3330, 2003
   
3. Schriger DL, Lorber B: Lowering the cut point for impaired fasting glucose: where is the evidence? Where is the logic? Diabetes Care 27:592–601, 2004[Free Full Text]
   
4. World Health Organization. Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications. Report of a WHO Consultation. Part 1: Diagnosis and Classification of Diabetes Mellitus. Geneva, World Health Org., 1999
   
5. Unwin N, Shaw J, Zimmet P, Alberti KGGM: Impaired glucose tolerance and impaired fasting glycaemia: the current status on definition and intervention. Diabet Med 19:708–723, 2002[Medline]
   
6. Vaccaro O, Ruffa G, Imperatore G, Iovino V, Rivellese AA, Riccardi G: Risk of diabetes in the new diagnostic category of impaired fasting glucose. Diabetes Care 22:1490–1493, 1999[Abstract/Free Full Text]
   
7. Decode Study Group, European Diabetes Epidemiology Group: Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria. Arch Intern Med 161:397–405, 2001[Abstract/Free Full Text]
   
8. Borch-Johnsen K, Colagiuri S, Balkau B: Creating a pandemic of prediabetes: the proposed new diagnostic criteria for impaired fasting glycemia. Diabetologia 47:1396–1402, 2004[Medline]
   
9. Dallo FJ, Weller SC: Effectiveness of diabetes mellitus screening recommendations. Proc Natl Acad Sci U S A 100:10574–10579, 2003[Abstract/Free Full Text]
   
10. Lindstrom J, Tuomilehto J: The diabetes risk score: a practical tool to predict type 2 diabetes risk. Diabetes Care 26:725–731
    
11. Glumer C, Cartensen B, Sandbaek A, Torsten L, Jorgensen T, Borch-Johnsen K: A Danish diabetes risk score for targeted screening. Diabetes Care 27:727–733, 2004[Abstract/Free Full Text]
    
12. De Backer G, Ambrosioni E, Borch-Johnsen K: European guidelines on cardiovascular disease prevention in clinical practice: Third Joint Task Force of European and other Societies on Cardiovascular Disease Prevention in Clinical Practice. Eur J Cardiol Prev Rehab 10:S1–S78, 2003
    
13. Tai ES, Goh ES, Lee JJM, Wong MS, Heng D, Huges K, Chew KS, Cutter J, Chew W, Gu K, Chia KS, Tan CE: Lowering the criterion for impaired fasting glucose: impact on disease prevalence and associated risk of diabetes and ischemic heart disease. Diabetes Care 27:1728–1734, 2004[Abstract/Free Full Text]
    
14. Blake DR, Meigs JB, Muller DC, Najjar SS, Andres R, Nathan DM: Impaired glucose tolerance, but not impaired fasting glucose, is associated with increased levels of coronary heart disease risk factors: results from the Baltimore Longitudinal Study on Aging. Diabetes 53:2095–100, 2004[Abstract/Free Full Text]
    
15. Hanefeld M, Koeh C, Schaper F, Fuecker K, Henkel E, Temelkova-Kurktschiev T: Postprandial plasma glucose is an independent risk factor for increased carotid intima-media thickness in non diabetic individuals: Atherosclerosis144:229–235, 1999[Medline]
    
16. Ceriello A: Impaired glucose tolerance and cardiovascular disease: the possible role of post-prandial hyperglycemia. Am Heart J147:803–807, 2004
    
17. Chiasson J-L, Josse RG, Gormis R, Hanefeld M, Karasik A, Laakso M, the STOP-NIDDM Trial Research Group: 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]
    
18. Tuomilehto J: A glucose tolerance test is important for clinical practice. Diabetes Care 25:1880.1882, 2002
    
19. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee: Screening and prevention. CJD 27:S10–S13, 2003
    

CiteULike

Del.icio.us

Digg

Reddit

Technorati

This article has been cited by other articles:

				S. Seicean, H. L. Kirchner, D. J. Gottlieb, N. M. Punjabi, H. Resnick, M. Sanders, R. Budhiraja, M. Singer, and S. Redline Sleep-Disordered Breathing and Impaired Glucose Metabolism in Normal-Weight and Overweight/Obese Individuals: The Sleep Heart Health Study Diabetes Care, May 1, 2008; 31(5): 1001 - 1006. [Abstract] [Full Text] [PDF]

				J. L. Kitzmiller, L. Dang-Kilduff, and M. M. Taslimi Gestational Diabetes After Delivery: Short-term management and long-term risks Diabetes Care, July 1, 2007; 30(Supplement_2): S225 - S235. [Full Text] [PDF]

				J. M. Dekker and B. Balkau Counterpoint: Impaired Fasting Glucose: The Case Against the New American Diabetes Association Guidelines Diabetes Care, May 1, 2006; 29(5): 1173 - 1175. [Full Text] [PDF]

				G. Brohall, C.-J. Behre, J. Hulthe, J. Wikstrand, and B. Fagerberg Prevalence of Diabetes and Impaired Glucose Tolerance in 64-Year-Old Swedish Women: Experiences of using repeated oral glucose tolerance tests Diabetes Care, February 1, 2006; 29(2): 363 - 367. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Vaccaro, O. Articles by Riccardi, G. Search for Related Content PubMed PubMed Citation Articles by Vaccaro, O. Articles by Riccardi, G. Social Bookmarking                What's this?