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This weeks Question:
Which has a higher sensitivity for predicting the progression to diabetes?

IGT Impaired Glucose Tolerance
IFG Impaired Fasting Glucose

The published data show that IGT has a much higher sensitivity for predicting progression to diabetes than does IFG.[6] This occurs at the cost of only a small reduction in specificity and positive predictive value. Thus, while the new category of IFG may broaden and improve our description of states of intermediate glucose metabolism, it should be seen as complementary to rather than a replacement for IGT. If data from other populations confirm these findings, then screening programs aimed at identifying people at risk of diabetes would lose a considerable amount of information by relying on fasting values alone rather than the OGTT.
This is consistent with the recommendations of the International Diabetes Federation IGT/IFG Consensus Workshop,[7] which concluded that IGT and IFG differ in their prevalence, population distribution, phenotype, gender distribution, and risk of total mortality and cardiovascular disease (CVD).

The recent publication of 2 successful intervention studies targeting subjects with impaired glucose tolerance (IGT), the Finnish Diabetes Prevention Study (DPS)[1] and the Diabetes Prevention Program (DPP) in the United States ,[2] has rekindled enthusiasm and interest for the prevention of type 2 diabetes. These studies confirm the strategies used in the first major lifestyle intervention study, the The Da Qing IGT and Diabetes Study.[3] in China. For those undertaking interventions, subjects with IGT and impaired fasting glycemia (IFG) are at highest risk of type 2 diabetes, so they are the most likely targets for interventions.
While IGT was introduced in the World Health Organization (WHO) classification of disorders of glucose tolerance in 1980, IFG is a "new kid on the block" resulting from the 1997 American Diabetes Association (ADA) Expert Committee [4] and the 1999 WHO Expert Committee reports.[5] IFG, "nondiabetic fasting hyperglycemia," is now included because subjects with this disorder also appear to be at greater risk for progression to diabetes and macrovascular disease. IFG refers to fasting glucose concentrations, which are lower than those required to diagnose diabetes but higher than the "normal" reference range. An individual with a fasting plasma glucose concentration (FPG) of 6.1 mmol/L (110 mg/dL) or greater (whole blood 5.6 mmol/L; 100 mg/dL) but less than 7.0 mmol/L (126 mg/dL) (whole blood 6.1 mmol/L; 110 mg/dL) is considered to have IFG. In introducing IFG, the ADA (but not the WHO) expert committee recommended that FPG rather than the oral glucose tolerance test (OGTT) should be the diagnostic test of choice both for clinical and epidemiological purposes. The ADA recommendation was mainly made on the basis of inconvenience of performing the OGTT in clinical practice.

IGT and IFG represent impaired glucose regulation, which refers to a metabolic state intermediate between normal glucose homeostasis and diabetes. Individuals who meet criteria for IGT and IFG are euglycemic in the circumstances of their day-to-day lives. IGT is often associated with the metabolic, or insulin resistance syndrome.

Are IFG and IGT One and the Same?

A major question is whether IGT and IFG are the same condition in disguise.
There had been concern that because the new category of IFG might not represent the same subjects as the IGT category, IFG would not be predictive of type 2 diabetes to the same degree as IGT. If the reason for diagnosing intermediate categories of glucose metabolism is to initiate treatment (lifestyle modification or pharmacotherapy) that will reduce the risk of progressing to diabetes, then it is important that IFG identifies either the same subjects as does IGT, or at least a group with a similar risk for progression. From the population perspective, the considerably lower sensitivity of IFG indicates that far fewer cases of diabetes could be prevented by targeting preventive measures on subjects with IFG than could be prevented by targeting IGT subjects.
The published data show that IGT has a much higher sensitivity for predicting progression to diabetes than does IFG.[6] This occurs at the cost of only a small reduction in specificity and positive predictive value. Thus, while the new category of IFG may broaden and improve our description of states of intermediate glucose metabolism, it should be seen as complementary to rather than a replacement for IGT. If data from other populations confirm these findings, then screening programs aimed at identifying people at risk of diabetes would lose a considerable amount of information by relying on fasting values alone rather than the OGTT.

This is consistent with the recommendations of the International Diabetes Federation IGT/IFG Consensus Workshop,[7] which concluded that IGT and IFG differ in their prevalence, population distribution, phenotype, gender distribution, and risk of total mortality and cardiovascular disease (CVD).

Risk Factors or Diseases?

Another major issue to consider is whether IGT and IFG should only be considered risk factors for type 2 diabetes (with IGT also being a risk determinant of cardiovascular disease) or are they, like diabetes, diseases in their own right? This issue has been considered in depth in by the recent International Diabetes Federation IGT/IFG Consensus Workshop.[7]
The International Diabetes Federation expert group sought to address, and hopefully clarify, 3 important questions:
1. Are the current definitions of IGT and IFG appropriate?
2. Are IFG and IGT risk factors, risk markers, or diseases?
3. What interventions (if any) should be recommended for people with IFG and IGT?
The conclusions of the International Diabetes Federation workshop were as follows:
1. The diagnostic thresholds for all categories of glucose intolerance should be revisited in the light of the latest evidence. There was no clear consensus (with current evidence) on whether IFG and IGT should be classified as diseases but they clearly represent risk factors and risk markers for diabetes and CVD, respectively.
2. Both IGT and IFG are similarly associated with an increased risk of diabetes, but IGT is more strongly associated with CVD outcomes.
3. Risks are higher when IGT and IFG coexist.
4. Lifestyle interventions are highly effective in delaying or preventing the onset of diabetes in people with IGT, as are pharmacologic agents such as metformin and acarbose. Lifestyle interventions may reduce cardiovascular and total mortality but they require further studies that address this issue directly.

References
1. Tuomilehto J, Lindstrom J, Eriksson JG, Valle, TT, Hamalainen, H, Ilanne-Parikka P, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med. 2001;344:1343-1350. Abstract
2. Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA et al, for the Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346:393-403. Abstract
3. Pan XR, Li GW, Hu YH, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and Diabetes Study. Diabetes Care. 1997;20:537-544. Abstract
4. American Diabetes Association: Report of the expert committee on the diagnosis and classification of diabetes mellitus. Diabetes Care. 1997;20:1183-1197. Abstract
5. World Health Organization. Definition, Diagnosis and Classification of Diabetes Mellitus and Its Complications; Part 1: Diagnosis and Classification of Diabetes Mellitus. WHO Department of Noncommunicable Disease Surveillance, Geneva, 1999.
6. Shaw JE, Zimmet PZ, de Courten M, et al. Impaired fasting glucose or impaired glucose tolerance: what best predicts future diabetes in Mauritius? Diabetes Care. 1999;22:399-402.
7. Unwin N, Shaw J, Zimmet P, Alberti KG. Impaired glucose tolerance and impaired fasting glycemia: the current status on definition and intervention. Diab Med. 2002;19:708-723.
Medscape Diabetes & Endocrinology 5(1), 2003. © 2003 Medscape

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