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Diagnosis, Prognosis, and Treatment of Impaired Glucose Tolerance and Impaired Fasting Glucose

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Summary (continued)



An accurate diagnosis of DM is required because the consequences for the individual are considerable and lifelong. The diagnosis of IFG or IGT is used as a risk indicator for future DM and/or CVD. The problem with these arbitrary classifications is that test reproducibility is poor, and this encourages repeat testing that adds to the uncertainty and confusion of the diagnosis when results are different.

Reproducibility of IGT and IFG

The observed reproducibility for both IGT and IFG classification in these studies was roughly 50 percent. The kappa coefficients for the IGT category were quite low and indicate overall fair agreement. The potential factors contributing to the variation and poor reproducibility were not assessed for this review.

The probability that a significant change has occurred in serial measurements can be estimated by calculating the reference change value (RCV). For FPG, the RCV = 2½ * 1.96 * (1.42 + 6.32)½ or 17.9 percent. For 2-hr PG, the RCV = 2½ * 1.96 * (1.42 + 16.62)½ or 46.4 percent. The difference between two fasting glucose values would therefore need to be greater than 17.9 percent to be significantly different. A lower RCV would increase the sensitivity to change, or reduce the variation noise, and could be achieved if the analytical and/or the biological variation are lowered.

In the best case scenario, the lowest biological variability reported for fasting glucose was an FPG CVI of 4.8 percent.84 If this value is used along with an intra-laboratory imprecision of 1 percent and no bias, the RCV can be reduced to 13.6 percent. This is the very best or lowest amount of variation possible for a fasting plasma glucose measurement.

Comparison of IFG and IGT diagnosis

This review also compared among studies the proportion of participants classified as IGT (2-hr PG), IGT (FPG and 2-hr PG), I-IGT, IFG, I-IFG, and IGT/IFG. Comparisons among these categories were statistically significant except for I-IGT versus IFG and I-IFG versus IGT/IFG. This exemplifies the importance of clearly distinguishing categories as this can affect the proportion of study subjects and the conclusions from prognosis and treatment data.

The reproducibility for both IGT and IFG categorization is poor by both observed and kappa analysis. Because of the large variability in glucose measurement, the absolute FPG and 2-hr PG measurements may be more informative than categorization into IFG and IGT, respectively. Comparison of IGT and IFG categories shows a wide degree of variation among populations.

The prevalence of IGT is greater than for IFG in almost all studies. High-risk populations have an equal or greater proportion of IFG compared to IGT diagnoses. Statistically, the proportion of study participants classified as IGT by 2-hr PG alone is greater than if the diagnostic criteria of both 2-hr PG and FPG are used. This will affect the conclusions of prognosis and possibly treatment data in population studies using only the 2-hr PG concentration (WHO epidemiological criteria).


This review provides further evidence of the relevance of the OGTT as a diagnostic test. Despite the many shortcomings of the OGTT reviewed here, it detects a very high-risk group for future DM and may either need to be more accessible to clinicians or replaced by a simpler test that provides comparable predictive information. The OGTT also detects a group at risk for CVD; and if IGT is causally related to CVD, the AR estimates suggest that its treatment may reduce CVD risk by as much as 20 percent to 40 percent.

These studies highlight the relevance of fasting and postchallenge glucometabolic abnormalities to clinically relevant outcomes. Intervention studies have already shown that DM can be prevented in these individuals with some interventions.

Risk for progression to DM

The results of this systematic review clearly show that IGT, IFG, I-IGT, I-IFG, and combined IGT/IFG are strong risk factors for future DM. The combined group has the strongest risk factor, and this observation is not surprising given the fact that the diagnostic threshold for DM is just a farther point along the dysglycemic spectrum than the threshold for either IFG or IGT.

Nevertheless, these large risk estimates clearly do suggest that any clinical approach directed at preventing DM should include a policy of detecting IFG or IGT. They do not support suggestions that measures of glucose are not necessary to detect individuals at risk for future DM. However, such a policy may be useful to reduce the number of individuals who require a glucose test.

Risk for CVD outcomes

The reviewed studies provide confirmation that IFG or IGT are risk factors for fatal and nonfatal CVD and are consistent with other studies that were excluded because whole blood or capillary samples were used to assay glucose levels. Moreover, the suggestion that IGT is a greater risk factor for CVD than IFG is supported by this systematic review but is based on the findings of a single study.85 This is not surprising given the fact that IGT is detected in response to stressing the physiology with a nonphysiological glucose load, thus exposing a degree of metabolic dysregulation that would not be apparent on the basis of fasting glucose levels alone.


Prevention of DM: lifestyle interventions

This systematic review clearly demonstrates that DM can be prevented or delayed with lifestyle modification. All but one of the five studies that evaluated a combined diet and exercise program found significant benefits, with a pooled relative risk of 54 percent for progression to diabetes. The only trial to show no effect of a combined diet and exercise intervention was of short duration (6-month followup). Interventions with diet or exercise alone showed mixed results between studies. Efforts to modify dietary intake and activity levels in individuals at increased risk for developing DM are clearly warranted.

Prevention of DM: pharmacotherapeutic interventions

Only four trials to date have evaluated the effect of pharmacotherapeutic interventions on the risk for developing DM in individuals with IGT. Two of these studies, one involving acarbose and one involving metformin, demonstrated reduced rates of progression to DM with a relative risk reduction of about 25 percent. Given this relative paucity of information, recommendation of pharmacological intervention for the prevention of DM would seem premature at this time.

Pediatric Population

Despite the paucity of population-based studies, several cohort studies in high-risk groups suggest that IGT is a significant and potentially growing problem in the pediatric population. Indeed, larger proportions of children may have IGT than is currently recognized. It is critical to acquire an understanding of the precursors of type 2 DM development in children and youth. However, few conclusions can be made based on the current pediatric literature. Further investigation of prevalence in children and adolescents is necessary to clarify the magnitude of the problem.


The reproducibility of the diagnosis of IGT with OGTT testing and the clinical significance of IFG versus IGT have not been widely examined in the pediatric literature. Although young age has been implicated as a predictor of poor reproducibility of OGTT results in adults, suggesting that reproducibility may be worse in adolescents and children, this was not the experience in one small pediatric study (n=10).77

Clearly, further investigation of the reliability of diagnostic criteria for IFG and IGT is warranted. Furthermore, given the importance of the prevention of type 2 DM, it may be advantageous to identify children who have disturbed glucose metabolism (insulin resistance and/or beta cell dysfunction) before they develop IFG or IGT.


An understanding of how disturbed glucose metabolism progresses to IGT and to type 2 DM is key to the primary prevention of DM. Currently, details of this progression are completely lacking in the pediatric population.

Prevalence data for type 2 DM suggest prognosis may vary with age, pubertal status, and ethnicity. Family history of DM, exposure to a diabetic environment in utero, fitness and physical activity, fat distribution, and characteristics of nutritional intake may also influence the prognosis of IFG and IGT. Longitudinal studies are required to examine mid- and long-term outcomes of IGT and the determinants of outcome in multiple ethnic groups and across a broad age range.

Investigation of other metabolic outcomes in children and adolescents with IFG and IGT would further improve our understanding of disturbance in health in this population. Better understanding of the prognosis of IGT in children and adolescents will clarify the need for intervention and contribute to optimal intervention study design.


A single study has described the pharmacological treatment of IGT, and no randomly controlled lifestyle intervention has been reported in the pediatric age group. Given the increasing rates of IFG/IGT, research on the optimal approach to the management of these children should be a research priority. This research should compare lifestyle intervention and pharmacotherapy and identify optimal methodologies for young populations and their families. Although glycemic status is a key outcome variable, other metabolic and psychosocial outcomes should also be examined.

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Analysis from this systematic evidence review suggests the following:

  • Diagnosis—The reproducibility for both IGT and IFG categorization is poor. Therefore the absolute FPG and 2-hr PG measurement may be more informative than categorization into IFG and IGT respectively. The distribution of study participants in the IGT category varies significantly with the diagnostic criteria used. This will affect findings in epidemiological studies evaluating prognosis and treatment.
  • Prognosis—Many studies consistently show that both IFG and IGT are strong risk factors for the development of DM. Fewer studies also show that they are risk factors for future CVD and all-cause mortality.
  • Treatment—There is evidence that combined diet and exercise, as well as drug therapy (metformin, acarbose), may be effective at preventing progression to DM in IGT subjects.
  • Pediatric population—IGT is relatively common in childhood, particularly in children who are overweight. Further clarification of population-based prevalence and investigation to improve understanding of the diagnosis, clinical significance, and optimal management of IFG and IGT in childhood is required.

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Availability of Full Report

The full evidence report from which this summary was taken was prepared for the Agency for Healthcare Research and Quality (AHRQ) by the McMaster Evidence-based Practice Center under Contract No. 290-02-0020. Printed copies may be obtained free of charge from the AHRQ Publications Clearinghouse by calling 800-358-9295. 9295. Requesters should ask for Evidence Report/Technology Assessment No. 128, Diagnosis, Prognosis, and Treatment of Impaired Glucose Tolerance and Impaired Fasting Glucose.

The Evidence Report is also online on the National Library of Medicine Bookshelf, or can be downloaded as a PDF File (8 MB) [Plugin Software Help].

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