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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
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
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
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
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
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.
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.
Return to Contents
Analysis from this systematic evidence review suggests the
- 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
- 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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AHRQ Publication Number No. 05-E026-1
Current as of August 2005