posted 11/13/02
Are the current definitions of impaired glucose tolerance (IGT)
and impaired fasting glycemia (IFG) appropriate? Are IFG and IGT risk factors,
risk markers or diseases? These are just a couple of the questions addressed.
Also, What interventions (if any) should be
recommended for people with IFG and IGT? These questions were addressed in a
workshop convened by the International Diabetes Federation to review the latest
information on these issues.
Impaired glucose tolerance and impaired fasting
glycemia: the current status on definition and intervention. A workshop was
convened by the International Diabetes Federation to review the latest
information relating to the risks associated with impaired glucose tolerance (IGT)
and impaired fasting glycemia (IFG) for future diabetes and cardiovascular
disease (CVD).
The workshop sought to address three questions: (i)
are the current definitions of IGT and IFG appropriate; (ii) are IFG and IGT
risk factors, risk markers or diseases; (iii) what interventions (if any) should
be recommended for people with IFG and IGT?
The determinants of elevated
fasting glucose and 2-h plasma glucose in an oral glucose tolerance test (2-HPG)
levels differ. Raised hepatic glucose output and a defect in early insulin
secretion are characteristic of the former, and peripheral insulin resistance is
most characteristic of the latter. Therefore, it is not surprising that the
concordance between the categories of IFG and IGT is limited.
In all prevalence studies to
date only half or less of people with IFG have IGT, and even a lower proportion
(20-30%) with IGT also have IFG.
In the majority of
populations studied, IGT is more prevalent than IFG, and there is a difference
in phenotype and gender distribution between the two categories.
IFG is substantially more
common amongst men and IGT slightly more common amongst women. The prevalence
of IFG tends to plateau in middle age whereas the prevalence of IGT rises into
old age. Both IFG and IGT are associated with a substantially increased risk of
developing diabetes, with the highest risk in people with combined IFG and IGT.
Because IGT is commoner than
IFG in most populations it is more sensitive (but slightly less specific) for
identifying people who will develop diabetes.
In most populations studied,
60% of people who develop diabetes have either IGT or IFG 5 years or so before,
with the other 40% having normal glucose tolerance at that time.
The limited published data
suggest that both isolated IFG (I-IFG) and isolated IGT (I-IGT) are similarly
associated with cardiovascular risk factors, such as hypertension and
dyslipidemia, with the highest risk in those with combined IFG and IGT. However,
some data have suggested that I-IGT is more strongly associated with
hypertension and dyslipidemia (features of the metabolic syndrome) than I-IFG.
In unadjusted analyses both
IFG and IGT are associated with CVD and total mortality.
In separate analyses for
fasting and 2-PPG adjusted for other cardiovascular risk factors (from the
DECODE study) there remains a continuous relationship between 2-PPG and
mortality, but an independent relationship with fasting glucose is only found
above 126 mg/dl.
Glycated hemoglobin (HbA1c)
levels are continuously and positively associated with CVD and total mortality
independent of other CVD risk factors.
Life style interventions,
including weight loss and increased physical activity, are highly effective in
preventing or delaying the onset of diabetes in people with IGT.
Two randomized controlled
trials of individuals with IGT found that life style intervention studies reduce
the risk of progressing to diabetes by 58%.
The oral hypoglycemic drugs
metformin and acarbose have also been shown to be effective, but less so than
the life style measures.
Similar data do not yet
exist for the effectiveness of such interventions in people with I-IFG.
Larger studies are required
to evaluate the effects of interventions on cardiovascular outcomes in people
with IGT.
Cost effective strategies to
identify people with IGT for intervention should be developed and evaluated. The
use of simple risk scores to assess who should undergo an oral glucose tolerance
test is one promising approach, although these will need to be
population-specific.
In conclusion
IGT and IFG differ in their
prevalence, population distribution, phenotype, and risk of total mortality and
CVD. The consensus of the workshop was:
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- Life style interventions are highly effective in delaying or preventing the onset of diabetes in people with IGT and may reduce CVD and total mortality, but the latter requires formal testing.
Source: Diabetes In Control
Dot Com: Diabetic Medicine 2002 19/9 (708-723)
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