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For anyone who settles for what some authorities call adequate control:
Susan
Markers of "Prediabetes" Seen to Independently Raise Mortality Risk CME
News Author: Steve Stiles
CME Author: Laurie Barclay, MD
Complete author affiliations and disclosures, and other CME information,
are available at the end of this activity.
Release Date: June 25, 2007; Valid for credit through June 25, 2008
Credits Available
Physicians - maximum of 0.25 AMA PRA Category 1 Credit(s)™ for physicians;
Family Physicians - up to 0.25 AAFP Prescribed credit(s) for physicians
All other healthcare professionals completing continuing education
credit for this activity will be issued a certificate of participation.
Physicians should only claim credit commensurate with the extent of
their participation in the activity.
from Heartwire — a professional news service of WebMD
June 25, 2007 — Markers of impaired glucose metabolism in nondiabetics
were independently related to increased risks of all-cause and
cardiovascular death in a large population-based study. The follow-up
time, averaging only about five years, suggests that such indicators of
"prediabetes" may represent significant mortality risk factors in their
own right, not simply predictors of a later high-risk condition, the
investigators speculate.
In the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab), 65%
of all cardiovascular deaths occurred in people with previously known or
newly identified diabetes or otherwise impaired glucose metabolism at
baseline, report Elizabeth LM Barr (International Diabetes Institute,
Caulfield, Victoria, Australia) and colleagues.
Compared with participants initially with normal glucose tolerance and
after researchers controlled for traditional CV risk factors, the group
writes, those with impaired fasting glucose metabolism or impaired
glucose tolerance showed a significant 50% to 60% increase in the risk
of death from any cause. The risk of CV death was more than doubled
among those initially with impaired fasting glucose (fasting plasma
glucose ≥ 6.1 and < 7.0 mmol/L with two-hour plasma glucose < 7.8 mmol/L).
Taken together, "these findings suggest that strategies to prevent
premature mortality, particularly cardiovascular-disease death, need to
be targeted not only to people with diabetes mellitus but also toward
people with milder forms of abnormal glucose metabolism." The group's
report was published online June 18, 2007, in Circulation.
In the analysis encompassing 10,428 participants, 298 (2.86%) died over
a median of 5.2 years. Of the 260 deaths for which a cause was known, a
third were due to CV disease. Of the 88 cardiovascular deaths, 57 (65%)
were among the participants initially with previously recognized or new
diabetes or impaired fasting glucose levels or tolerance, all of which —
except for newly diagnosed diabetes — were significant independent risk
factors for death from any cause.
Mortality Risks, HR (95% CI), by Baseline Metabolic Status Compared to
7662 Participants Initially With Normal Glucose Tolerance*
Endpoint IFG
(n = 610) IGT
(n = 1298) NDM
(n = 433) KDM
(n = 425)
All-cause mortality 1.6 (1.0 -2.4) 1.5 (1.1 - 2.0) 1.3 (0.9 - 2.0) 2.3
(1.6 - 3.2)
CV mortality 2.5 (1.2 - 5.1) 1.2 (0.7 - 2.2) 1.8 (0.9 - 3.6) 2.6 (1.4 - 4.7)
*Adjusted for age, sex, previously reported CV disease, waist
circumference, lipid-lowering medication use, total
cholesterol:high-density lipoprotein cholesterol ratio, and smoking
status. All-cause mortality also adjusted for hypertension (BP ≥ 140/90
or antihypertensive drug use). CV mortality also adjusted for diastolic
blood pressure.
DM = diabetes mellitus; FPG = fasting plasma glucose; PG = plasma
glucose; normal glucose tolerance = FPG < 6.1 mmol/L and 2-hour PG < 7.8
mmol/L; IFG = impaired FPG (≥ 6.1 and < 7.0 mmol/L with 2-hour PG < 7.8
mmol/L); IGT = impaired glucose tolerance (2-hour PG ≥ 7.8 and < 11.1
mmol/L with FPG < 7.0 mmol/L); NDM = newly diagnosed DM (no
physician-diagnosed DM but FPG ≥ 7.0 mmol/L or 2-hour PG ≥ 11.1 mmol/L);
KDM = known DM (physician-diagnosed DM and on hypoglycemic medication,
or had FPG ≥ 7.0 mmol/L or 2-hour PG ≥ 11.1 mmol/L).
Those initially with known diabetes or impaired glucose tolerance had
independently elevated risks of non-CV death: HR 2.3 (95% CI, 1.5-3.6)
and 1.6 (1.1-2.3), respectively. Of the 172 deaths with a known non-CV
cause, 59% were attributed to "malignant neoplasm," the authors write.
Noting that the risk of all-cause mortality, but not CV-mortality,
reached significance for those initially with impaired glucose
tolerance, Barr et al write that even with the small sample size, "it is
possible to infer that in the present study cohort, impaired glucose
tolerance may increase the risk of cancer mortality."
Often in prior studies tracking mortality associated with impaired
glucose metabolism in nondiabetics, the group notes, it has been
difficult to distinguish any risk from baseline glucose abnormalities
from risk directly related to diabetes developing later. In the current
study, the glucose-related markers predicted mortality "after only a
relatively short period of follow-up," suggesting that later diabetes
onset "was not a major pathway to death and that impaired fasting
glucose and impaired glucose tolerance are genuine risk factors for
mortality and not just precursors of diabetes mellitus."
The AusDiab report says the study received financial support from Abbott
Australasia, Alphapharm, AstraZeneca, Aventis Pharma, Bio-Rad
Laboratories, Bristol-Myers Squibb, Eli Lilly Australia,
GlaxoSmithKline, Merck Sharp & Dohme, Multiplex, Novartis
Pharmaceuticals, Novo Nordisk Pharmaceuticals, Pfizer, Roche Diagnostics
Australia, and Sanofi-Synthelabo. Coauthor Dr Timothy A Welborn
(University of Western Australia, Nedlands) has received speaker
payments from Novo Nordisk Pharmaceuticals, Eli Lilly,
Sanofi-Synthelabo, Aventis Pharma, and Servier, and is an consultant and
advisor to the boards of Abbott Australasia, Roche Diagnostics
Australia, Sanofi-Synthelabo, and Aventis Pharma.
Circulation. Published online June 18, 200