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The Importance of Testing for Pre-diabetes—Using the Right Tool
therefore be used to diagnose patients as having diabetes or pre- with type 2 diabetes after they received the anti-inflammatory drug
diabetes.
18
Along with setting these thresholds, the authors identified a anakinra.
19,20
Promising as some of these developments may be, they are
number of advantages for the use of HbA
1c
in diagnosing diabetes, still a long way from routine clinical use.
19
including the fact that laboratory measures that express long-term
glycemic exposure should provide a better marker for presence and Conclusion
severity of disease than single measures of glucose concentration.
18
Other Diabetes is one of the most prevalent chronic diseases affecting the US
advantages of HbA
1c
focused on the convenience and ease of sample healthcare system today. While it is important to address the acute and
collection for the patient, as no fasting or other preparation is necessary.
18
chronic treatment needs of those already diagnosed, an increasing
emphasis is being placed on disease prevention and screening.
Despite this correlation of HbA
1c
percentages to risk of developing Pre-diabetes is an important stage on the spectrum between normal
diabetic complications, significant limiting factors for the use of this blood sugar and frank hyperglycemia. Patients can benefit greatly from
assay remain. Some include hemoglobinopathies and conditions of the early detection of this state. Studies have shown that patients with
altered red cell turnover, as previously described. Others include the diabetes often show signs of early diabetic complications at the time of
observations that HbA
1c
levels tend to rise with age, or differ among diagnosis. Early intervention with lifestyle modifications and/or
ethnic groups.
18
The lack of standardization of the HbA
1c
assay pharmacological therapy can often delay, and in some cases prevent,
worldwide also continues to be a limiting factor. While the current the progression from pre-diabetes to diabetes. Despite the availability
recommended method for diagnosing diabetes remains the OGTT, HbA
1c
of various testing methods, venous blood sampling and core laboratory
may become a useful diagnostic test in years to come. analysis remain the standard. Fasting plasma glucose levels, and
specifically OGTTs, detect pre-diabetes most reliably. While POCT
Genotyping and Antibody Screening devices are convenient and readily available, variables such as operator
The future of diabetes screening is promising and may involve effects continue to plague the reliability of POCT devices as diagnostic
genotyping and antibody screening. Multiple clinical trials are currently tools. Future diagnostic tests may include HbA
1c
testing or genotyping
under way using type 1 diabetes as the template for autoimmune- and antibody screening. The HbA
1c
assay, while familiar to both
mediated causes of diabetes. These trials suggest that the risk for clinicians and patients, has not been evaluated for diagnosis of
developing type 1 diabetes is a combination of the presence of high-risk diabetes or pre-diabetes. Genotyping and antibody screening are
human leukocyte antigen (HLA) genes and autoantibodies.
19
Early showing promise as these tests are furthering the understanding of
observations include the idea that patients who are genetically at risk type 2 diabetes through research in the realm of type 1 diabetes. It
but do not have autoantibodies have a lower risk of developing type 1 seems that causes of type 2 diabetes may be similar to those of type 1,
diabetes unless there is a triggering event.
19
The nature of the necessary especially in the setting of the body’s autoimmune response to
triggering event is not yet known. Antibody screening, in turn, could be pancreatic islet cells. To date, however, this research is in its early
used as an indicator of whether an immune response against pancreatic stages and is not yet ready for routine clinical use. n
islets has been activated.
Olga S Chajewski, MD, is a PGY-2 Pathology Resident at
Currently, four major antibodies have been identified: insulin antibodies
Baystate Medical Center in Springfield. She is a resident
(IAA), glutamic acid decarboxylase (GAD65), a tyrosine-kinase-like member of the College of American Pathologists (CAP).
molecule (IA-2), and the zinc transporter ZnT8. Having any two of the four
She graduated with a medical degree from the Medical
University of South Carolina in Charleston and completed
is considered positive for an activated immune response.
19
As more
a year of post-graduate surgical training at Waterbury
discoveries are made with regard to type 1 diabetes, researchers are Hospital in Connecticut.
finding that the diagnostic divide between type 1 and type 2 diabetes is
getting smaller, suggesting the possible utility of these new developments
James H Nichols, PhD, DABCC, FACB, is a Professor
in the future diagnosis of type 2 diabetes and pre-diabetes. Type 2 diabetes
of Pathology at Tufts University School of Medicine
is defined by the combination of insulin resistance and inadequate insulin and Medical Director of Clinical Chemistry for Baystate
secretion. Based on type 1 diabetes research, it has been observed that
Health System in Springfield, Massachusetts. Previously,
he spent several years at Johns Hopkins School of
insulin resistance can accelerate the effect of the autoimmune attack on
Medicine as Associate Director of Chemistry and
islets, thus showing an overlap between type 1 and type 2 diabetes.
19
Director of the Postdoctoral Training Program.
Similarly, inflammation has been examined in type 1 diabetes and, recently,
in type 2 diabetes. A new study from 2007 showed some benefit in patients
1. Sacks DB, et al., Clin Chem, 2002;48:436–72. 9. (DPP) Diabetes Prevention Research Group, N Engl J Med, 14. Buchanan TA, et al., Diabetes, 2002;51:2796–803.
2. Aroda VR, et al., J Clin Endocrinol Metab, 2008;93:3259–65. 2002;346:393–403. 15. Nichols JH, Principles & Practice of Point-of-Care Testing,
3. Alberti KGMM, Diabetes Obes Metab, 2007;9(Suppl. 1):12–16. 10. (DPP) The Diabetes Prevention Program, Diabetes Care, Philadelphia: Lippincot Williams & Wilkins, 2002;
4. Cheng C, et al., Metabolism, 2006;55:434–8. 1999;22:623–34. 194–213.
5. Tai ES, et al., Diabet Med, 2000;17:771–5. 11. (DPP) The Diabetes Prevention Program Research Group, 16. Nathan DM, et al., Diabetes Care, 2008;31:1473–8.
6. Diabetes Control and Complications Trial Research Group, Diabetes Care, 2000;23:1619–29. 17. Titus K, CAP Today, June 2009;23:1.
N Engl J Med, 1993;329:978–86. 12. American Diabetes Association, Diabetes Care, 2004;27 18. Nathan DM, et al., Diabetes Care, 2009;32:1327–34.
7. DCCT Research Group, Diabetes, 1995;44:968–83. (Suppl. 1):S47–54. 19. Titus K, CAP Today, 2009;23:1.
8. The DECODE Study Group, Arch Int Med, 2001;161:397–405. 13. Chiasson JL, et al., Lancet, 2002;359:2072–7. 20. Larsen CM, et al., N Engl J Med, 2007;356:1517–26.
US ENDOCRINOLOGY 25
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