Hemoglobin A1c (HbA1c) is a common and practical measure of average glucose (blood sugar) levels during the preceding three to four months. It is used both to diagnose diabetes and to measure diabetic control. Hemoglobin A comprises 97 percent of the hemoglobin found in normal red blood cells. HbA1c is a subtype of Hemoglobin A to which glucose binds permanently. The higher the amount of glucose in the blood, the higher the level of HbA1c will be. The average lifespan of a normal red blood cell is 90 to 120 days, which is why HbA1c will measure glucose levels over that period of time.
Diseases that affect Hemoglobin and/or red blood cells may affect the measurement of HbA1c. Take, for example, sickle cell disease (SCD) and sickle cell trait (SCT). Both are genetic diseases that cause Hemoglobin A to be replaced by Hemoglobin S in red blood cells. SCD requires two abnormal, or altered, genes while SCT requires one abnormal gene. A child born of parents who both have SCT has a high likelihood of having SCD. SCT is fairly common, affecting eight to ten percent of black people but less than one percent of white people. The red blood cells in individuals with SCT contain 60 to 70 percent hemoglobin A and 30 to 40 percent Hemoglobin S. Hemoglobin S causes red blood cells to be deformed. It also causes these red blood cells to be removed from circulation by the spleen earlier than the 90 to 120 days that normal red blood cells live. Therefore it has been postulated that because SCT causes red blood cells to contain less Hemoglobin A and the cells to last a shorter time in circulation, levels of HbA1c in those with SCT may be artificially lower than they really are.
A recent study done at Brown University set out to prove this theory. While other smaller studies have shown no correlation between SCT and levels of HbA1c, the Brown study was a large study that had an unusually high percentage of participants with SCT (28 percent). They measured not just HbA1c levels but did two-hour glucose tolerance tests on the study volunteers. What they found was that there was indeed a connection between SCT and artificially lower levels of HbA1c. The authors suggested that HbA1c may systematically underestimate elevated glucose levels and rates of diabetes in black people with SCT.
The findings of this study may partly explain why the prevalence of diabetes in the black community is higher than the population in general. It may also explain why the rates of diabetic complications are higher in black people. Of course more research is needed but perhaps if black patients do not know whether or not they have SCT they should be routinely tested for it and, if positive, other ways of testing for and monitoring diabetes should be considered.
For more information go to www.ngsp.org/factors.asp or www.cdc.gov/ncbddd/sicklecell/traits.html
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