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Reflecting on Hemoglobin A1C, 1,5-Anhydroglucitol, and the Glycated Proteins Fructosamine and Glycated Albumin

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Reflecting on Hemoglobin A1C, 1,5-Anhydroglucitol, and the Glycated Proteins Fructosamine and Glycated Albumin In Brief This article reviews the advantages and limitations of the current glycemic FROM biomarkers, including A1C, 1,5-anhydroglucitol, and the glycated proteins fructosamine and glycated albumin. It provides patient encounter case studies R and related discussion to guide health care professionals on the appropriate ESEARCH TO PRACTICE/GLYCEMIC use of the various glycemic biomarkers in clinical practice. The Challenge of the Use of Glycemic Biomarkers in Diabetes: Reflecting on Hemoglobin A1C, 1,5-Anhydroglucitol, and the Glycated Proteins Fructosamine and Glycated Albumin M ARKERS: Frequent evaluation, as well as pre- nique to assess glycemic control.5 It cise measurement, of glycemic control provides information about the degree Lorena Alarcon-Casas Wright, MD, is a crucial part of optimal care for of glucose control during the previ- and Irl B. Hirsch, MD patients with diabetes. Glycemic bio- ous 8–12 weeks in the nonpregnant A 6 markers are important tools used to population. A1C has been used as a R determine whether a patient’s meta- primary treatment target for diabetes EVIEW O bolic control has been maintained because of the large intervention stud- within the target range, but most ies in both type 1 and type 2 diabetes importantly, theyare used as surro- associating improved glycemic control F gates to estimate and reduce the risk with a decreased risk of microvascular THE of chronic diabetes complications. disease.7,8 Below, we review clinical instances in It should be noted that early use T which A1C should not be used and of A1C in these two landmark stud- OOLS reflect on the use of other glycemic ies could not be extrapolated to biomarkers that can be used in sub- others because of the lack of assay stitution, as well as their individual standardization of A1C. Currently, W limitations. the National Glycohemoglobin E Standardization Program (NGSP) A LL Hemoglobin A1C has decreased potential technical In 1969, an increase in an “unusual” errors, and standardization is close to L OVE, PERHA hemoglobin was first observed in universal.7 patients with diabetes.1 It was later However, in addition to the impor- learned that, in red blood cells (RBCs), tance of standardization, it is also glucose binds to the α-amino position important to be aware of other clini- of hemoglobin β-chains (valine) in an cal situations in which A1C may not aldimine or Schiff base linkage, and be an accurate reflection of glycemic P this process could partially re arrange control in diabetes. S T in a reversible manner to form a OO DEARLY? ketoamine linkage, resulting in a “gly- Average Glycemia Versus Glycemic cated” hemoglobin, or hemoglobin Variability A1C. 2,3 In 1976, it was reported that Exposure to dysglycemia in diabe- A1C reflects the mean blood glucose tes can be simplified as a function concentration over previous weeks to of several components, including months and that its periodic moni- the duration and severity of chronic toring could provide a useful way of hyperglycemia and the acute fluctua- documenting glycemic control.4 tions of glucose over a time period. Currently, A1C is a widely used A1C in a patient with a normal hema- glycemic marker and is considered by tological profile is the reflection of the American Diabetes Association, that patient’s average glucose control along with self-monitoring of blood during the previous 2–3 months; as glucose (SMBG), as the primary tech- such, A1C is mainly a reflection of the Diabetes Spectrum Volume 25, Number 3, 2012 141 first component of dysglycemia, with targeted more aggressively. But, as of associated with hemoglobin concen- contributions from postprandial and now, there is no definitive proof that trations and negatively associated with fasting hyperglycemia.8,9 improving glycemic variability can erythropoietin dose.20 In addition to Recent studies in vitro10–12 and in change the natural history of diabetic erythropoietin, medications that affect humans13,14 strongly suggest a second vascular disease. One problem is that RBC mass, such as dapsone,21 will component, namely, the acute excur- there is not a perfect serum biomarker affect A1C results. sions of glucose around a mean value of glycemic variability. The falsely lowered A1C may lead (i.e., hyperglycemic glucose fluctua- to the wrong assumption of adequate tions but also hypoglycemic exposure A1C: Sources of Misinterpretation glycemic control. Table 1 summarizes around mean glucose) described as sources of misinterpretation for A1C 1. RBC lifespan “glycemic variability.” Glycemic vari- and other glycemic biomarkers. RBCs are freely permeable to glucose. ability may be a significant risk factor As a result, glucose enters the cells 2. Presence of hemoglobinopathies for microvascular complications, and attaches to hemoglobin at a rate along with A1C and genetics, and it Hemoglobinopathies such as sickle dependent on the serum blood glucose. cell traits (hemoglobin S) and other may help to explain why some patients Hence, A1C glycation is dynamic and develop microvascular complications abnormal hemoglobin variants such as depends not only on average glycemia hemoglobin C and E can lead to falsely and others having the same A1C do but also in the rate of production (and high or low A1C readings depend- not. In a study involving patients destruction) of RBCs. Conditions that ing on the laboratory methodology with either type 1 or type 2 diabetes affect RBC lifespan will invariably used.22–24 Comprehensive information using continuous glucose monitoring have an impact on A1C results. regarding A1C assay interferences in (CGM), the standard deviation (SD; a RBCs that have a short lifespan patients with hemoglobinopathies is measure of variability) had no impact secondary to destruction (i.e., hemo- found at the NGSP Web site.7 on A1C in type 2 diabetic patients but lytic anemia,17 destruction through the did influence A1C in type 1 diabetic passage of abnormal heart valves,18 3. Iron status patients.15 or splenomegaly) will result in a low Previous studies suggest that iron defi- It is therefore important to be A1C independent of the mean serum ciency with25 and without25,26 anemia aware that A1C in general is a crude glucose. This situation is also pres- affect the level of A1C independent of marker of dysglycemia. It is also ent in circumstances in which the glycemia. Iron is important for hemo- important to note that postprandial bone marrow increases the produc- globin synthesis and RBC production. hyperglycemia does not necessarily tion of young RBCs (reticulocytes), In negative iron balance status, the equate to glycemic variability; instead, as seen in patients with chronic iron and hemoglobin deficiencies are postprandial hyperglycemia should be kidney disease (CKD) who receive followed by deficient RBC production, regarded as a component of glycemic erythropoietin treatment for anemia; translating to a slow turnover of RBCs variability.16 post-hemorrhage, as the healthy bone and mostly “mature” cells circulat- As a result of the development of marrow is stimulated by hypoxia; or ing in the bloodstream, allowing more outpatient CGM capabilities, glyce- after a blood transfusion.19 A1C val- time for glycation and falsely increas- mic variability is being studied and ues have been found to be positively ing the values of A1C. Table 1. The Most Common Sources of Error in the Interpretation of Glycemic Biomarkers Sources of Error A1C Glycated Proteins 1,5-AG Mechanism Conditions or treatments that Conditions or treatments that Conditions or treatments that alter RBC half-life alter protein metabolism alter renal function or thresh- old for glucose Falsely High • Iron deficiency • Hypothyroidism • CKD stage 4–5 Values • Anemia • Cirrhosis of the liver • Hemoglobinopathies • Race: African American, Hispanic, Asian Falsely Low • Hemolysis • Hypoalbuminemia: • Pregnancy Values • Reticulocytosis protein-losing enteropathy, • Chronic liver disease • Hemoglobinopathies nephrotic syndrome, liver • Glucokinase–maturity- • Post-hemorrhage or failure onset diabetes of the young post-transfusion • Hyperthyroidism • Drugs: iron, erythropoietin, • Hyperuricemia dapsone • Hypertriglyceridemia • Uremia • Nonalcoholic fatty liver • Splenomegaly disease 142 Diabetes Spectrum Volume 25, Number 3, 2012 Data from the National Health and production of A1C),33 and differences uninterpretable A1C, patients with 34 Nutrition Examination Survey 1999– in RBC transmembrane gradients. CKD frequently receive erythro- FROM 200627 found that iron deficiency Recently, a cross-sectional study poietin, with the expectation of an was, not surprisingly, more common in African-American and white increase in the production of RBCs in women than in men and that this people with and without diabe- as part of treatment, and, as a result, R iron deficiency was not necessar- tes was conducted to investigate such increase in proportion of young ESEARCH TO PRACTICE/GLYCEMIC ily accompanied by anemia. Among such racial disparities in A1C and RBCs will result in an erroneous low women, 13.7% had iron deficiency, included glycemic biomarkers that A1C value. and 30% of iron-deficient women would be unaffected by hemoglobin In advanced CKD, alternative had anemia. Iron deficiency is much glycation and erythrocyte turnover markers of glycemia such as fructos- less common in men; 1.6% had iron (fructosamine and 1,5-anhydroglu- amine and glycated albumin (GA) may deficiency, and 33% of iron-deficient citol [1,5-AG]). 35 The results were in be preferable.39 men had anemia. In this representative agreement with previous studies that healthy, adult, American population A1C is higher in African-American Glycated Proteins sample, it was found that iron defi- people; however, they also had sig- In addition to hemoglobin, other ciency shifted A1C slightly upward at nificantly higher values of other proteins in the plasma can become gly- the lower end of the A1C spectrum glycated proteins compared to white cated. Glucose can attach to proteins independent of fasting glucose level.27 people before and after adjustment and form ketoamines or fructos- These observations were also reported for covariates and fasting glucose.
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