# Glycated hemoglobin

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Form of hemoglobin chemically linked to a sugar

"A1C" redirects here. For other uses, see [A1C (disambiguation)](/source/A1C_(disambiguation)).

Medical diagnostic method

Glycated hemoglobin MedlinePlus 003640 eMedicine 2049478 LOINC 41995-2

**Glycated hemoglobin**, also called **glycohemoglobin**, is a form of [hemoglobin](/source/Hemoglobin) (Hb) that is chemically linked to a sugar.[note 1] Most [monosaccharides](/source/Monosaccharide), including [glucose](/source/Glucose), [galactose](/source/Galactose), and [fructose](/source/Fructose), spontaneously (that is, [non-enzymatically](/source/Enzyme)) bond with hemoglobin when they are present in the bloodstream. However, glucose is only 21% as likely to do so as galactose and 13% as likely to do so as fructose, which may explain why glucose is used as the primary metabolic fuel in humans.[1][2]

The formation of excess sugar-hemoglobin linkages indicates the presence of excessive sugar in the bloodstream and is an indicator of [diabetes](/source/Diabetes) or other hormone diseases in high concentration (HbA1c > 6.4%).[3] A1c is of particular interest because it is easy to detect. The process by which sugars attach to hemoglobin is called [glycation](/source/Glycation) and the reference system is based on HbA1c, defined as beta-N-1-deoxy fructosyl hemoglobin as a component.[4]

There are several ways to measure glycated hemoglobin, of which **HbA1c** (or simply **A1c**) is a standard single test.[5] HbA1c is measured primarily to determine the three-month average [blood sugar level](/source/Blood_sugar_level) and is used as a standard diagnostic test for evaluating the risk of complications of [diabetes](/source/Diabetes) and as an assessment of [glycemic control](/source/Glycemic_control).[5][6] The test is considered a three-month average because the average lifespan of a red blood cell is three to four months. Normal levels of glucose produce a normal amount of glycated hemoglobin. As the average amount of plasma glucose increases, the fraction of glycated hemoglobin increases predictably. In diabetes, higher amounts of glycated hemoglobin, indicating higher blood glucose levels, have been associated with [cardiovascular disease](/source/Cardiovascular_disease), [nephropathy](/source/Nephropathy), [neuropathy](/source/Neuropathy), and [retinopathy](/source/Retinopathy).[7]

## Terminology

[Glycated](/source/Glycation) hemoglobin is preferred over [glycosylated](/source/Glycosylation) hemoglobin to reflect the correct (non-enzymatic) process. Early literature often used *glycosylated* as it was unclear which process was involved until further research was performed. The terms are still sometimes used interchangeably in English-language literature.[8]

The naming of HbA1c derives from hemoglobin type A being separated on [cation exchange chromatography](/source/Ion_chromatography). The first fraction to separate, considered to be pure hemoglobin A, was designated HbA0, and the following fractions were designated HbA1a, HbA1b, and HbA1c, in their order of [elution](/source/Elution). Improved separation techniques have subsequently led to the isolation of more [subfractions](https://en.wiktionary.org/wiki/subfraction).[9]

## History

Hemoglobin A1c was first separated from other forms of hemoglobin by Huisman and Meyering in 1958 using a [chromatographic column](/source/Chromatography).[10] It was first characterized as a [glycoprotein](/source/Glycoprotein) by Bookchin and Gallop in 1968.[11] Its increase in diabetes was first described in 1969 by [Samuel Rahbar](/source/Samuel_Rahbar) and coworkers.[12] The reactions leading to its formation were characterized by Bunn and coworkers in 1975.[13]

The use of hemoglobin A1c for monitoring the degree of control of glucose metabolism in diabetic patients was proposed in 1976 by [Anthony Cerami](/source/Anthony_Cerami), Ronald Koenig, and coworkers.[14]

## Damage mechanisms

Glycated hemoglobin causes an increase of highly reactive [free radicals](/source/Radical_(chemistry)) inside blood cells, altering the properties of their [cell membranes](/source/Cell_membrane). This leads to [blood cell aggregation](/source/Erythrocyte_aggregation) and increased blood [viscosity](/source/Viscosity), which results in impaired blood flow.[15]

Another way glycated hemoglobin causes damage is via [inflammation](/source/Inflammation), which results in [atherosclerotic](/source/Atherosclerosis) plaque ([atheroma](/source/Atheroma)) formation. Free-radical build-up promotes the [excitation](/source/Excited_state) of [Fe2+](/source/Ferrous)-hemoglobin through [Fe3+](/source/Ferric)-Hb into abnormal [ferryl](/source/Ferryl) hemoglobin (Fe4+-Hb). Fe4+ is unstable and reacts with specific [amino acids](/source/Amino_acid) in hemoglobin to regain its Fe3+ [oxidation state](/source/Oxidation_state). Hemoglobin molecules clump together via [cross-linking reactions](/source/Cross-link), and these hemoglobin clumps (multimers) promote cell damage and the release of Fe4+-hemoglobin into the [matrix](/source/Extracellular_matrix) of innermost layers ([subendothelium](/source/Tunica_intima)) of arteries and veins. This results in increased permeability of interior surface ([endothelium](/source/Endothelium)) of blood vessels and production of pro-inflammatory [monocyte](/source/Monocyte) [adhesion](/source/Adhesion) proteins, which promote [macrophage](/source/Macrophage) accumulation in blood vessel surfaces, ultimately leading to harmful plaques in these vessels.[15]

Highly glycated Hb-[AGEs](/source/Advanced_glycation_end-product) go through [vascular smooth muscle](/source/Vascular_smooth_muscle) layer and inactivate [acetylcholine](/source/Acetylcholine)-induced endothelium-dependent relaxation, possibly through binding to [nitric oxide](/source/Nitric_oxide) (NO), preventing its normal function. NO is a potent [vasodilator](/source/Vasodilation) and also inhibits the formation of plaque-promoting [LDLs](/source/Low-density_lipoprotein) (sometimes called "bad cholesterol") [oxidized](/source/Redox) form.[15]

This overall degradation of blood cells also releases [heme](/source/Heme) from them. Loose heme can cause oxidation of endothelial and LDL proteins, which results in plaques.[15]

Glycation pathway via Amadori rearrangement (in HbA1c, R is typically N-terminal valine).[16]

## Principle in medical diagnostics

Glycation of proteins is a frequent occurrence, but in the case of hemoglobin, a nonenzymatic condensation reaction occurs between glucose and the N-end of the [beta chain](/source/Beta_chain). This reaction produces a [Schiff base](/source/Schiff_base) (R−N=CHR', R=beta chain, CHR'=glucose-derived), which is itself converted to 1-deoxyfructose. This second conversion is an example of an [Amadori rearrangement](/source/Amadori_rearrangement).[*[citation needed](https://en.wikipedia.org/wiki/Wikipedia:Citation_needed)*]

When blood glucose levels are high, [glucose](/source/Glucose) molecules attach to the hemoglobin in [red blood cells](/source/Red_blood_cell). The longer hyperglycemia occurs in blood, the more glucose binds to hemoglobin in the red blood cells and the higher the glycated hemoglobin.[17]

Once a hemoglobin molecule is glycated, it remains that way. A buildup of glycated hemoglobin within the red cell, therefore, reflects the average level of glucose to which the cell has been exposed during its [life cycle](/source/Red_blood_cell#Life_cycle). Measuring glycated hemoglobin assesses the effectiveness of therapy by monitoring long-term serum glucose regulation.

A1c is a weighted average of blood glucose levels during the life of the red blood cells (117 days for men and 106 days in women[18]). Therefore, glucose levels on days nearer to the test contribute substantially more to the level of A1c than the levels on days further from the test.[19]

This is also supported by data from clinical practice showing that HbA1c levels improved significantly after 20 days from the start or intensification of glucose-lowering treatment.[20]

## Measurement

Several techniques are used to measure hemoglobin A1c. Laboratories may use [high-performance liquid chromatography](/source/High-performance_liquid_chromatography), [immunoassay](/source/Immunoassay), [enzymatic](/source/Enzymatic) assay, [capillary electrophoresis](/source/Capillary_electrophoresis), or [boronate affinity chromatography](/source/Boronate_affinity_chromatography). [Point of care](/source/Point_of_care) (e.g., doctor's office) devices use immunoassay boronate affinity chromatography.[17]

In the United States, HbA1c testing laboratories are certified by the National Glycohemoglobin Standardization Program to standardize them against the results of the 1993 [Diabetes Control and Complications Trial](/source/Diabetes_Control_and_Complications_Trial) (DCCT).[21] An additional percentage scale, Mono S has previously been in use by Sweden and KO500 is in use in Japan.[22][23]

### Switch to IFCC units

The American Diabetes Association, [European Association for the Study of Diabetes](/source/European_Association_for_the_Study_of_Diabetes), and [International Diabetes Federation](/source/International_Diabetes_Federation) have agreed that, in the future, HbA1c is to be reported in the [International Federation of Clinical Chemistry and Laboratory Medicine](/source/International_Federation_of_Clinical_Chemistry_and_Laboratory_Medicine) (IFCC) units.[24] IFCC reporting was introduced in Europe except for the UK in 2003;[25] the UK carried out dual reporting from 1 June 2009[26] until 1 October 2011.

Conversion between DCCT and IFCC is by the following equation:[27]

- I F C C H B A 1 c ( mmol mol ) = [ D C C T H B A 1 c ( % ) − 2.14 ] × 10.929 {\displaystyle \mathrm {IFCC\ HBA1c} \,{\Big (}{\frac {\text{mmol}}{\text{mol}}}{\Big )}=[\mathrm {DCCT\ HBA1c} \,(\%)-2.14]\times 10.929}

"IFCC" HbA1c "DCCT" HbA1c "Mono S" HbA1c[23] (mmol/mol) (%) (%) 10 3.1 2.0 20 4.0 2.9 30 4.9 3.9 40 5.8 4.8 45 6.3 5.3 50 6.7 5.8 55 7.2 6.3 60 7.6 6.8 65 8.1 7.2 70 8.6 7.7 80 9.5 8.7 90 10.4 9.6 100 11.3 10.6

## Interpretation of results

Laboratory results may differ depending on the analytical technique, the age of the subject, and biological variation among individuals. Higher levels of HbA1c are found in people with persistently elevated blood sugar, as in [diabetes mellitus](/source/Diabetes_mellitus). While diabetic patient treatment goals vary, many include a target range of HbA1c values. A diabetic person with good glucose control has an HbA1c level that is close to or within the reference range.[*[citation needed](https://en.wikipedia.org/wiki/Wikipedia:Citation_needed)*]

The International Diabetes Federation and the American College of Endocrinology recommend HbA1c values below 48 mmol/mol (6.5 DCCT %), while the [American Diabetes Association](/source/American_Diabetes_Association) recommends HbA1c be below 53 mmol/mol (7.0 DCCT %) for most patients.[28] Results from large trials in 2008–09 suggested that a target below 53 mmol/mol (7.0 DCCT %) for older adults with type 2 diabetes may be excessive: Below 53 mmol/mol, the health benefits of reduced A1c become smaller, and the intensive glycemic control required to reach this level leads to an increased rate of dangerous hypoglycemic episodes.[29]

A retrospective study of 47,970 type 2 diabetes patients, aged 50 years and older, found that patients with an HbA1c more than 48 mmol/mol (6.5 DCCT %) had an increased mortality rate,[30] but a later international study contradicted these findings.[31][32][33]

A review of the [UKPDS](/source/UKPDS), Action to Control Cardiovascular Risk in Diabetes (ACCORD), Advance and Veterans Affairs Diabetes Trials (VADT) estimated that the risks of the main complications of diabetes ([diabetic retinopathy](/source/Diabetic_retinopathy), [diabetic nephropathy](/source/Diabetic_nephropathy), [diabetic neuropathy](/source/Diabetic_neuropathy), and [macrovascular disease](/source/Macrovascular_disease)) decreased by about 3% for every 1 mmol/mol decrease in HbA1c.[34]

However, a trial by ACCORD designed specifically to determine whether reducing HbA1c below 42 mmol/mol (6.0 DCCT %) using increased amounts of medication would reduce the rate of cardiovascular events found higher mortality with this intensive therapy, so much so that the trial was terminated 17 months early.[35]

Practitioners must consider patients' health, their risk of hypoglycemia, and their specific health risks when setting a target HbA1c level. Because patients are responsible for averting or responding to their own hypoglycemic episodes, their input and the doctors' assessments of the patients' [self-care](/source/Self-care) skills are also important.[*[citation needed](https://en.wikipedia.org/wiki/Wikipedia:Citation_needed)*]

Persistent elevations in blood sugar (and, therefore, HbA1c) increase the risk of long-term vascular complications of diabetes, such as [coronary disease](/source/Coronary_disease), [heart attack](/source/Heart_attack), [stroke](/source/Stroke), [heart failure](/source/Heart_failure), [kidney failure](/source/Chronic_kidney_disease), [blindness](/source/Blindness), [erectile dysfunction](/source/Erectile_dysfunction), [neuropathy](/source/Neuropathy) (loss of sensation, especially in the feet), [gangrene](/source/Gangrene), and [gastroparesis](/source/Gastroparesis) (slowed emptying of the stomach). Poor blood glucose control also increases the risk of short-term complications of surgery, such as poor [wound healing](/source/Wound_healing).[*[citation needed](https://en.wikipedia.org/wiki/Wikipedia:Citation_needed)*]

[All-cause mortality](/source/Mortality_rate) is higher above 64 mmol/mol (8.0 DCCT%) HbA1c as well as below 42 mmol/mol (6.0 DCCT %) in diabetic patients, and above 42 mmol/mol (6.0 DCCT %) as well as below 31 mmol/mol (5.0 DCCT %) in non-diabetic persons, indicating the risks of [hyperglycemia](/source/Hyperglycemia) and [hypoglycemia](/source/Hypoglycemia), respectively.[7] Similar risk results are seen for [cardiovascular disease](/source/Cardiovascular_disease).[7]

The 2022 ADA guidelines reaffirmed the recommendation that HbA1c should be maintained below 7.0% for most patients. Higher target values are appropriate for children and adolescents, patients with extensive co-morbid illness and those with a history of severe hypoglycemia. More stringent targets (<6.0%) are preferred for pregnant patients if this can be achieved without significant hypoglycemia.[36]

### Factors other than glucose that affect A1c

Lower-than-expected levels of HbA1c can be seen in people with shortened red blood cell lifespans, such as with [glucose-6-phosphate dehydrogenase deficiency](/source/Glucose-6-phosphate_dehydrogenase_deficiency), [sickle-cell disease](/source/Sickle-cell_disease), or any other condition causing premature red blood cell death. For these patients, alternate assessment with [fructosamine](/source/Fructosamine) or glycated [albumin](/source/Albumin) is recommended; these methods reflect glycemic control over the preceding 2–3 weeks.[37] Blood donation will result in rapid replacement of lost RBCs with newly formed red blood cells. Since these new RBCs will have only existed for a short period of time, their presence will lead HbA1c to underestimate the actual average levels. There may also be distortions resulting from [blood donation](/source/Blood_donation) during the preceding two months, due to an abnormal synchronization of the age of the RBCs, resulting in an older than normal average blood cell life (resulting in an overestimate of actual average blood glucose levels). Conversely, higher-than-expected levels can be seen in people with a longer red blood cell lifespan, such as with iron deficiency.[38]

Results can be unreliable in many circumstances, for example after blood loss, after surgery, blood transfusions, anemia, or high erythrocyte turnover; in the presence of chronic renal or liver disease; after administration of high-dose vitamin C; or [erythropoetin](/source/Erythropoetin) treatment.[39][40] [Hypothyroidism](/source/Hypothyroidism) can artificially raise the A1c.[41][42][43] In general, the [reference range](/source/Reference_range) (that found in healthy young persons), is about 30–33 mmol/mol (4.9–5.2 DCCT %).[44] The mean HbA1c for diabetics type 1 in Sweden in 2014 was 63 mmol/mol (7.9 DCCT%) and for type 2, 61 mmol/mol (7.7 DCCT%).[45] HbA1c levels show a small, but statistically significant, progressive uptick with age; the clinical importance of this increase is unclear.[37]

A study indicated that it is possible to predict HbA1c values years in advance, by analyzing blood glucose patterns measured using [continuous glucose monitors](/source/Continuous_glucose_monitors) [46]

### Mapping from A1c to estimated average glucose

The approximate mapping between HbA1c values given in DCCT percentage (%) and eAG (estimated average glucose) measurements is given by the following equation:[39]

- eAG(mg/dL) = 28.7 × A1c − 46.7 eAG(mmol/L) = 1.59 × A1c − 2.59 (Data in parentheses are 95% [confidence intervals](/source/Confidence_interval)>)

HbA1c eAG % mmol/mol[47] mmol/L mg/dL 5 31 5.4 (4.2–6.7) 97 (76–120) 6 42 7.0 (5.5–8.5) 126 (100–152) 7 53 8.6 (6.8–10.3) 154 (123–185) 8 64 10.2 (8.1–12.1) 183 (147–217) 9 75 11.8 (9.4–13.9) 212 (170–249) 10 86 13.4 (10.7–15.7) 240 (193–282) 11 97 14.9 (12.0–17.5) 269 (217–314) 12 108 16.5 (13.3–19.3) 298 (240–347) 13 119 18.1 (15–21) 326 (260–380) 14 130 19.7 (16–23) 355 (290–410) 15 140 21.3 (17–25) 384 (310–440) 16 151 22.9 (19–26) 413 (330–480) 17 162 24.5 (20–28) 441 (460–510) 18 173 26.1 (21–30) 470 (380–540) 19 184 27.7 (23–32) 499 (410–570)

### Normal, prediabetic, and diabetic ranges

The 2010 [American Diabetes Association](/source/American_Diabetes_Association) Standards of Medical Care in Diabetes added the HbA1c ≥ 48 mmol/mol (≥6.5 DCCT %) as another criterion for the diagnosis of diabetes.[48]

Diagnostic standard for HbA1c in diabetes[49] Diagnosis "IFCC" HbA1c "DCCT" HbA1c "Mono S" HbA1c Normal < 40 mmol/mol < 5.7% < 4.7% Prediabetes 40–47 mmol/mol 5.7–6.4% 4.7–5.4% Diabetes ≥ 48 mmol/mol ≥ 6.5% > 5.5%

## Indications and uses

Glycated hemoglobin testing is recommended for both checking the blood sugar control in people who might be prediabetic and monitoring blood sugar control in patients with more elevated levels, termed diabetes mellitus. For a single blood sample, it provides far more revealing information on glycemic behavior than a fasting blood sugar value. However, fasting blood sugar tests are crucial in making treatment decisions. The American Diabetes Association guidelines are similar to others in advising that the glycated hemoglobin test be performed at least twice a year in patients with diabetes who are meeting treatment goals (and who have stable glycemic control) and quarterly in patients with diabetes whose therapy has changed or who are not meeting glycemic goals.[50][36]

Glycated hemoglobin measurement is not appropriate where a change in diet or treatment has been made within six weeks. Likewise, the test assumes a normal red blood cell aging process and mix of hemoglobin subtypes (predominantly HbA in normal adults). Hence, people with recent blood loss, [hemolytic anemia](/source/Hemolytic_anemia), or genetic differences in the hemoglobin molecule ([hemoglobinopathy](/source/Hemoglobinopathy)) such as [sickle-cell disease](/source/Sickle-cell_disease) and other conditions, as well as those who have donated blood recently, are not suitable for this test.[51]

Due to glycated hemoglobin's variability, additional measures should be checked in patients at or near recommended goals. People with HbA1c values at 64 mmol/mol or less should be provided additional testing to determine whether the HbA1c values are due to averaging out high blood glucose ([hyperglycemia](/source/Hyperglycemia)) with low blood glucose ([hypoglycemia](/source/Hypoglycemia)) or the HbA1c is more reflective of an elevated blood glucose that does not vary much throughout the day. Devices such as continuous [blood glucose monitoring](/source/Blood_glucose_monitoring) allow people with diabetes to determine their blood glucose levels on a continuous basis, testing every few minutes. Continuous use of blood glucose monitors is becoming more common, and the devices are covered by many health insurance plans, including [Medicare](/source/Medicare_(United_States)) in the United States. The supplies tend to be expensive, since the sensors must be changed at least every 2 weeks. Another useful test in determining if HbA1c values are due to wide variations of blood glucose throughout the day is [1,5-anhydroglucitol](/source/1%2C5-Anhydroglucitol), also known as [GlycoMark](/source/GlycoMark). GlycoMark reflects only the times that the person experiences hyperglycemia above 180 mg/dL over a two-week period.[*[citation needed](https://en.wikipedia.org/wiki/Wikipedia:Citation_needed)*]

Concentrations of hemoglobin A1 (HbA1) are increased, both in diabetic patients and in patients with [kidney failure](/source/Kidney_failure), when measured by [ion-exchange chromatography](/source/Ion-exchange_chromatography). The thiobarbituric acid method (a chemical method specific for the detection of glycation) shows that patients with kidney failure have values for glycated hemoglobin similar to those observed in normal subjects, suggesting that the high values in these patients are a result of binding of something other than glucose to hemoglobin.[52]

In [autoimmune hemolytic anemia](/source/Autoimmune_hemolytic_anemia), concentrations of HbA1 is undetectable. Administration of [prednisolone](/source/Prednisolone) will allow the HbA1 to be detected.[53] The alternative [fructosamine](/source/Fructosamine) test may be used in these circumstances and it also reflects an average of blood glucose levels over the preceding 2 to 3 weeks.[54]

All the major institutions such as the International Expert Committee Report, drawn from the International Diabetes Federation, the European Association for the Study of Diabetes, and the American Diabetes Association, suggest the HbA1c level of 48 mmol/mol (6.5 DCCT %) as a diagnostic level.[55] The Committee Report further states that, when HbA1c testing cannot be done, the fasting and glucose-tolerance tests should be done. Screening for diabetes during pregnancy continues to require fasting and glucose-tolerance measurements for [gestational diabetes](/source/Gestational_diabetes) at 24 to 28 weeks gestation, although glycated hemoglobin may be used for screening at the first prenatal visit.[37]

## Modification by diet

[Meta-analysis](/source/Meta-analysis) has shown [probiotics](/source/Probiotic) to cause a statistically significant reduction in glycated hemoglobin in [type-2 diabetics](/source/Type_2_diabetes).[56] Trials with multiple strains of probiotics had statistically significant reductions in glycated hemoglobin, whereas trials with single strains did not.[56]

## Standardization and traceability

Most clinical studies recommend the use of HbA1c assays that are traceable to the DCCT assay.[57] The National Glycohemoglobin Standardization Program (NGSP) and IFCC have improved assay standardization.[37] For initial diagnosis of diabetes, only HbA1c methods that are NGSP-certified should be used, not [point-of-care testing](/source/Point-of-care_testing) devices.[36] Analytical performance has been a problem with earlier [point-of-care](/source/Point-of-care) devices for HbA1c testing, specifically large standard deviations and negative bias.[37]

## Veterinary medicine

HbA1c testing has not been found useful in the monitoring during the treatment of cats and dogs with diabetes, and is not generally used; monitoring of [fructosamine](/source/Fructosamine) levels is favoured instead.[58]

## See also

- [Diabetes mellitus](/source/Diabetes_mellitus)

- [Hemoglobin A2](/source/Hemoglobin_A2)

- [Prediabetes](/source/Prediabetes)

- [Proteopedia](/source/Proteopedia): [Structure of glycated hemoglobin](https://proteopedia.org/wiki/index.php/Glycated_hemoglobin)

## Notes

1. **[^](#cite_ref-1)** "Glycosylated haemoglobin" is a common misnomer because glycation and glycosylation are different processes, of which only the former is relevant in this case. Glycation is a non-enzymatic process, while glycosylation is enzymatic.

## References

1. **[^](#cite_ref-pmid12192669_2-0)** Bunn HF, Higgins PJ (July 1981). "Reaction of monosaccharides with proteins: possible evolutionary significance". *Science*. **213** (4504): 222–4. [Bibcode](/source/Bibcode_(identifier)):[1981Sci...213..222B](https://ui.adsabs.harvard.edu/abs/1981Sci...213..222B). [doi](/source/Doi_(identifier)):[10.1126/science.12192669](https://doi.org/10.1126%2Fscience.12192669). [PMID](/source/PMID_(identifier)) [12192669](https://pubmed.ncbi.nlm.nih.gov/12192669).

1. **[^](#cite_ref-3)** McPherson JD, Shilton BH, Walton DJ (March 1988). "Role of fructose in glycation and cross-linking of proteins". *Biochemistry*. **27** (6): 1901–7. [doi](/source/Doi_(identifier)):[10.1021/bi00406a016](https://doi.org/10.1021%2Fbi00406a016). [PMID](/source/PMID_(identifier)) [3132203](https://pubmed.ncbi.nlm.nih.gov/3132203).

1. **[^](#cite_ref-4)** Pongudom, Saranya (1 November 2019). ["Determination of Normal HbA1C Levels in Non-Diabetic Patients with Hemoglobin E"](http://www.annclinlabsci.org/content/49/6/804.long). *[Annals of Clinical & Laboratory Science](/source/Annals_of_Clinical_%26_Laboratory_Science)*. **49** (6): 804–9. [PMID](/source/PMID_(identifier)) [31882432](https://pubmed.ncbi.nlm.nih.gov/31882432).

1. **[^](#cite_ref-pmid16112961_5-0)** Miedema K (2005). "Standardization of HbA1c and Optimal Range of Monitoring". *Scandinavian Journal of Clinical and Laboratory Investigation*. **240**: 61–72. [doi](/source/Doi_(identifier)):[10.1080/00365510500236143](https://doi.org/10.1080%2F00365510500236143). [PMID](/source/PMID_(identifier)) [16112961](https://pubmed.ncbi.nlm.nih.gov/16112961). [S2CID](/source/S2CID_(identifier)) [30162967](https://api.semanticscholar.org/CorpusID:30162967).

1. ^ [***a***](#cite_ref-umich_6-0) [***b***](#cite_ref-umich_6-1) Elizabeth Weiser Caswell Diabetes Institute. [Hemoglobin A1c Fact Sheet](https://diabetes.med.umich.edu/about/resources-health-professionals/hemoglobin-a1c-fact-sheet). Accessed 2024-07-02.

1. **[^](#cite_ref-7)** ["2. Glycated haemoglobin (HbA1c) for the diagnosis of diabetes"](https://www.ncbi.nlm.nih.gov/books/NBK304271/). [*Use of Glycated Haemoglobin (HbA1c) in the Diagnosis of Diabetes Mellitus: Abbreviated Report of a WHO Consultation*](https://www.ncbi.nlm.nih.gov/books/NBK304267/). WHO Guidelines Approved by the Guidelines Review Committee. World Health Organization. 2011. [PMID](/source/PMID_(identifier)) [26158184](https://pubmed.ncbi.nlm.nih.gov/26158184). NBK304271.

1. ^ [***a***](#cite_ref-pmid28760792_8-0) [***b***](#cite_ref-pmid28760792_8-1) [***c***](#cite_ref-pmid28760792_8-2) Cavero-Redondo I, Peleteiro B, Martínez-Vizcaíno V (2017). ["Glycated haemoglobin A1c as a risk factor of cardiovascular outcomes and all-cause mortality in diabetic and non-diabetic populations: a systematic review and meta-analysis"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5642750). *[BMJ Open](/source/BMJ_Open)*. **7** (7) e015949. [doi](/source/Doi_(identifier)):[10.1136/bmjopen-2017-015949](https://doi.org/10.1136%2Fbmjopen-2017-015949). [PMC](/source/PMC_(identifier)) [5642750](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5642750). [PMID](/source/PMID_(identifier)) [28760792](https://pubmed.ncbi.nlm.nih.gov/28760792).

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1. **[^](#cite_ref-27)** ["Standardisation of the reference method for the measurement of HbA1c to improve diabetes care"](https://web.archive.org/web/20110722031224/http://www.acb.org.uk/docs/hba1c.pdf) (PDF) (Press release). [Association for Clinical Biochemistry and Laboratory Medicine](/source/Association_for_Clinical_Biochemistry_and_Laboratory_Medicine) (with [Diabetes UK](/source/Diabetes_UK)). April 2008. Archived from [the original](http://www.acb.org.uk/docs/hba1c.pdf) (PDF) on 2011-07-22. Retrieved 2009-07-02.

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## External links

Wikimedia Commons has media related to [Glycated hemoglobin](https://commons.wikimedia.org/wiki/Category:Glycated_hemoglobin).

[Scholia](https://www.wikidata.org/wiki/Wikidata:Scholia) has a profile for [**glycated haemoglobin (Q311213)**](https://iw.toolforge.org/scholia/Q311213).

- [Health Information: Diabetes](https://www.niddk.nih.gov/health-information/diabetes) — National Institutes of Health (NIH): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) - [National Diabetes Information Clearinghouse](https://web.archive.org/web/20100221034416/http://diabetes.niddk.nih.gov/) — NIDDK (old site, archived 2010-02-21)

- [Standards of Care in Diabetes](https://professional.diabetes.org/standards-of-care), American Diabetes Association Professional Practice Committee - [Standards of Care in Diabetes — 2024](https://ada.silverchair-cdn.com/ada/content_public/journal/care/issue/47/supplement_1/15/standards-of-care-2024.pdf) (pdf), American Diabetes Association Professional Practice Committee

v t e Clinical biochemistry blood tests Electrolytes Sodium Potassium Chloride Calcium Renal function Creatinine Urea BUN-to-creatinine ratio Plasma osmolality Serum osmolal gap Acid-base Anion gap Arterial blood gas Base excess Bicarbonate CO2 content Lactate Iron tests Ferritin Serum iron Transferrin saturation Total iron-binding capacity Transferrin Transferrin receptor Hormones ACTH stimulation test Thyroid function tests Thyroid-stimulating hormone Metabolism Blood glucose Hemoglobin A1c Lipid panel LDL HDL Triglycerides Total cholesterol Basic metabolic panel Comprehensive metabolic panel Cardiovascular Cardiac marker Troponin test CPK-MB test Lactate dehydrogenase Myoglobin Glycogen phosphorylase isoenzyme BB Liver function tests Proteins Human serum albumin Serum total protein ALP transaminases ALT AST AST/ALT ratio GGT Bilirubin Unconjugated Conjugated Pancreas Amylase Lipase Pancreatic lipase Small molecules Blood sugar level Hypoglycemia Hyperglycemia Nitrogenous Azotemia Hyperuricemia Hypouricemia Proteins LFT Elevated transaminases Elevated ALP Hypoproteinemia Hypoalbuminemia Hyperproteinemia Other Elevated alpha-fetoprotein

v t e Proteins that contain heme (hemoproteins) Globins Hemoglobin Subunits Alpha locus on 16: α HBA1 HBA2 pseudo ζ HBZ θ HBQ1 μ HBM Beta locus on 11: β HBB δ HBD γ HBG1 HBG2 ε HBE1 Tetramers stages of development: Embryonic Hb Gower 1 (ζ2ε2) Hb Gower 2 (α2ε2) Hb Portland I (ζ2γ2) Hb Portland II (ζ2β2) Hb Portland III (ζ2δ2) Fetal HbF/Fetal (α2γ2) HbA (α2β2) Adult HbA (α2β2) HbA2 (α2δ2) HbF/Fetal (α2γ2) pathology: HbH (β4) Barts (γ4) HbD (α2βD2) HbS (α2βS2) HbC (α2βC2) HbE (α2βE2) HbO (α2βO2) Compounds Carboxyhemoglobin Carbaminohemoglobin Oxyhemoglobin/Deoxyhemoglobin Sulfhemoglobin Other human Glycated hemoglobin Methemoglobin Nonhuman Chlorocruorin Erythrocruorin Other human: Myoglobin Metmyoglobin Neuroglobin Cytoglobin plant: Leghemoglobin Other Cytochrome Cytochrome b Cytochrome P450 Methemalbumin see also disorders of globin and globulin proteins

v t e Diabetes Types Type 1 Type 2 Type 3 Type 3c (pancreatogenic) Type 5 LADA Gestational diabetes Diabetes and pregnancy Prediabetes Impaired fasting glucose Impaired glucose tolerance Insulin resistance Ketosis-prone diabetes (KPD) MODY Type 1 2 3 4 5 6 Neonatal Transient Permanent MIDD Blood tests Blood sugar level Biomarkers Glycated hemoglobin Glucose tolerance test Postprandial glucose test Fructosamine Glucose test C-peptide Noninvasive glucose monitor Insulin tolerance test Homeostatic model assessment Management Prevention Diet in diabetes Diabetes medication Insulin therapy intensive conventional pulsatile Diabetic shoes Cure Embryonic stem cells Artificial pancreas Other Gastric bypass surgery Complications Diabetic comas Hypoglycemia Ketoacidosis Hyperosmolar hyperglycemic state Diabetic foot ulcer Neuropathic arthropathy Organs in diabetes Blood vessels Muscle Kidney Nerves Retina Heart Diabetes-related skin disease Diabetic dermopathy Diabetic bulla Diabetic cheiroarthropathy Diabetic foot ulcer Hyperglycemia Hypoglycemia Advocacy and organizations T1International Open Insulin Project Breakthrough T1D International Diabetes Federation World Diabetes Day Diabetes UK Other Outline of diabetes Glossary of diabetes Epidemiology of diabetes History of diabetes Notable people with type 1 diabetes

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Adapted from the Wikipedia article [Glycated hemoglobin](https://en.wikipedia.org/wiki/Glycated_hemoglobin) by Wikipedia contributors ([contributor history](https://en.wikipedia.org/wiki/Glycated_hemoglobin?action=history)). Available under [Creative Commons Attribution-ShareAlike 4.0 International](https://creativecommons.org/licenses/by-sa/4.0/). Changes may have been made.