Glycated

hemoglobin

Glycated hemoglobin (HbA1c, hemoglobin

A1c, A1c, or less commonly HbA1c,
HgbA1c, Hb1c, etc.) is a form of
hemoglobin (abbreviated Hb) that is
chemically linked to a sugar. Most
monosaccharides, including glucose,
galactose and fructose, spontaneously
(i.e. non-enzymatically) bind with
hemoglobin, when present in the
bloodstream of humans. However, glucose
is less likely to do so than galactose and
fructose (7.5 times less than fructose and
4.7 times less than galactose), which may
explain why glucose is used as the primary
metabolic fuel in humans.[1][2]

Glycated hemoglobin
MedlinePlus 003640

eMedicine 2049478

LOINC 41995-2
The formation of the sugar-Hb linkage
indicates the presence of excessive sugar
in the bloodstream, often indicative of
diabetes. A1C is of particular interest
because it is easy to detect.

The process by which sugars attach to Hb

is called glycation. HbA1c is a measure of
the beta-N-1-deoxy fructosyl component of
hemoglobin.[3]

It is measured primarily to determine the

three-month average blood sugar level and
can be used as a diagnostic test for
diabetes mellitus and as an assessment
test for glycemic control in people with
diabetes.[4] The test is limited to a three-
month average because the average
lifespan of a red blood cell is four months.
Since individual red blood cells have
varying lifespans, the test is used as a
limited measure of three 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 in a predictable
way. In diabetes, higher amounts of
glycated hemoglobin, indicating poorer
control of blood glucose levels, have been
associated with cardiovascular disease,
nephropathy, neuropathy, and retinopathy.
Terminology
Glycated hemoglobin is preferred over
glycosylated hemoglobin to reflect the
correct (non-enyzmatic) 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.[5]

The naming of HbA1c derives from

Hemoglobin type A being separated on
cation exchange chromatography. The
first fraction to separate, probably
considered to be pure Hemoglobin A, was
designated HbA0, and the following
fractions were designated HbA1a, HbA1b,
and HbA1c, in their order of elution.
Improved separation techniques have
subsequently led to the isolation of more
subfractions.[6]

History
Hemoglobin A1c was first separated from
other forms of hemoglobin by Huisman
and Meyering in 1958 using a
chromatographic column.[7] It was first
characterized as a glycoprotein by
Bookchin and Gallop in 1968.[8] Its
increase in diabetes was first described in
1969 by Samuel Rahbar et al.[9] The
reactions leading to its formation were
characterized by Bunn and his coworkers
in 1975.[10]

The use of hemoglobin A1c for monitoring

the degree of control of glucose
metabolism in diabetic patients was
proposed in 1976 by Anthony Cerami,
Ronald Koenig and coworkers.[11]

Damage mechanisms
Glycated hemoglobin causes an increase
of highly reactive free radicals inside blood
cells. Radicals alter blood cell membrane
properties. This leads to blood cell
aggregation and increased blood viscosity,
which results in impaired blood flow.[12]

Another way glycated Hb causes damage

is via inflammation, which results in
atherosclerotic plaque (atheroma)
formation. Free-radical build-up promotes
the excitation of Fe2+-Hb through Fe3+-Hb
into abnormal ferryl Hb (Fe4+-Hb). Fe4+ is
unstable and reacts with specific amino
acids in Hb to regain its Fe3+ oxidation
state. Hb molecules clump together via
cross-linking reactions,and these Hb
clumps (multimers) promote cell damage
and the release of Fe4+-Hb into the matrix
of innermost layers (subendothelium) of
arteries and veins. This results in
increased permeability of interior surface
(endothelium) of blood vessels and
production of pro-inflammatory monocyte
adhesion proteins, which promote
macrophage accumulation in blood vessel
surfaces, ultimately leading to harmful
plaques in these vessels.[12]

Highly glycated Hb-AGEs go through

vascular smooth muscle layer and
inactivate acetylcholine-induced
endothelium-dependent relaxation,
possibly through binding to nitric oxide
(NO), preventing its normal function. NO is
a potent vasodilator and also inhibits
formation of plaque-promoting LDLs (i.e.
“bad cholesterol”) oxidized form.[12]

This overall degradation of blood cells also

releases heme from them. Loose heme
can cause oxidation of endothelial and
LDL proteins, which results in plaques.[12]

Glycation pathway via Amadori Rearrangement (in

HbA1c, R is typically N-terminal valine).[13]

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. This reaction produces a
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. When blood glucose levels
are high, glucose molecules attach to the
hemoglobin in red blood cells. The longer
hyperglycemia occurs in blood, the more
glucose binds to hemoglobin in the red
blood cells and the higher the glycated
hemoglobin.

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. 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[14]). Therefore, glucose
levels on days nearer to the test contribute
substantially more to the level of A1c than
the levels in days further from the test.[15]

This is also supported by data from

clinical practice showing that HbA1c levels
improved significantly after 20 days from
start or intensification of glucose-lowering
treatment.[16]

Measurement
Several techniques are used to measure
hemoglobin A1c. Laboratories use high-
performance liquid chromatography (the
HbA1c result is calculated as a ratio to
total hemoglobin using a chromatogram);
immunoassay; enzymatic assay; capillary
electrophoresis; or boronate affinity
chromatography. Point of care (e.g.,
doctor's office) devices use immunoassay
ororonate affinity chromatography.

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 (DCCT).[17] An
additional percentage scale, Mono S has
previously been in use by Sweden and
KO500 is in use in Japan.[18][19]
Switch to IFCC units …

The American Diabetes Association,

European Association for the Study of
Diabetes, and International Diabetes
Federation have agreed that, in the future,
HbA1c is to be reported in the International
Federation of Clinical Chemistry and
Laboratory Medicine (IFCC) units.[20] IFCC
reporting was introduced in Europe except
for the UK in 2003;[21] the UK carried out
dual reporting from 1 June 2009 [22] until 1
October 2011.

Conversion between DCCT and IFCC is by

the following equation:[23]
IFCC-HbA1c DCCT-HbA1c Mono S- HbA1c[19]

(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. While diabetic patient
treatment goals vary, many include a
target range of HbA1c values. A diabetic
person with good glucose control has a
HbA1c level that is close to or within the
reference range.

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
recommends HbA1c be below
53 mmol/mol (7.0 DCCT %) for most
patients.[24] Recent results from large trials
suggest that a target below 53 mmol/mol
(7 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.[25]

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,[26] but a later
international study contradicted these
findings.[27][28][29]

A review of the 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, diabetic
nephropathy, diabetic neuropathy, and
macrovascular disease) decreased by
about 3% for every 1 mmol/mol decrease
in HbA1c.[30]
However, a trial by ACCORD designed
specifically to determine whether reducing
HbA1c below 6.0% 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.[31]

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 skills are also
important.

Persistent elevations in blood sugar (and,

therefore, HbA1c) increase the risk of long-
term vascular complications of diabetes,
such as coronary disease, heart attack,
stroke, heart failure, kidney failure,
blindness, erectile dysfunction, neuropathy
(loss of sensation, especially in the feet),
gangrene, and 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.
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,
sickle-cell disease, or any other condition
causing premature red blood cell death.
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, which
occurred as long as two months before
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 vitamin B12 or folate deficiency.[32]

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 treatment.[33] In
general, the reference range (that found in
healthy young persons), is about 30–
33 mmol/mol (4.9–5.2 DCCT %).[34] 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%).[35]

The approximate mapping between HbA1c

values given in DCCT percentage (%) and
eAG (estimated average glucose)
measurements is given by the following
equation:[33]

eAG(mg/dl) = 28.7 × A1C − 46.7

eAG(mmol/l) = 1.59 × A1C − 2.59
 Data in parentheses are 95% confidence
intervals
HbA1c eAG

% mmol/mol[36] 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
Standards of Medical Care in Diabetes
added the =HbA1c ≥ 48 mmol/mol (≥6.5
DCCT %) as another criterion for the
diagnosis of diabetes.[37]
Diagnostic Standard for HbA1C in Diabetes[38]
HbA1C Diagnosis

<5.7% Normal

5.7-6.4% Prediabetes

>6.5% Diabetes

Indications and use

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.[39]
Glycated hemoglobin measurement is not
appropriate where a change in diet or
treatment has been made within 6 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, or
genetic differences in the hemoglobin
molecule (hemoglobinopathy) such as
sickle-cell disease and other conditions, as
well as those who have donated blood
recently, are not suitable for this test.

Due to glycated hemoglobin's variability

(as shown in the table above), 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) with low blood glucose
(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 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, but not by
Medicare 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, also known as GlycoMark.
GlycoMark reflects only the times that the
person experiences hyperglycemia above
180 mg/dl over a two-week period.

Concentrations of hemoglobin A1 (HbA1)

are increased, both in diabetic patients
and in patients with kidney failure, when
measured by 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.[40]

In autoimmune hemolytic anemia,

concentrations of HbA1 is undetectable.
Administration of prednisolone will allow
the HbA1 to be detected.[41] The
alternative 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.

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.[42] The Committee Report
further states that, when HbA1c testing
cannot be done, the fasting and glucose-
tolerance tests be done.
Diagnosis of diabetes during pregnancy
continues to require fasting and glucose-
tolerance measurements for gestational
diabetes, and not the glycated
hemoglobin.

Modification by diet
Meta-analysis has shown probiotics to
cause a statistically significant reduction
in glycated hemoglobin in type 2
diabetics.[43] Trials with multiple strains of
probiotics had statistically significant
reductions in glycated hemoglobin,
whereas trials with single strains did
not.[43]
Standardization and
traceability
Hemoglobin A1c is now standardized and
traceable to IFCC methods HPLC-CE and
HPLC-MS. The change to the newer unit of
mmol/mol is part of this standardization.
The standardized test does not test for
iodine levels in the blood; hypothyroidism
or iodine supplementation are known to
artificially raise the A1c.[44]

Veterinary medicine
HbA1c has not been found useful in the
treatment of cats and dogs with diabetes,
and is not generally used; fructosamine is
favoured instead.[45]

See also
Diabetes mellitus
Hemoglobin A2
Prediabetes
Proteopedia: Structure of glycated
hemoglobin

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Hypothyroidism Falsely Raises HbA1c
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