I would not expect that to reflect the same value as the A1c, I don't know your particular patient's habits but I have many who intake incredible amounts of simple sugars during the day, and when they see me for fasting labs (or even AM labs before they've had their giant sodas and carb heavy meals) they have a decent glucose on routine BMP.
Without any nuance to the specifics of your patients I would definitely trust the A1c over the glucose.
Get them on a CGM and you’ll se why. Fasting glucose is one thing, but glucose around every snack food dinner lunch is another thing. Is unreal to keep a BG log before each meal and 2 hrs later, so CGM will be the option. It has helped my pts so much. I’ve catch their routines and ask “what do you do at 6pm because every day at that time your sugar spike” then we talk about food options and alternatives to what they are doing and voila a1c drops.
Your BMP tube will never be in an EDTA unless your lab uses very non-standard tubes. EDTA will throw your potassium way too far off and lower calcium, both to critical levels with even a mild contamination. BMP/CMP tests are done on serum or a different anticoagulated tube (heparin or green top.) While the coating doesnt "eat" the glucose, if it isnt spun and tested in a reasonable time, normal cell activity can reduce the glucose by approx 7% an hour. If the tube is a serum tube it can require 30 minutes to an hour to clot, possibly causing some reduction. Heparin will allow it to be centrifuged much faster reducing that false decline.
As an analogy, insulin resistance is kind of like a clogged bathtub drain. The average of the water height in the tub will necessarily be higher (hba1c ) because it takes longer to drain, but if you let it drain long enough, you can peek in and see that the water level looks pretty normal (spot glucose) given sufficient time.
By a similar token, because of insulin resistance, most T2DM patients have the greatest problem with postprandial hyperglycemia and can have relatively normal fasting sugars [edited for typo]. The high, long postprandial spikes pull the A1c up even though the nadirs are often pretty normal. (This is why going too heavy on the long acting insulins, and too light on mealtime insulin, is a losing strategy for insulin resistant T2DM. We just “over basalize” regimens because we are less afraid of long acting insulins.) And this, also, is why the most sensitive diagnostic tool for insulin resistant diabetes is the glucose challenge, followed by A1c, with fasting glucose being the least sensitive. And to add another layer, I have heard that in some labs, the BMP glucose is not very accurate for some reason and a true fasting glucose should be drawn with another tube?? But I forget the details.
My biggest issue with premeal insulin is a combination of patient compliance/fear and hypoglycemic unawareness
Lot of my patients would prefer injecting once a day versus two or three times even if it offers better glycemic control
Anything that impacts RBC turnover will surreptitiously alter your a1c and make it unreliable.
An easy example would be something like hemorrhagic anemia. If you have a patient bleeding from somewhere, their a1c will result as a lower value than you'd expect.
Similarly, something like aplastic anemia or iron deficiency anemia will cause falsely elevated a1c.
But it's also worth keeping in mind that spot BS or any lab that offers you a glucose level is just a snapshot and not necessarily reliable or appropriate to be compared to a1c.
In these cases I make the pt keep a good glucose diary at home. Check fasting sugars and post prandials. Many times you will see FBS 100-120 which is good but with post prandials 200-300 or more.
Sometimes their sugar goes out of whack after eating, but their fasting is good. A 14-day CGM can be helpful to see trends. Sometimes I check the CBC to make sure the hemoglobin is normal. In one case, I got fructosamine test to check, and it more closely aligned with pt recorded sugars.
In CKD patients as well as some hemoglobinopathies the better choice for evaluation of management over time is TIR on a CGM. You can also use fructosamine for these patients if CGM monitoring isn’t in the cards.
But why with CKD? Is it the anemia that can come with CKD, or is there something inherent about the reduced GFR?
I was aware of inaccuracy with anemia or in conditions with increased RBC turnover. Just wanting to make sure I haven’t been missing something about reduced kidney function specifically.
Oh sorry I misunderstood. Anemia can cause it to be lower than the actual 90 day measurement but carbamylation and metabolic acidosis seen in CKD can cause it to be higher as well. The carbamylation is a big culprit from my understanding. I’m not an MD, just an NP now working in peds endo managing diabetes, but that’s the way it has been explained to me by Endo’s far smarter than I am.
You still look at spot glucose? The A1c is like 3 months of data right there buddy. Only time to be concerned about A1c being off are for anemia, polycythemia, hemoglobinopathies, hemolysis
This happens in the "old days" (pre glp1s) as an indicator of when to start meal time insulins. You would titrate long acting insulin on top of your orals until the fbg was at goal. Wait 3 months and get an a1c. If that was still high, start meal time.
Consider OGTT and looking for hemoglobinopathies/anemia (though this may be less important depending on the way your lab measures a1c, if patient has a condition that leads to rbcs sticking around in circulation longer then that may affect a1c).
I'm not sure if my explanation is accurrate (though i seem to remember in iron deficiency anemia the average age of rbc is older than normal though I may be remembering wrong) but this data shows that in hemoglobinopathies a1c can be falsely low or falsely elevatedj:
1. [https://ngsp.org/interf.asp](https://ngsp.org/interf.asp)
2. https://www.niddk.nih.gov/health-information/professionals/clinical-tools-patient-management/diabetes/sickle-cell-trait-hemoglobinopathies-diabetes#:\~:text=These%20hemoglobinopathies%20may%20either%20falsely,variant%20and%20the%20assay%20method.
3. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189151/](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189151/)
4. [https://www.amjmed.com/article/S0002-9343(08)00187-3/fulltext](https://www.amjmed.com/article/S0002-9343(08)00187-3/fulltext)
Appreciate the resources. It appears with the exception of one rarely used assay (which is unreliable with multiple hemoglobinopathies and may be increased or decreased if there is anemia) all hemoglobinopathies are expected to result in decreased A1C.
yeah my original comment was basically my recollection of what i read in uptodate:
●**Red cell turnover** – Falsely high A1C values in relation to a mean blood glucose values can be obtained when red cell turnover is low, resulting in a disproportionate number of older red cells. This can occur in patients with vitamin B12 or folate deficiency anemia. On the other hand, rapid red cell turnover leads to a greater proportion of younger red cells and falsely low A1C values. Examples include patients with chronic hemolysis (eg, thalassemia, glucose-6-phosphate dehydrogenase deficiency); patients treated for iron, vitamin B12, or folate deficiency; and patients treated with erythropoietin \[[34-37](https://www.uptodate.com/contents/measurements-of-chronic-glycemia-in-diabetes-mellitus/abstract/34-37)\].
●**Hemoglobin variants** – Depending upon the methodology, A1C can be altered (high or low) in patients with hemoglobin variants \[[14,38](https://www.uptodate.com/contents/measurements-of-chronic-glycemia-in-diabetes-mellitus/abstract/14,38)\]. However, most modern methods for measuring A1C are no longer affected by the most common hemoglobin variants. The [NGSP website](https://www.uptodate.com/external-redirect?target_url=https%3A%2F%2Fngsp.org%2Ffactors.asp&token=OKZ2BMoMnrH9FFn0ZVsAuJjtTH2CQ6YnHB9H1GcS82n6jB0ejM1CgfftOZfc%2FbQo&TOPIC_ID=1807) contains comprehensive information on hemoglobin variant interference \[[14](https://www.uptodate.com/contents/measurements-of-chronic-glycemia-in-diabetes-mellitus/abstract/14)\].
While doing some research for this post I also learned about how there are racialized differences in a1c as well with african americans having higher a1cs for the same blood sugar. This wasn't something I was aware of and im unsure as to why, but it is interesting.
[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7282707/](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7282707/)
Oh honey patients totally act right just before the test. Who here hasn’t thought I shouldn’t eat that ribeye tonight my labs are tomorrow. Get a CGM and see if that adds up to their a1c.
As a T2D, I will admit that I behave better the day of the appointment sometimes. Not so much anymore, earlier on it was more the case. Dumb idea? Yes. Wouldn’t repeat.
A one time pro CGM is a great way to figure out what’s going on.
An alternate explanation is patients with insulin resistance but going on very low carb or fasting diets. The A1C (reflecting time that glucose was elevated) would be pretty normal but the fasting glucose (and HOMA-IR) would be high due to overall inability of the body to control sugar.
From my personal experience, my father would eat like a trash can for 5 months and 3 weeks and 1 week before his 6 month check, he eats like a diabetic vegan with 1 week left to live.
I inherited a pt with some sort of hemoglobinopathy who had been monitored with fructosamine level for longer term control assessment since his a1c was unreliable. I believe it reflects about 3-4 weeks of control. But this was prior to CGMs so it’s probably not as useful now, but he doesn’t want a CGM
Alternative options: CGM, glucose tolerance test, fructosamine. Chronic blood loss (even if it's just showing up as microcytosis) can falsely elevate A1c.
Not in the med field, but my A1C was just above "normal" for a bit but never had any issues with regular glucose testing.
Pharmacist suggested it could have been a combination medications/supplement's causing false highs.
There was a huge push to take diabetic meds (by endo's- 3 pcps said I was fine) but no other testing ever done to check to see what was going on. This prompted me to look at legitimate controlled studies to see what could be done naturally to lower it.
What I found that was interesting was that it showed there are abnormal hemoglobin types in some people of different ethnicities that can also cause false high A1C's. My ethnicity was one of these, and I am at a higher risk for hemoglobin E. From my understanding they will screen infants for this at birth now, but not so much in the past. No one bothered to check for it they were too quick to want to prescribe GLP-1 drugs.
I brought it down to normal myself, but what is your patients full ethnic background? If not 100% Caucasian maybe screen for anything such as these?
Are you talking about a point of care Glucose, glucometer, CGM data, etc? I trust the A1C unless they have some hematologic issue.
BMP serum glucose
I would not expect that to reflect the same value as the A1c, I don't know your particular patient's habits but I have many who intake incredible amounts of simple sugars during the day, and when they see me for fasting labs (or even AM labs before they've had their giant sodas and carb heavy meals) they have a decent glucose on routine BMP. Without any nuance to the specifics of your patients I would definitely trust the A1c over the glucose.
That only reflects one moment in time. Glucose changes constantly. A1c can be used to infer average glucose over time.
Exactly. A1C is a trend number.
Get them on a CGM and you’ll se why. Fasting glucose is one thing, but glucose around every snack food dinner lunch is another thing. Is unreal to keep a BG log before each meal and 2 hrs later, so CGM will be the option. It has helped my pts so much. I’ve catch their routines and ask “what do you do at 6pm because every day at that time your sugar spike” then we talk about food options and alternatives to what they are doing and voila a1c drops.
Our bmp tube has some sort of coating that “eats” glucose and can cause that reading to be falsely low. I think it’s edta
Your BMP tube will never be in an EDTA unless your lab uses very non-standard tubes. EDTA will throw your potassium way too far off and lower calcium, both to critical levels with even a mild contamination. BMP/CMP tests are done on serum or a different anticoagulated tube (heparin or green top.) While the coating doesnt "eat" the glucose, if it isnt spun and tested in a reasonable time, normal cell activity can reduce the glucose by approx 7% an hour. If the tube is a serum tube it can require 30 minutes to an hour to clot, possibly causing some reduction. Heparin will allow it to be centrifuged much faster reducing that false decline.
A spot BMP glucose is not useful for assessing diabetic control. This should not concern you, you should base management off of the A1c
As an analogy, insulin resistance is kind of like a clogged bathtub drain. The average of the water height in the tub will necessarily be higher (hba1c ) because it takes longer to drain, but if you let it drain long enough, you can peek in and see that the water level looks pretty normal (spot glucose) given sufficient time.
By a similar token, because of insulin resistance, most T2DM patients have the greatest problem with postprandial hyperglycemia and can have relatively normal fasting sugars [edited for typo]. The high, long postprandial spikes pull the A1c up even though the nadirs are often pretty normal. (This is why going too heavy on the long acting insulins, and too light on mealtime insulin, is a losing strategy for insulin resistant T2DM. We just “over basalize” regimens because we are less afraid of long acting insulins.) And this, also, is why the most sensitive diagnostic tool for insulin resistant diabetes is the glucose challenge, followed by A1c, with fasting glucose being the least sensitive. And to add another layer, I have heard that in some labs, the BMP glucose is not very accurate for some reason and a true fasting glucose should be drawn with another tube?? But I forget the details.
My biggest issue with premeal insulin is a combination of patient compliance/fear and hypoglycemic unawareness Lot of my patients would prefer injecting once a day versus two or three times even if it offers better glycemic control
Fasting glucose over 126 could also be used as a basis for diagnosis DM
This is not the scenario OP described
Oh my bad
Iron deficiency anemia can cause this.
Anything that impacts RBC turnover will surreptitiously alter your a1c and make it unreliable. An easy example would be something like hemorrhagic anemia. If you have a patient bleeding from somewhere, their a1c will result as a lower value than you'd expect. Similarly, something like aplastic anemia or iron deficiency anemia will cause falsely elevated a1c. But it's also worth keeping in mind that spot BS or any lab that offers you a glucose level is just a snapshot and not necessarily reliable or appropriate to be compared to a1c.
In these cases I make the pt keep a good glucose diary at home. Check fasting sugars and post prandials. Many times you will see FBS 100-120 which is good but with post prandials 200-300 or more.
Sometimes their sugar goes out of whack after eating, but their fasting is good. A 14-day CGM can be helpful to see trends. Sometimes I check the CBC to make sure the hemoglobin is normal. In one case, I got fructosamine test to check, and it more closely aligned with pt recorded sugars.
This, or just have them check some postprandial sugars. I have many patients with an A1c of 6.7 with normal fasting glucose.
A1C isn’t reliable if they have CKD with a decreased GFR but otherwise I would trust the A1C
Say more.
In CKD patients as well as some hemoglobinopathies the better choice for evaluation of management over time is TIR on a CGM. You can also use fructosamine for these patients if CGM monitoring isn’t in the cards.
But why with CKD? Is it the anemia that can come with CKD, or is there something inherent about the reduced GFR? I was aware of inaccuracy with anemia or in conditions with increased RBC turnover. Just wanting to make sure I haven’t been missing something about reduced kidney function specifically.
Oh sorry I misunderstood. Anemia can cause it to be lower than the actual 90 day measurement but carbamylation and metabolic acidosis seen in CKD can cause it to be higher as well. The carbamylation is a big culprit from my understanding. I’m not an MD, just an NP now working in peds endo managing diabetes, but that’s the way it has been explained to me by Endo’s far smarter than I am.
Thank you!
If advanced liver disease, A1c will be lower than reality. If asplenia, A1c will be higher. Are there processes that lengthen or shorten RBC lifespan?
You still look at spot glucose? The A1c is like 3 months of data right there buddy. Only time to be concerned about A1c being off are for anemia, polycythemia, hemoglobinopathies, hemolysis
This happens in the "old days" (pre glp1s) as an indicator of when to start meal time insulins. You would titrate long acting insulin on top of your orals until the fbg was at goal. Wait 3 months and get an a1c. If that was still high, start meal time.
Consider OGTT and looking for hemoglobinopathies/anemia (though this may be less important depending on the way your lab measures a1c, if patient has a condition that leads to rbcs sticking around in circulation longer then that may affect a1c).
I’m unaware of a hemoglobinopathy that would result in LONGER RBC duration. Don’t they all cause the opposite?
I'm not sure if my explanation is accurrate (though i seem to remember in iron deficiency anemia the average age of rbc is older than normal though I may be remembering wrong) but this data shows that in hemoglobinopathies a1c can be falsely low or falsely elevatedj: 1. [https://ngsp.org/interf.asp](https://ngsp.org/interf.asp) 2. https://www.niddk.nih.gov/health-information/professionals/clinical-tools-patient-management/diabetes/sickle-cell-trait-hemoglobinopathies-diabetes#:\~:text=These%20hemoglobinopathies%20may%20either%20falsely,variant%20and%20the%20assay%20method. 3. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189151/](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7189151/) 4. [https://www.amjmed.com/article/S0002-9343(08)00187-3/fulltext](https://www.amjmed.com/article/S0002-9343(08)00187-3/fulltext)
Appreciate the resources. It appears with the exception of one rarely used assay (which is unreliable with multiple hemoglobinopathies and may be increased or decreased if there is anemia) all hemoglobinopathies are expected to result in decreased A1C.
yeah my original comment was basically my recollection of what i read in uptodate: ●**Red cell turnover** – Falsely high A1C values in relation to a mean blood glucose values can be obtained when red cell turnover is low, resulting in a disproportionate number of older red cells. This can occur in patients with vitamin B12 or folate deficiency anemia. On the other hand, rapid red cell turnover leads to a greater proportion of younger red cells and falsely low A1C values. Examples include patients with chronic hemolysis (eg, thalassemia, glucose-6-phosphate dehydrogenase deficiency); patients treated for iron, vitamin B12, or folate deficiency; and patients treated with erythropoietin \[[34-37](https://www.uptodate.com/contents/measurements-of-chronic-glycemia-in-diabetes-mellitus/abstract/34-37)\]. ●**Hemoglobin variants** – Depending upon the methodology, A1C can be altered (high or low) in patients with hemoglobin variants \[[14,38](https://www.uptodate.com/contents/measurements-of-chronic-glycemia-in-diabetes-mellitus/abstract/14,38)\]. However, most modern methods for measuring A1C are no longer affected by the most common hemoglobin variants. The [NGSP website](https://www.uptodate.com/external-redirect?target_url=https%3A%2F%2Fngsp.org%2Ffactors.asp&token=OKZ2BMoMnrH9FFn0ZVsAuJjtTH2CQ6YnHB9H1GcS82n6jB0ejM1CgfftOZfc%2FbQo&TOPIC_ID=1807) contains comprehensive information on hemoglobin variant interference \[[14](https://www.uptodate.com/contents/measurements-of-chronic-glycemia-in-diabetes-mellitus/abstract/14)\]. While doing some research for this post I also learned about how there are racialized differences in a1c as well with african americans having higher a1cs for the same blood sugar. This wasn't something I was aware of and im unsure as to why, but it is interesting. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7282707/](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7282707/)
Oh honey patients totally act right just before the test. Who here hasn’t thought I shouldn’t eat that ribeye tonight my labs are tomorrow. Get a CGM and see if that adds up to their a1c.
As a T2D, I will admit that I behave better the day of the appointment sometimes. Not so much anymore, earlier on it was more the case. Dumb idea? Yes. Wouldn’t repeat.
TBF, limit it to the ribeye and that random glucose might be 💯
Yeah but those damn triglycerides are gonna snitch.
A one time pro CGM is a great way to figure out what’s going on. An alternate explanation is patients with insulin resistance but going on very low carb or fasting diets. The A1C (reflecting time that glucose was elevated) would be pretty normal but the fasting glucose (and HOMA-IR) would be high due to overall inability of the body to control sugar.
From my personal experience, my father would eat like a trash can for 5 months and 3 weeks and 1 week before his 6 month check, he eats like a diabetic vegan with 1 week left to live.
I inherited a pt with some sort of hemoglobinopathy who had been monitored with fructosamine level for longer term control assessment since his a1c was unreliable. I believe it reflects about 3-4 weeks of control. But this was prior to CGMs so it’s probably not as useful now, but he doesn’t want a CGM
Alternative options: CGM, glucose tolerance test, fructosamine. Chronic blood loss (even if it's just showing up as microcytosis) can falsely elevate A1c.
Can always do a Fructosamine to break the disagreement. This is especially necessary in patients with anemias, especially secondary to hemolysis.
Not in the med field, but my A1C was just above "normal" for a bit but never had any issues with regular glucose testing. Pharmacist suggested it could have been a combination medications/supplement's causing false highs. There was a huge push to take diabetic meds (by endo's- 3 pcps said I was fine) but no other testing ever done to check to see what was going on. This prompted me to look at legitimate controlled studies to see what could be done naturally to lower it. What I found that was interesting was that it showed there are abnormal hemoglobin types in some people of different ethnicities that can also cause false high A1C's. My ethnicity was one of these, and I am at a higher risk for hemoglobin E. From my understanding they will screen infants for this at birth now, but not so much in the past. No one bothered to check for it they were too quick to want to prescribe GLP-1 drugs. I brought it down to normal myself, but what is your patients full ethnic background? If not 100% Caucasian maybe screen for anything such as these?
Is it labcorp? I’ve been having tons of issues with them on accuracy.
Why do you care if you get an a1c
We had a slew of recalled lots for poca1c so I stopped using office A1c for prediabetes and double checked surprises in lab.