Tag Archives: diabetes

Vabysmo better than Eylea?

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Yosemite/Rhine Studies: a critical analysis

The Yosemite and Rhine Studies were twin randomized, double-masked, multicenter non-inferiority trials comparing the efficacy of faricimab (Vabysmo) vs aflibercept (Eylea) in the treatment of diabetic macular edema.

The study abstract begins with the statement, “To reduce treatment burden and optimize patient outcomes in diabetic macular oedema, we present the 1-year results from two phase 3 trials of faricimab, a novel angiopoeitin-2 and vascular endothelial growth factor-A bispecific antibody.”  However, analysis of the data reveals the study report did NOT demonstrate reduced treatment burden at one year.  It did demonstrate potential non-inferiority of faricimab compared with aflibercept with an increased treatment burden in the faricimab arms of the studies. 

Treatment burden was greater in both faricimab treatment arms of both studies compared with aflibercept. Table 1 reveals 25% greater injections in the faricimab q8 week group compared with aflibercept.  The faricimab group received 10 injections at 52 weeks compared with aflibercept at 9 injections.  The faricimab group did not experienced a reduced treatment burden compared with aflibercept.  Moreover, the faricimab group sustained a more intense treatment burden to meet the “non-inferiority” assessment compared with aflibercept.  

Table 1. Injection schedule for faricimab (Fq8) and aflibercept (Aq8) q8 week study arms.

wk#1481216202428323640444852total
Fq81111110101010110
Aq8111110101010109

There was only one subgroup of eyes that received one less injection of faricimab at one year compared with aflibercept.  There were 63 eyes of 286 (22%) in Yosemite and 66 eyes of 308 (21%) in Rhine who underwent 7 faricimab injections within the group randomized to “personalized treatment interval” (PTI) compared with 8 injections in the aflibercept group.  Unfortunately, the visual and anatomic outcomes of this subgroup of faricimab eyes were reported a part of the entire PTI group, which overall had more injections than the aflibercept group. 

The primary outcome of the study was the number of letters of improvement on the standard ETDRS chart. However, because of the uneven staggered injection schedule between the q8 week treatments groups, the method to calculate the visual improvement outcome favored faricimab over aflibercept.  The study design called for averaging the measurements of visual improvement over a three-month time frame (i.e. at week 48, 52, and 56).  As a result, the three averaged measurements for faricimab (Fq8) was 4 weeks, 8 weeks, and 4 weeks post-injection (average 5.3 weeks), while the three measurements for aflibercept (Aq8) were 8, 4, and 8 weeks post injection (average 6.6 weeks).  Thus, the unevenly staggered injection schedule resulted in a final visual endpoint measurement inappropriately in favor of faricimab.  

Even in the subgroup of faricimab (Fpti) that touted one 16week treatment interval, the visual acuity measurements were taken at 16weeks, 4weeks, and 8 weeks post-injection.  This represents an average of 9.3 weeks post-injection; this is nowhere near the measurement taken at 16 weeks.  In addition, the acuity outcomes in the Fpti group were reported as a group without reporting the acuity gains made specifically by the subgroup of eyes extended to a 16-week interval.  Therefore, the reported acuity gains do not apply to this subgroup with extended treatment.       

A secondary outcome of the study was the central subfield macular thickness (CST).  This measurement shows the anatomic improvement in macular edema.  The slope of the thickness curve trended toward a more rapid decrease in both arms of faricimab compared with aflibercept during the monthly injection stage (initial loading stage).  Analysis of the results after the loading stage (monthly injections), both faricimab and aflibercept showed a similar jagged curve demonstrating a drop-off of treatment effect during the no-treatment month.  A similar jagged response is not seen in the Fpti group as the treatment intervals varied within that group.  The rebound in edema seen in both faricimab and aflibercept suggests the durability of the treatment effect may be similar.  These studies did not perform a direct comparison of faricimab and aflibercept on the same personalized treatment interval protocol.

Remarkably, these limitations of the study were not discussed in the published article and the FDA granted approval of faricimab for use in the United States based on these data drawn from an imperfect study design that favored faricimab.  More research is needed in order to determine if faricimab is truly non-inferior to aflibercept and whether faricimab may offer a reduced treatment burden.  

UPDATE Oct 2022: I have been using Vabysmo in the office. I am please with the results in patients with wet AMD in that I can extend the treatment interval further than with older drugs. However, patients with large serous pigment epithelial detachments (PED) appear to be at greater risk of vision loss from rips in the PED. I have not been impressed with superior effectiveness of Vabysmo in patients with diabetic retinopathy.

By Scott E. Pautler, MD

For a telemedicine consultation with Dr Pautler, please send email request to spautler@rvaf.com. We accept Medicare and most insurances in Florida. Please include contact information (including phone number) in the email. We are unable to provide consultation for those living outside the state of Florida with the exception of limited one-time consultations with residents of the following states: Alabama, Arkansas, Connecticut, Georgia, Minnesota, and Washington.

Copyright  © 2022 Designs Unlimited of Florida

Yosemite and Rhine Studies: an editorial

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Faricimab was recently approved by the FDA for the treatment of diabetic macular edema (DME). It is the first drug which simultaneously blocks vascular endothelial growth factor A (VEGF-A) and angiopoietin-2 (Ang 2). The anti-VEGF-A action is shared with bevacizumab, ranibizumab, and aflibercept; and stabilizes microvascular permeability and inhibits neovascularization. The Ang 2 inhibition works via the angiopoietin and Tie signaling pathway to reduce microvascular permeability by a pathway independent of VEGF-A blockade. Preclinical studies suggested that faricimab might be more effective than simple anti-VEGF inhibition in treating diabetic macular edema. In particular, there were expectations for improvement over the status quo in duration of action. If similar efficacy with lesser treatment burden were possible, this would help overtaxed clinicians and patients and begin to close the real-world versus randomized trial performance gap.1

The results of two identical, phase 3 randomized clinical trials, YOSEMITE and RHINE, were recently published, allowing clinicians the opportunity to assess how the efficacy of faricimab matches the promise of the preclinical studies.2 There were 3 groups in the randomization: faricimab 6 mg q 8 weeks (F8), faricimab 6 mg with a personalized treatment interval (FPTI), and aflibercept 2 mg q 8 weeks (A8). The study authors reported the following in their paper:

  1. With A8 as the comparator, both F8 and FPTI were noninferior (4 letter margin) based on a primary outcome of mean change in best-corrected visual acuity at 1 year, averaged over weeks 48, 52, and 56.
  2. There were no differences in safety events among the 3 groups.
  3. In the FPTI group, more than 70% of patients achieved every-12-week dosing or longer at 1 year.
  4. Reductions in CST and proportions of eyes without center-involved DME (CI-DME) over 1 year consistently favored faricimab over aflibercept.
  5. Faricimab demonstrated a potential for extended durability in treating CI-DME.

Based on the evidence in the paper, are the claims substantiated? 

With respect to noninferiority of mean change in best corrected visual acuity, the answer is qualified by the authors’ method of measurement. Because the three groups got last injections at different times, there was no single visit for which assessment of final visual acuity was intuitive. Therefore, the authors averaged the visual acuities measured at 48, 52, and 56 weeks. For the F8 group, the 3 components of the average were 4 weeks post-injection (the measurements taken at 48 weeks), 8 weeks post-injection (the measurements taken at 52 weeks), and 4 weeks post-injection (the measurements taken at 56 weeks), implying that the average last visual acuity was at 5.33 weeks post-injection ([4+8+4]/3=5.33). For the A8 group, the 3 components of the average were 8 weeks post-injection (the measurements taken at 48 weeks), 4 weeks post-injection (the measurements taken at 52 weeks), and 8 weeks post-injection (the measurements taken at 56 weeks), implying that the average last visual acuity was at 6.66 weeks post-injection ([8+4+8]/3=6.66). That is, the A8 group was disadvantaged relative to the F8 group by virtue of the F8 group having more injections in the first year, and an injection nearer to the outcome measurement times. This issue might have been averted had the F8 group received the same 5 initial monthly injections as the A8 group.    

It is difficult to provide an analogous comparative calculation for the FPTI group. The relevant information is depicted in figure 3B, but the scale of the figure is microscopic, and only estimates can be made. For example, the YOSEMITE panel of figure 3B, the red-boxed subgroup, appears to comprise 63 patients. For these patients, the 3 components of the average were 16 weeks post-injection (the measurements taken at 48 weeks), 4 weeks post-injection (the measurements taken at 52 weeks), and 8 weeks post-injection (the measurements taken at 56 weeks), implying that the average last visual acuity was at 9.3 weeks post-injection ([16+4+8]/3=9.3). Likewise, for the RHINE panel of figure 3B, the red-boxed subgroup, appears to comprise 67 patients with the average last visual acuity at 9.3 weeks.  At the other extreme of the figure (the bottom) sits the group of eyes that could never be extended beyond 4 weeks.  For YOSEMITE and RHINE this group appears to comprise 19 and 23 patients, respectively. The average last visual acuity for these eyes would be 4 weeks. In between these extremes of the figure, one would need to do an analogous calculation for every row in the figure, pooling all the results for an overall average. This is clearly more than a reader can be asked to do. The authors should have done it and reported the result in the paper, to allow the reader to see if the outcome time for the FPTI group is comparable to the A8 group. The suspicion is that they are not comparable.

Regarding the claim that the safety results of the three groups were equivalent, we agree with the authors’ interpretation. There is no evidence that faricimab is less safe to use over the 52 weeks of follow-up reported.

The authors claim that over 70% of the FPTI group were able to enter the q 12 week dosing interval. The specific term they chose was “achieved” to signal this distinction. However, entering 12 week dosing is different from demonstrating that faricimab can sustain such intervals. The primary outcome at 52 weeks did not give enough time to determine if those eyes entering 12 week or longer durations could sustain that performance, or whether they would regress to require shorter interval injections. In YOSEMITE, 169 eyes (59%) and in RHINE, 172 eyes (56%) completed one 12wk interval to be assessed for successful completion. The reader has no idea if this proportion will be sustained in the second year of the trial, and it would be an unfounded assumption to expect the entrance to q12 week intervals to be maintained. This outcome will be of great interest when the 2-year results are reported. Only 22%/21% (Yosemite/Rhine) actually completed a 16-week interval and none were treated long enough to determine sustainability of this interval.

Another problem with the authors’ claim on duration of effect has to do with a form of spin, specifically type 3 spin, in the classification of Demla and colleagues.3 A reader might think that this achievement by faricimab distinguishes it from aflibercept, but that inference would not be warranted because of the study design. There was no aflibercept personalized treatment interval arm of the randomization, which would be required to make a claim that increased duration between injections was an advantage of faricimab. While true that a drug company investing in faricimab has no obligation to provide an opportunity for the competitor’s comparator drug to perform as well, the authors cannot claim that the feature displayed by faricimab is a differentiator worthy of a clinician’s choice as a deciding factor in the question of which drug to use. It is also true that the authors don’t make this claim differentiating the drugs, but in presenting asymmetric evidence as they do, an erroneous inference is easy to make, which we seek to avert.

The authors’ claim of superior drying effectiveness for faricimab is supported by the presented data, but unremarked by the authors was evidence of similar durations of drying action of faricimab and aflibercept. To see this, examine figure 3C. The slope of the thickness curve trended toward a more rapid decrease in both arms of faricimab compared with aflibercept during the monthly injection stage (initial loading stage).  In an analysis of the graphs after the loading stage (monthly injections), both faricimab and aflibercept showed a similar jagged curve demonstrating a drop-off of treatment effect during the no-treatment month. A jagged response is not seen in the FPTI group because the treatment intervals varied within that group.  The zig-zag rebound of edema seen in both faricimab (F8) and aflibercept (A8) groups suggests the durability of the treatment effect may be similar between the two drugs.  These studies did not perform a direct comparison of faricimab and aflibercept on the same personalized treatment interval protocol.

The authors’ contention that faricimab rendered a higher proportion of eyes free of CI-DME is warranted by the data they present.

Finally, the authors emphasize the potential of faricimab for lesser burden of treatment because of potential longer durability. This emphasis is unsupported by the evidence presented. The F8 group received 10 injections. The A8 group received 9 injections – hence no decreased burden favoring faricimab over aflibercept in this comparison. It is more complicated to analyze in the FPTI group because the needed information is not reported, but we can make some inferences. There were 63 eyes of 286 (22%) in Yosemite and 66 eyes of 308 (21%) in Rhine that achieved the opportunity to extend treatment; these eyes underwent a total of 8 faricimab injections at week 52.  This number represents the least number of scheduled injections and only one less than the aflibercept group. The remainder of eyes were scheduled to have more than 8 injections, but the pooled average is difficult to parse from figure 3B.  We can easily note that from the figure that the greatest number of injections at week 52 in this arm of the study was 14 injections in eyes that required monthly treatment (19 eyes (7%) in Yosemite, and 22 eyes (7%) in Rhine).  This is far more than the 9 injections of A8, and does not demonstrate a reduced treatment burden among eyes in the faricimab group compared with aflibercept. When the remainder of eyes between the extremes of figure 3B are added in to the calculation of average treatment burden, which we encourage the authors to report, we suspect that it was greater for the FPTI arm of the study than for A8, not less.  

In summary, YOSEMITE and RHINE provide data that faricimab as administered in the studies was equivalent to aflibercept in the primary visual outcome, and superior to aflibercept as given in the study in drying the macula. No data were presented supporting a claim that treatment burden is less with faricimab than aflibercept. The published data show that a proportion of eyes can be managed with a reduced injection burden with faricimab, but provide no evidence that this would differentiate faricimab from aflibercept were aflibercept plugged into the same personal treatment interval algorithm. There was no arm of the study that would allow such a comparison to be made. The published data substantiate that faricimab has a greater macular drying effect than aflibercept, but the see-saw central subfield thickness curve in the non-loading phase of the first year suggests that the duration of drying by faricimab is no greater than with aflibercept.

The FDA has approved faricimab for the treatment of CI-DME based on YOSEMITE and RHINE. Retinal specialists will be making choices of which drug to use. An economic perspective will enter into the decision. The clinical decision will not be based exclusively on efficacy. The offered average costs for aflibercept and faricimab to the editorialists are $1747 and $2168, respectively. Is the $441 differential cost a reasonable price to pay for the documented differences in drug performance? Our opinion is no. There is no published difference in visual outcomes, nor any published difference in durability, because it wasn’t checked. There is a difference in macular drying, analogous to the superior drying effect of aflibercept over bevacizumab in the better-vision group of protocol T (eyes with CI-DME)or in the aflibercept versus bevacizumab group in SCORE-2 (eyes with central retinal vein occlusion with macular edema).4,5 We, and many others, did not think that differences warranted the use of aflibercept over the less expensive bevacizumab in cases similar to those in the better seeing group of protocol T or eyes like those studied in SCORE-2, nor do we think that drying difference seen in YOSEMITE and RHINE between faricimab and aflibercept is reason to choose the more expensive drug. We congratulate the authors of these studies for providing ophthalmologists with new options for treating diabetic macular edema, but nothing they have published suggests that this option marks a milestone in reducing treatment burden in DME. The 2-year results will be more informative for decision-making than the 1-year results, and we encourage the authors to remedy the flaws in their year -1 results data presentation so that the 2-year data are more useful.

By David J. Browning, MD, PhD and Scott E. Pautler, MD

References

   1.   Kiss S, Liu Y, Brown J, et al. Clinical utilization of anti-vascular endothelial growth-factor agents and patient monitoring in retinal vein occlusion and diabetic macular edema. Clin Ophthalmol 2014;8:1611-1621.

   2.   Wykoff CC, Abreu F, Adamis AP, et al. Efficacy, durability, and safety of intravitreal faricimab with extended dosing up to every 16 weeks in patients with diabetic macular oedema (YOSEMITE and RHINE): two randomised, double-masked, phase 3 trials. Lancet 2022;DOI:https://doi.org/10.1016/S0140-6736(22)00018-6.

   3.   Demla S, Shinn E, Ottwell R, Arthur W, Khattab M, Hartwell M, Wright DN, Vassar M. Evaluaton of “spin” in the abstracts of systematic reviews and meta-analyses focused on cataract therapies. Am J Ophthalmol 2021;228:47-57.

   4.   Diabetic Retinopathy Clinical Research Network, Welss JA, Glassman AR, Ayala AR, Jampol LM, Aiello LP, Antoszyk AN, Arnold-Bush AN, Baker CW, Bressler NM, Browning DJ, Elman MJ, Ferris FJ, Friedman SJ, Melia M, Pieramici D, Sun JK, Beck RW. Aflibercept, bevacizumab, or ranibizumab for diabetic macular edema. N Engl J Med 2015;372:1193-1203.

   5.   Scott IU, VanVeldhuisen PC, Ip MS, et al, SCORE2 Investigator group. Effect of bevacizumab vs aflibercept on visual acuity among patients with macular edema due to central retinal vein occlusion: the SCORE2 randomized clinical trial. JAMA 2017;317:2072-2087.

Diabetic Vitreous Hemorrhage

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Eye Anatomy

What is diabetic vitreous hemorrhage?

            Diabetic vitreous hemorrhage means blood has leaked into the vitreous gel of the eye as a result of diabetic damage. The vitreous is a clear gel that fills the center of the eye and helps to hold the retina in place against the eye-wall like wallpaper in a room.  The retina is a thin layer of delicate nerve tissue, which acts like film in a camera.  In the eye, light is focused onto the retina, which “takes the picture” and sends the image to the brain.  The retina has many fine blood vessels that may become damaged from diabetes leading to bleeding into the vitreous.  Blood in the vitreous (vitreous hemorrhage) interferes with vision. 

What symptoms does diabetic vitreous hemorrhage cause?

            Diabetic vitreous hemorrhage usually causes many new floaters in the vision.  Floaters may appear as round specks, hair-like or bug-like debris, or clouds moving in your vision as though they were in front of your eye.  They are more noticeable when looking at a blank surface and may interfere with the good vision in the fellow eye.  If vitreous hemorrhage is severe, the vision may be severely limited.  Patients may only see shadows or light, but no details.

            Flashes are brief streaks of light that are usually seen off to the side, especially at night when you turn your head or eyes.  Flashes are caused by vitreous gel pulling on the retina with eye movement.  They may be seen in the setting of diabetic vitreous hemorrhage, but are not worrisome in themselves.

Although many people have occasional floaters or flashes of light, the sudden onset of many new floaters with or without flashes is an important sign of abnormal pulling on the retina by the vitreous.  In some people with these symptoms, the retina may tear and detach resulting in loss of vision.  Therefore, these new symptoms warrant prompt evaluation.

What causes diabetic vitreous hemorrhage?

            Diabetes can cause vitreous hemorrhage by weakening the blood vessels in the retina and by causing the vitreous gel to shrink and pull on the retinal vessels.  Aging also causes changes in the vitreous gel and can cause it to pull on the retina.  In any given patient with diabetes, both weakened retinal blood vessels, as well as tugging on the blood vessels from the vitreous play a role in causing vitreous hemorrhage.  However, in some eyes weakened blood vessels may be the main reason and in other eyes the main reason for bleeding may be tugging from the vitreous.  This is an important issue as diabetic vitreous hemorrhage may be treated differently depending on its underlying cause.   

How is diabetic vitreous hemorrhage treated?

            The most important step is to have a thorough eye examination with ultrasonography.  The ultrasound machine uses sound waves to safely and effectively “look through” the blood in the vitreous to see if the retina is attached.  If a retinal detachment is found, surgery is required in an attempt to repair it.  If no retinal detachment is found on ultrasound exam, your doctor may allow the vitreous hemorrhage to clear on its own with time.  The ultrasound exam may be repeated periodically to assure the retina remains attached.  If the hemorrhage does not clear on its own, vitrectomy surgery as a one-day surgery in the hospital operating room may be considered.  The amount of visual return depends on several factors including the health of the underlying retina.     

            In an effort to prevent additional bleeding, the underlying diabetic retinopathy may be treated with medication injections (e.g. Avastin, Lucentis, or Eylea) into the eye.  These injections can usually be given without significant pain by using anesthetics.  The injections reduce the risk of future bleeding, but do not hasten the clearing of the bleeding that has already occurred.   These medication injections may be especially important if no previous laser (or insufficient laser) has been given for diabetic retinal damage (diabetic retinopathy) prior to the vitreous hemorrhage.  Medication injections do not help with tugging on the retinal blood vessels by the vitreous.  Indeed, in rare cases the injections may increase the tugging.  Therefore, if tugging from the vitreous is determined to be the main factor in causing the diabetic vitreous hemorrhage, injections may not be used.  Instead, vitrectomy surgery is more effective at relieving the tugging.  

            Once the vitreous hemorrhage has cleared over time with observation or with vitrectomy surgery, laser is often used to stabilize the retinal blood vessels that have been weakened from diabetes.  This helps reduce the chances of reoccurrence of vitreous hemorrhage in the future.

What should I be on the lookout for?

            After examination or treatment for a vitreous hemorrhage, you should notify your doctor if you have a burst of new floaters, a loss of side vision, or pain.  Sometimes, retinal tears or a retinal detachment occur at a later date after the examination.

By Scott E. Pautler, MD

For a telemedicine consultation with Dr Pautler, please send email request to spautler@rvaf.com. We accept Medicare and most insurances in Florida. Please include contact information (including phone number) in the email. We are unable to provide consultation for those living outside the state of Florida with the exception of limited one-time consultations with residents of the following states: Alabama, Arkansas, Connecticut, Georgia, Minnesota, and Washington.

Copyright 2021 Designs Unlimited of Florida.  All Rights Reserved.

Iluvien Fluocinolone Implant for Diabetic Macular Edema

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Iluvien
Iluvien Implant

What is the Iluvien implant?

The Iluvien implant is shaped like a small thin tube so that it can be injected into the eye in the office with a needle attached to an injector. The tube contains a corticosteroid medicine that is released into the eye slowly for up to 2-3 years. Repeated injections may be performed. When the tube-like implant is empty it remains in the eye and usually causes no problems.

What is the Iluvien implant used for?

The Iluvien implant decreases inflammation, leaky vessels and swelling inside the eye. It has been approved to treat diabetic macular edema. It helps keep the vision from worsening and may improve vision over time.

How is an Iluvien implant inserted into the eye?

Anesthetic solutions are used to make the procedure pain-free. The eye is treated with an iodine solution in an effort to prevent infection and an instrument is used to gently keep the lids open during the injection. A pressure sensation may be felt as the implant is injected into the eye with a very thin, short needle. The procedure is very brief.

What are the possible side-effects?

It is normal to experience a red area on the white of the eye, which disappears in one to two weeks. It is rare to see the tube floating in the vision. Most eyes require cataract surgery several months after injection of the implant. About 30-40% of eyes experience a pressure increase (glaucoma) in the eye. Although the pressure is not usually painful, it may require eye drops to prevent permanent loss of vision. In 1-5% of eyes, glaucoma surgery is needed. Rare risks of injection include bleeding, infection, retinal detachment, and loss of vision/loss of the eye. Please report any severe loss of vision to the doctor without delay.

How do I care for the eye?

You may be given eye drops and instructions on how to use them. Physical activity is not limited. Tylenol or Ibuprofen may be used if there is discomfort, but severe pain should be reported to your doctor without delay. If you have any questions or concerns, please call the office.

By Scott E. Pautler, MD

For a telemedicine consultation with Dr Pautler, please send email request to spautler@rvaf.com. We accept Medicare and most insurances in Florida. Please include contact information (including phone number) in the email. We are unable to provide consultation for those living outside the state of Florida with the exception of limited one-time consultations with residents of the following states: Alabama, Arkansas, Connecticut, Georgia, Minnesota, and Washington.

Copyright © 2014-2022 Designs Unlimited of Florida. All Rights Reserved.

Better Diabetes Management with the Hemoglobin A1c Test

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What is hemoglobin A1C?

Hemoglobin A1C is a blood test that measures the average blood sugar level in the blood over the past two or three months. Specifically, this test measures the amount of sugar that permanently attaches to hemoglobin, a protein in red blood cells. Because red blood cells live for about three months, this test shows the average blood sugar level during that time. This test gives some of the information that you could get if you measured your blood sugar every day continuously throughout the day and night.

Why is hemoglobin A1C important?

We know high blood sugar damages blood vessels and may cause blindness, kidney failure, nerve damage, amputation, heart attack, stroke, and premature death. Managing blood sugar dramatically reduces the risk of these complications. The hemoglobin A1C test helps to determine whether your blood sugar control has been adequate to minimize damage from diabetes.

Do I need both hemoglobin A1C and standard blood sugar testing?

Yes. Each test gives different information about blood sugar control. For example, your fasting blood sugar may be normal, but if your hemoglobin A1C is high, then you know there are times in the day that the blood sugars are too high and you are still at risk of having complications from diabetes. On the other hand, if your hemoglobin A1C is high, you need spot checks of the blood sugar level to know specifically what part of the day in which you may need to manage differently.

How do results from hemoglobin A1C compare with blood sugar levels?

The hemoglobin A1C test measures the percent of hemoglobin that is chemically bound to sugar. The normal range of hemoglobin A1C is 4-6%, which corresponds to an average blood sugar level of 60-120 mg/dl. Your doctor will help determine what level is best for you, but generally a hemoglobin A1C greater than 7% (average blood sugar equal to 140 mg/dl) means that measures must be taken to achieve better management.

The hemoglobin A1C  test results may be inaccurate in certain conditions. The test results may be falsely low in the following situations: the use of dapsone, certain types of anemia, mechanical heart valves, recent blood transfusion, enlarged spleen, treatment with erythropoietin, severely elevated triglycerides, high-dose vitamin C or E.

Conversely, test results may be falsely elevated in the following situations: untreated hypothyroidism, after surgical removal of the spleen, Iron deficiency, vitamin B12 deficiency, reduced red blood cell production by the bone marrow, chronic alcoholism, chronic kidney disease.

If there is a question about the reliability of the test results, other means of testing may be considered, such as the fructosamine test.

Hemoglobin A1cBlood Sugar
A1c(mg/dL)
4%60
5%90
6%120
7%150
8%180
9%210
10%240
11%270
12%300
13%330

What can I do if my hemoglobin A1C results are high?

While it is important to keep blood sugar levels from being too high, it is also important not to risk frequent or severe episodes of dangerously low blood sugar levels. You and your doctor will evaluate your situation to determine which of the following factors may be playing a role:

  • Too little exercise
  • Inadequate medication type or dosing
  • Too much food
  • Wrong types of food
  • Increased stress
  • Infection

The hemoglobin A1C test provides you with more information to maintain good management of your diabetes. Better control means a longer, healthier life. And any positive change in your care, no matter how small, makes a difference. For example, each 1% decrease in the hemoglobin A1C reduces the risk of eye and kidney damage by 37% and reduces the risk of diabetes-related death by 21%. The more you are involved with your health care, the greater the likelihood of living a longer and healthier life.

By Scott E. Pautler, MD

For a telemedicine consultation with Dr Pautler, please send email request to spautler@rvaf.com. We accept Medicare and most insurances in Florida. Please include contact information (including phone number) in the email. We are unable to provide consultation for those living outside the state of Florida with the exception of limited one-time consultations with residents of the following states: Alabama, Arkansas, Connecticut, Georgia, Minnesota, and Washington.

Copyright  © 2014-2022 Designs Unlimited of Florida.  All Rights Reserved.

Diabetic Retinopathy

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Diabetes mellitus is a group of conditions characterized by abnormally high blood sugar levels.  Short-term side effects include increased thirst, frequent urination, and weight changes.  Long-term complications include numbness of the hands and feet, loss of vision, kidney failure, as well as hardening of the arteries leading to amputation, heart attack, stroke, and premature death.  Diabetes affects about one million Floridians and 16 million Americans.  It is the leading cause of blindness in America among adults.  Several studies have proven that strict control of blood sugar levels dramatically decreases the risk of blindness and other complications of diabetes.  The National Eye Institute proved that laser treatment may save vision if diabetic eye damage is detected early.  The American Diabetes Association recommends annual eye examinations for all adults with diabetes to prevent blindness.

What is the retina?

The retina is a thin layer of delicate nerve tissue, which lines the inside wall of the eye like the film in a camera.  In the eye, light is focused onto the retina, which “takes the picture” and sends the image to the brain.  The retina has two main areas.  The macula is the central area that gives you sharp, central vision and color vision.  The peripheral retina is the part of the retina that gives you side vision and night vision.

What is diabetic retinopathy?

Diabetic retinopathy is a condition that occurs after many years of high blood sugar.  It consists of damage to tiny blood vessels within the retina resulting in abnormal leakage of fluid and blood inside the eye.  If not detected or treated, diabetic retinopathy may cause bleeding, scar tissue formation, retinal detachment, and blindness.

Stages of diabetic retinopathy:

Non-proliferative diabetic retinopathy: The first stage of retinal damage consisting of a weakening or blockage of tiny blood vessels, which does not require treatment with laser unless macular edema develops.

Diabetic macular edema: Swelling of the central retina (the macula) due to abnormal leakage of fluid from small blood vessels weakened by diabetes.  Blurring of central vision may advance to legal blindness.

Proliferative diabetic retinopathy: The second stage of diabetic retinopathy in which abnormal, weak blood vessels begin to grow from the retina into the clear gel (vitreous) which fills the inside of the eye.  If not treated, this serious stage often results in blindness from bleeding.  Symptoms include new “floaters” or sudden loss of vision.  Retinal detachment may occur from diabetic scar tissue, which pulls the retina off the eye wall.  Retinal detachment causes a dark shadow in the vision or total loss of vision.  Laser and vitrectomy surgery best control these problems if detected early.

How is diabetic retinopathy diagnosed?

Because no symptoms may be present until severe damage to the retina has occurred, it is essential that all adults with diabetes have a complete, dilated eye examination at least once a year.  The eye doctor can see into the eye with an ophthalmoscope to diagnose retinopathy.  If significant changes are found, photographs can be taken to record the changes. A fluorescein angiogram may be performed in the office by injecting a fluorescent dye into the vein of the arm while photographs are taken of the retina.  It supplies important information about the health of the retinal blood vessels.

How is diabetic retinopathy treated?

No treatment is needed if the vision is not threatened.  If blood vessel damage is significant, painless injections of medicine (Avastin) may be required to improve vision. Laser treatment performed in the office can often prevent severe visual loss.  Laser produces heat, which serves to cauterize the damaged retinal blood vessels.  Usually there is no pain, but if extensive laser is needed, an anesthetic injection may be given around the eye.  In severe cases of bleeding and scar tissue formation, vitrectomy surgery is performed as a one-day surgery in the hospital.  With laser and vitrectomy surgery, most people can retain useful vision. However, some people lose vision despite all efforts with treatment.

What can I do to prevent diabetic damage?

Strict control of the blood sugar has been proven to reduce the rate of progression of diabetic retinopathy by about 70%.  In addition, loss of vision can be minimized by optimal control of other health problems such as physical inactivity, obesity, hypertension (<130/<80), cholesterol (<200) and triglycerides (<150), heart failure, and kidney failure.  Tobacco use is strongly discouraged.  Daily aspirin use is recommended.

PREVENT BLINDNESS THROUGH GOOD MANAGEMENT OF DIABETES AND REGULAR DILATED EYE EXAMINATIONS.

By Scott E. Pautler, MD

For a telemedicine consultation with Dr Pautler, please send email request to spautler@rvaf.com. We accept Medicare and most insurances in Florida. Please include contact information (including phone number) in the email. We are unable to provide consultation for those living outside the state of Florida with the exception of limited one-time consultations with residents of the following states: Alabama, Arkansas, Connecticut, Georgia, Minnesota, and Washington.

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