HbA1C and Retinopathy
teamwork helps to
improve diabetic control
Controlling your diabetes can slow down diabetic complications and retinopathy. In practice this means that conditions such as retinopathy may stopped in most people, and good sight maintained. In a few people the retinopathy may still progress, but at a much slower rate. See DCCT and UKPDS.
The progression rate of retinopathy is 37% less for each 10mmol/l (1%) reduction in the HbA1C or 1mmol/l of blood sugar. Teamwork is crucial to good diabetic control: the patient is the focus, but assistance from many health professionals is usually needed to assist good control.
- HbA1c is linked to retinopathy 2012
- mulitple risk factors including micoraneurysms 2012
- elevated HbA1c can be used to caculate a risk index 2012
- Asian patients get more retinopthy for the same HbA1c.
- In addition, retinopathy can develop despite good control, if the control years previously was poor ('legacy effect'). (Shown by DCCT and UKPDs studies.)
|At the onset of type 2 diabetes||48mmol/ l (6.5%) is the target|
|if well, and diet or tablet controlled||HbA1c less than 48mmol/ l (6.5%)|
|if very ill||higher levels may be accepted|
|if using insulin and keen to control diabetes and able to test glucose 4-6 times day (basal bolus insulin/pump)||HbA1c
48-58 mmol/ l (6.5-7.5%)
(without many hypos)
|if using insulin and keen to control diabetes and able to test glucose <4 times day (basal bolus insulin/pump)..the average patient||HbA1c ~ 58 mmol/ l (7.5%)
(or as low as possible without many hypos)
testing your glucose level is essential for most people with diabetes, especially insulin users
- This means that if your diabetes is controlled (HbA1c less than about 53mmol/ l (7%) retinopathy may never develop, or develop very slowly.
- Such good control is easier to achieve if your have type 2 diabetes and use tablets. Eventually though, the pancreas stops producing any insulin and eventually most people with type 2 diabetes eventually need insulin, and then control is harder.
- Whatever your type of diabetes, if you use insulin, such good control is
harder to achieve. But the lower the better, so if your HbA1c is 53mmol/ l (7%), you
will develop retinopathy at a much slower rate than someone whose level
is 75mmol/ l (9.0%) .
As each percentage point (10mmol/l) of HbA1c translates into a massive 37% difference in progression rate, your retinopathy will be 2 x 37%, = 74% slower, to develop.
- Retinopathy may develop after 14 years of poorly controlled type 1 diabetes (type 2 less than 14 years as it may be diagnosed late).
- Converting HbA1c, table
Enlarge If your HbA1C is 53mmol/ l (7%) retinopathy may develop, but it is much slower to develop than if it is 75mmol/l (9%) . If your HbA1C is 53mmol/ l (7%) , you will have about 74% less progression after 2 years than if it is 75mmol/l (9%). Blue...no retinopathy; red... retinopathy
What is your HbA1c? Is it below 75mmol/l (9%) ? If not, can you get it lower? Ask your nurse for help.
enlarge The relationship between your sugar level and retinopathy and kidney disease is illustrated here.
If you suddenly improve control and your HbA1C drops the retinopathy may
need laser treatment. The benefits of an HbA1C drop, say from 53-75mmol/l (9 to 7%), are
long term. The retinopathy may actually deteriorate in the short term, and
so require laser. If this is difficult to understand, ask your ophthalmologist
After two-three years however, assuming you have any laser that may be necessary, you will be better off and the retinopathy will be less active than it would otherwise have been. Retinopathy progression detail.
The ACCORD study noticed extra deaths in the very intensive glucose control arm. This group of patients had to achieve HbA1c <48mmol/ l (6.5%), and risks were increased 25 % versus the group that achieved 53-64mmol/ l (7.0-7.9%). Reports such as BMJ suggest that
- very intensive glucose control (as a target <6.5%) may not be ideal if patients have CVD (cerebrovascular disease) and have been diabetic 10y, until we know more
- the problem may have been caused by the combination of multiple dose insulin regimes AND hypoglycaemic agents, possibly because of hypos on the heart QT interval
- we should aim for this level if it can be achieved easily...eg in the first 10y of diabetes
Predictive index of HbA1c (PI)
- we have to use the old units to use this index!
- Calculate the years spent >Hba1c 6%................retinopathy will not develop unless index >36.
- Mmol/l..multiply by 10
- earlier in smokers/hypertensives, later in none-smokers/normotensives
Example 1, a type 1 patient:
Patient: diagnosed type 1 diabetes at onset of 1990. HbA1c 9% in that year...index =2 for that year. For next 23 years, HbA1c 7%, so by 2013 index has reached 24 (22y at 7% [7%-6%=1, x 22y=predictive index 22] +1 year at 8% [8%=6%=2, 1 year= predictive index 2].
As the predicitive index is only 24, patient will not develop retinopathy.
Second example, a type 2 patient:
The study below only examined type 1 patients, but there is no reason why it should not apply for type 2. Patient diagnosed diabetc 1993, HbAc3 7.5% since then, PI =20 x 1.5= 30.
But patient has retinopathy...I assume this is becuase the diabetes had been present sometime before the diagnosis, perhaps 1y at 9%, 1y at 8%, 1y at 7%, pervious ly 6%.....extra PI = (9-6=3) + (8-6=2) + (7-6=1) 6, so tatal PI = 30 +6, 36, so this would explain why there is retinopathy.
A predictive index for retinopathy development using hba1c values in younger onset type 1 diabetes
A. Hirose, S. Kitano, Y. Uchigata, taken from EASDec poster 2012
Introduction: retrospective study; Purpose: to evaluate a predictive index for retinopathy development using HbA1c values in a long-term follow-up study of younger onset type 1 diabetes.
Methods: to study the influence of hyperglycemia on retinopathy development as accurately as possible, we selected younger onset diabetics (to minimize the influence of hypertension and dyslipidemia) with continuous HbA1c data substantially just after the onset of diabetes (to minimize the influence of metabolic memory). Major inclusion criteria were: (1) type 1 diabetes diagnosed before the age of 30 years; (2) first visit to the Diabetes Centre between 1988 and 1990 within 12 months after onset; (3) follow-up during 20 years after onset with HbA1c values measured in the Centre. Each patient underwent a principally annual fundus examination through dilated pupils by Centre ophthalmologists. Retinopathy for a given year was defined as positive by a level of 15/<15 or more severe on the final Retinopathy Severity scale of the Early Treatment Diabetic Retinopathy Study. The first year of retinopathy development was established when two consecutive retinopathy-positive years were detected. Patients without a 20th year fundus examination were excluded. HbA1c (Japan Diabetes Society value≈ National Glycohemoglobin Standardization Program value-0.4 (%)) was measured by high performance liquid chromatography. A current year's excess HbA1c value was calculated by the year's mean HbA1c minus a hypothetical normal HbA1c threshold 6.0(%). Then the Xth year's predictive index (PI) was calculated by cumulating the yearly excess HbA1c values from the 1st to Xth year.
Results. Of the 15 patients (6 males and 9 females), 5 developed retinopathy with PI values of 36.3～43.1 during the 20-year follow-up, while 10 did not, with maximum PI values of 3.4～32.5.
Conclusions. This index could be valuable in predicting the development of retinopathy in younger onset type 1 diabetes.