Tight control of HbA1c levels has assumed great importance in
diabetes
management. It has been enshrined in the QOF (Quality and Outcomes
Framework) of the New GP Contract as being an evidence based proposal.
Multiple drugs are licenced on the understanding that they reduce HbA1c
levels and that this is a good thing. So should it surprise us that a meta
-
analysis of trials of roisiglitazone shows a raised risk of myocardial
infarction
and an increase in cardiovascular deaths? (1)
I think the evidence to support tight glylcaemic control in reducing
complications of type 2 diabetes is poor. In fact the reduction in
diabetes
related endpoints, mortality and stroke from using metformin is not
explicable on the basis of glycaemic control. This isn’t just my opinion,
it is
what was written in the original paper of UKPDS 34, which is still the
paper I
see quoted as showing that tight glycaemic control reduces diabetic
complications. (2)
Should you choose to review the data of UKPDS 33 which compared tight
glycaemic control with sulphonylureas or insulin with conventional
treatment
you will see little benefit from tight control. (3) Tight control made no
difference to absolute rates of angina, heart failure, stroke, renal
failure, nor
vitreous haemorrhage. Tight control reduced the risk of going blind in one
eye, of suffering a fatal MI or of having an amputation by fewer than 1
per
1000 patient years, and then with no statistical significance. The
outcomes
which did show some clinical benefit were cataract extractions, retinal
photocoagulation and non-fatal MI and all –cause mortality, that is if you
can
call absolute risk reductions of between 1 and 3 per 1000 patient years as
being clinically relevant. Would you make the major lifestyle changes
required
by these two groups of treatment if after 10 years your largest single
risk
reduction was a 1 in 30 chance of not needing retinal photocoagulation? I
wouldn’t.
The wonder with drug licencing is that we continue to accept
surrogate
endpoints in trials to licence new treatments for conditions for which we
already have treatments. Our patients deserve better than they are
currently
being offered by those who promote tight glycaemic control. Show me better
data or accept that the control of blood glucose means metformin –anything
else is merely for symptom control.
References
1. Study links diabetes drug to heart deaths. BMJ 2007; 334: 1073
2. Effect of Intensive blood-glucose control with metformin on
complications in overweight patients with type 2 diabetes (UKPDS 34).
Lancet
1998; 352: 854-865
3. Intensive blood-glucose control with sulphonylureas or insulin
compared with conventional treatment and risks of complications in
patients
with type 2 diabetes (UKPDS 33). Lancet 1998; 352: 837- 853
Competing interests:
I have co-authored with Adrian
Edwards , Glyn Elwin and Rhys
Williams a paper on explaining
risk information over the
internet to patients with
diabetes. That project was
funded by the BMJ group
Rapid Response:
Glycaemic control is more myth than fact
Tight control of HbA1c levels has assumed great importance in
diabetes
management. It has been enshrined in the QOF (Quality and Outcomes
Framework) of the New GP Contract as being an evidence based proposal.
Multiple drugs are licenced on the understanding that they reduce HbA1c
levels and that this is a good thing. So should it surprise us that a meta
-
analysis of trials of roisiglitazone shows a raised risk of myocardial
infarction
and an increase in cardiovascular deaths? (1)
I think the evidence to support tight glylcaemic control in reducing
complications of type 2 diabetes is poor. In fact the reduction in
diabetes
related endpoints, mortality and stroke from using metformin is not
explicable on the basis of glycaemic control. This isn’t just my opinion,
it is
what was written in the original paper of UKPDS 34, which is still the
paper I
see quoted as showing that tight glycaemic control reduces diabetic
complications. (2)
Should you choose to review the data of UKPDS 33 which compared tight
glycaemic control with sulphonylureas or insulin with conventional
treatment
you will see little benefit from tight control. (3) Tight control made no
difference to absolute rates of angina, heart failure, stroke, renal
failure, nor
vitreous haemorrhage. Tight control reduced the risk of going blind in one
eye, of suffering a fatal MI or of having an amputation by fewer than 1
per
1000 patient years, and then with no statistical significance. The
outcomes
which did show some clinical benefit were cataract extractions, retinal
photocoagulation and non-fatal MI and all –cause mortality, that is if you
can
call absolute risk reductions of between 1 and 3 per 1000 patient years as
being clinically relevant. Would you make the major lifestyle changes
required
by these two groups of treatment if after 10 years your largest single
risk
reduction was a 1 in 30 chance of not needing retinal photocoagulation? I
wouldn’t.
The wonder with drug licencing is that we continue to accept
surrogate
endpoints in trials to licence new treatments for conditions for which we
already have treatments. Our patients deserve better than they are
currently
being offered by those who promote tight glycaemic control. Show me better
data or accept that the control of blood glucose means metformin –anything
else is merely for symptom control.
References
1. Study links diabetes drug to heart deaths. BMJ 2007; 334: 1073
2. Effect of Intensive blood-glucose control with metformin on
complications in overweight patients with type 2 diabetes (UKPDS 34).
Lancet
1998; 352: 854-865
3. Intensive blood-glucose control with sulphonylureas or insulin
compared with conventional treatment and risks of complications in
patients
with type 2 diabetes (UKPDS 33). Lancet 1998; 352: 837- 853
Competing interests:
I have co-authored with Adrian
Edwards , Glyn Elwin and Rhys
Williams a paper on explaining
risk information over the
internet to patients with
diabetes. That project was
funded by the BMJ group
Competing interests: No competing interests