New QOF glycaemia targets are achievable and based on a balanced review of available evidence
In their editorial, Lehman and Krumholz(1) raise concerns that the
revision of the HbA1c targets in the GMS quality and outcomes framework
(QOF) may pose a risk to people with diabetes. They suggest that huge
numbers of patients will need to be given additional treatment including
insulin in order that 50% of patients have an HbA1c of 7.0% or less.
Interestingly they make no comment on the recently updated NICE(2)
guidelines and ADA/EASD consensus statement(3) advocating an HbA1c target
of <7.0%. In fact, glycaemic control among people with diabetes in the
UK is rather better than they seem to think. Data on HbA1c values amongst
the 464,000 people in the 2005-2006 National Diabetes Audit demonstrate
that 45% already had values of 7.0% or less, 72% were below 8% and 85%
were under 9%.(4) Thus, the small changes in the distribution of glycaemia
may already have been achieved, even before publication of the revised QOF
targets, particularly given the rapid rise in numbers of newly diagnosed
patients in the last few years. Furthermore, the authors ignore the
potential contribution of advice concerning diet and physical activity.
Lehman and Krumholz conclude that the revised QOF indicators
encourage "tighter glycaemic control for all patients with type 2
diabetes". This is not the case. The previous HbA1c targets (7.5% and 10%)
were replaced by three (7%, 8% and 9%) in order to promote a downward
shift in the distribution of blood glucose, while encouraging GPs to agree
safe and appropriate targets with individual patients (as NICE recommended
in 20082), but also to provide incentives at more points across the HbA1c
distribution, thereby reducing perverse incentives to focus care away from
those at greatest risk.
The editorial does not present a balanced view of the recent trial
data in the context of the large body of evidence of the association
between hyperglycaemia and the complications of diabetes. Concerns are
raised about excess mortality in the ACCORD trial which led to its early
termination.(5) While the reasons for this are unclear, the HbA1c target
(6.0%, achieved median 6.4%) was much lower than that advocated in the
QOF, the trial only recruited people with poor control (above 8%), HbA1c
was reduced very rapidly (by 1.4% over four months), and a significant
proportion of patients were prescribed Rosiglitazone, all of which suggest
that the findings may not be directly relevant to a QOF target of ¡Ü7.0%
for 50% of patients. Furthermore, mortality was not increased in the
intensively treated groups in the three other recently reported trials
(ADVANCE,(6) UKPDS 10 year follow up,(7) and the Veteran Affairs Diabetes
Trial(8)). Indeed in the UKPDS mortality was 13% lower in the
sulphonylurea and insulin group and 27% lower in the metformin group.(7)
Observational studies demonstrate a continuous relationship between
glycaemia and risk of mortality and cardiovascular events; a 1% higher
HbA1c was independently associated with a 28% higher risk of death from
all causes in the EPIC-Norfolk cohort,(9) and a 21% higher risk of death
related to diabetes in the UKPDS cohort.(10) This association extends
below the diagnostic cut-off for diabetes and does not exhibit a
threshold, suggesting that as with blood pressure and cholesterol, the
lower the HbA1c the better in the long term, providing that treatment does
not cause problems in the short term. Results from trials of interventions
to lower blood glucose are broadly consistent with the observational data.
Indeed all four of the recently published trials reported a lower risk of
cardiovascular events associated with intensive treatment,(5-8) albeit
only the one with longer follow-up (UKPDS)(7) achieving statistical
significance. It is notable that the benefits in terms of cardiovascular
risk reduction only start to appear after several years in all the trials.
The editorial focussed mainly on cardiovascular complications. While
these are clearly common and costly they are not the only complications
associated with hyperglycaemia. Even the trials cited in the editorial
added to the large body of evidence that intensive treatment of
hyperglycaemia is associated with reduced risk of non-trivial
microvascular complications such as nephropathy. Microvascular
complications are likely to become increasingly important as simultaneous
treatment of multiple risk factors (blood pressure, cholesterol and blood
glucose) leads to the reduced rates of cardiovascular events seen in
recent trials among patients with diabetes. One consequence of this is
that these trials have tended to be underpowered to detect between-group
differences in cardiovascular outcomes within three to five years. This
has led to some incorrectly interpreting 'a lack of evidence of effect' as
'evidence of lack of any effect'. Blood glucose is an independent
cardiovascular risk factor, albeit not a very strong one. Good management
of newly diagnosed and longstanding diabetes should include intensive
management of multiple risk factors. Such an approach can reduce mortality
by half,(11) and is encouraged by the QOF indicators which relate to
several risk factors, not simply glycaemia.
The editorial concentrated on longstanding type 2 diabetes, but the
QOF also applies to type 1. There is presumably no challenge to the
findings of the DCCT/EDIC studies demonstrating significant long-term
reductions in risk of microvascular and macrovascular disease associated
with intensive treatment of blood glucose.(12) Interestingly, these
important benefits were not apparent early in the DCCT follow-up. Indeed
the trial might have been stopped due to the initial excess of adverse
events in the intensive treatment arm, something that should perhaps be
borne in mind when interpreting the results of trials of intensive
treatment among patients with type 2 diabetes.
While there is some suggestion that the QOF has facilitated
improvements in the delivery of care,(13) doubts remain about the overall
cost-effectiveness of this previously untested, expensive policy. This
topic might have been a more appropriate focus for a potentially
influential editorial than a narrow perspective on a single QOF target. It
is unfortunate that the reports on which NHS employers and the
profession's negotiators based their decision, and which provide some of
the rationale for the recommendations, are only now available in the
public domain.(4) They serve to demonstrate that targets for glycaemia
have a stronger evidence base than many of the other QOF indicators.
People with diabetes and their professional advisers should continue
to negotiate individually-tailored, safe and appropriate targets for all
risk factors but should avoid rapid reductions of HbA1c to below 6.5%.
They can have confidence that the modest changes encouraged by the revised
QOF targets are safe and will lead to further reductions in risk and
health service costs over time.
References
1. Lehman R, Krumholz HM. Tight control of blood glucose in long
standing type 2 diabetes. British Medical Journal 2009;338(mar05_2):b800.
2. NICE. Type 2 diabetes: the management of type 2 diabetes (update).
London: National Institute for Health and Clinical Excellence, 2008.
3. Nathan DM, Buse JB, Davidson MB, Ferrannini E, Holman RR, Sherwin
R, et al. Medical Management of Hyperglycemia in Type 2 Diabetes: A
Consensus Algorithm for the Initiation and Adjustment of Therapy: A
consensus statement of the American Diabetes Association and the European
Association for the Study of Diabetes. Diabetes Care 2009;32(1):193-203.
4. Graffy J, Griffin S. Review of the Quality and Outcomes Framework
for Diabetes: Current Indicators 2007 - 2008. Manchester: National Primary
Care Research and Development Centre, 2008. http://www.npcrdc.ac.uk/Publications/Diabetes_200708.pdf.
5. The Action to Control Cardiovasculr Risk in Diabetes Study Group.
Effects of Intensive Glucose Lowering in Type 2 Diabetes. New England
Journal of Medicine 2008;358(24):2545-2559.
6. The ADVANCE Collaborative Group. Intensive Blood Glucose Control
and Vascular Outcomes in Patients with Type 2 Diabetes. New England
Journal of Medicine 2008;358(24):2560-2572.
7. Holman RR, Paul SK, Bethel MA, Matthews DR, Neil HA. 10-year
follow-up of intensive glucose control in type 2 diabetes. New England
Journal of Medicine 2008;359(15):1577-89.
8. Duckworth W, Abraira C, Moritz T, Reda D, Emanuele N, Reaven PD,
et al. Glucose control and vascular complications in veterans with type 2
diabetes. New England Journal of Medicine 2009;360(2):129-39.
9. Khaw KT, Wareham N, Luben R, Bingham S, Oakes S, Welch A, et al.
Glycated haemoglobin, diabetes, and mortality in men in Norfolk cohort of
european prospective investigation of cancer and nutrition (EPIC-
Norfolk). British Medical Journal 2001;322(7277):15-18.
10. Stratton I, Adler AG, Neil HA, Matthews DR, Manley SE, Cull C, et
al. Association of glycaemia with macrovascular and microvascular
complications of type 2 diabetes (UKPDS 35): prospective observational
study. British Medical Journal 2000;321:405-412.
11. Gaede P, Lund-Andersen H, Parving H-H, Pedersen O. Effect of a
Multifactorial Intervention on Mortality in Type 2 Diabetes. New England
Journal of Medicine 2008;358(6):580-591.
12. Nathan DM, Cleary PA, Backlund JY, Genuth SM, Lachin JM, Orchard
TJ, et al. Intensive diabetes treatment and cardiovascular disease in
patients with type 1 diabetes. New England Journal of Medicine
2005;353(25):2643-53.
13. Campbell S, Reeves D, Kontopantelis E, Middleton E, Sibbald B,
Roland M. Quality of primary care in England with the introduction of pay
for performance. New England Journal of Medicine 2007;357(2):181-90.
Competing interests:
Simon Griffin and Jonathan Graffy were members of the expert reference group providing advice on the QOF diabetes targets
Rapid Response:
New QOF glycaemia targets are achievable and based on a balanced review of available evidence
In their editorial, Lehman and Krumholz(1) raise concerns that the
revision of the HbA1c targets in the GMS quality and outcomes framework
(QOF) may pose a risk to people with diabetes. They suggest that huge
numbers of patients will need to be given additional treatment including
insulin in order that 50% of patients have an HbA1c of 7.0% or less.
Interestingly they make no comment on the recently updated NICE(2)
guidelines and ADA/EASD consensus statement(3) advocating an HbA1c target
of <7.0%. In fact, glycaemic control among people with diabetes in the
UK is rather better than they seem to think. Data on HbA1c values amongst
the 464,000 people in the 2005-2006 National Diabetes Audit demonstrate
that 45% already had values of 7.0% or less, 72% were below 8% and 85%
were under 9%.(4) Thus, the small changes in the distribution of glycaemia
may already have been achieved, even before publication of the revised QOF
targets, particularly given the rapid rise in numbers of newly diagnosed
patients in the last few years. Furthermore, the authors ignore the
potential contribution of advice concerning diet and physical activity.
Lehman and Krumholz conclude that the revised QOF indicators
encourage "tighter glycaemic control for all patients with type 2
diabetes". This is not the case. The previous HbA1c targets (7.5% and 10%)
were replaced by three (7%, 8% and 9%) in order to promote a downward
shift in the distribution of blood glucose, while encouraging GPs to agree
safe and appropriate targets with individual patients (as NICE recommended
in 20082), but also to provide incentives at more points across the HbA1c
distribution, thereby reducing perverse incentives to focus care away from
those at greatest risk.
The editorial does not present a balanced view of the recent trial
data in the context of the large body of evidence of the association
between hyperglycaemia and the complications of diabetes. Concerns are
raised about excess mortality in the ACCORD trial which led to its early
termination.(5) While the reasons for this are unclear, the HbA1c target
(6.0%, achieved median 6.4%) was much lower than that advocated in the
QOF, the trial only recruited people with poor control (above 8%), HbA1c
was reduced very rapidly (by 1.4% over four months), and a significant
proportion of patients were prescribed Rosiglitazone, all of which suggest
that the findings may not be directly relevant to a QOF target of ¡Ü7.0%
for 50% of patients. Furthermore, mortality was not increased in the
intensively treated groups in the three other recently reported trials
(ADVANCE,(6) UKPDS 10 year follow up,(7) and the Veteran Affairs Diabetes
Trial(8)). Indeed in the UKPDS mortality was 13% lower in the
sulphonylurea and insulin group and 27% lower in the metformin group.(7)
Observational studies demonstrate a continuous relationship between
glycaemia and risk of mortality and cardiovascular events; a 1% higher
HbA1c was independently associated with a 28% higher risk of death from
all causes in the EPIC-Norfolk cohort,(9) and a 21% higher risk of death
related to diabetes in the UKPDS cohort.(10) This association extends
below the diagnostic cut-off for diabetes and does not exhibit a
threshold, suggesting that as with blood pressure and cholesterol, the
lower the HbA1c the better in the long term, providing that treatment does
not cause problems in the short term. Results from trials of interventions
to lower blood glucose are broadly consistent with the observational data.
Indeed all four of the recently published trials reported a lower risk of
cardiovascular events associated with intensive treatment,(5-8) albeit
only the one with longer follow-up (UKPDS)(7) achieving statistical
significance. It is notable that the benefits in terms of cardiovascular
risk reduction only start to appear after several years in all the trials.
The editorial focussed mainly on cardiovascular complications. While
these are clearly common and costly they are not the only complications
associated with hyperglycaemia. Even the trials cited in the editorial
added to the large body of evidence that intensive treatment of
hyperglycaemia is associated with reduced risk of non-trivial
microvascular complications such as nephropathy. Microvascular
complications are likely to become increasingly important as simultaneous
treatment of multiple risk factors (blood pressure, cholesterol and blood
glucose) leads to the reduced rates of cardiovascular events seen in
recent trials among patients with diabetes. One consequence of this is
that these trials have tended to be underpowered to detect between-group
differences in cardiovascular outcomes within three to five years. This
has led to some incorrectly interpreting 'a lack of evidence of effect' as
'evidence of lack of any effect'. Blood glucose is an independent
cardiovascular risk factor, albeit not a very strong one. Good management
of newly diagnosed and longstanding diabetes should include intensive
management of multiple risk factors. Such an approach can reduce mortality
by half,(11) and is encouraged by the QOF indicators which relate to
several risk factors, not simply glycaemia.
The editorial concentrated on longstanding type 2 diabetes, but the
QOF also applies to type 1. There is presumably no challenge to the
findings of the DCCT/EDIC studies demonstrating significant long-term
reductions in risk of microvascular and macrovascular disease associated
with intensive treatment of blood glucose.(12) Interestingly, these
important benefits were not apparent early in the DCCT follow-up. Indeed
the trial might have been stopped due to the initial excess of adverse
events in the intensive treatment arm, something that should perhaps be
borne in mind when interpreting the results of trials of intensive
treatment among patients with type 2 diabetes.
While there is some suggestion that the QOF has facilitated
improvements in the delivery of care,(13) doubts remain about the overall
cost-effectiveness of this previously untested, expensive policy. This
topic might have been a more appropriate focus for a potentially
influential editorial than a narrow perspective on a single QOF target. It
is unfortunate that the reports on which NHS employers and the
profession's negotiators based their decision, and which provide some of
the rationale for the recommendations, are only now available in the
public domain.(4) They serve to demonstrate that targets for glycaemia
have a stronger evidence base than many of the other QOF indicators.
People with diabetes and their professional advisers should continue
to negotiate individually-tailored, safe and appropriate targets for all
risk factors but should avoid rapid reductions of HbA1c to below 6.5%.
They can have confidence that the modest changes encouraged by the revised
QOF targets are safe and will lead to further reductions in risk and
health service costs over time.
References
1. Lehman R, Krumholz HM. Tight control of blood glucose in long
standing type 2 diabetes. British Medical Journal 2009;338(mar05_2):b800.
2. NICE. Type 2 diabetes: the management of type 2 diabetes (update).
London: National Institute for Health and Clinical Excellence, 2008.
3. Nathan DM, Buse JB, Davidson MB, Ferrannini E, Holman RR, Sherwin
R, et al. Medical Management of Hyperglycemia in Type 2 Diabetes: A
Consensus Algorithm for the Initiation and Adjustment of Therapy: A
consensus statement of the American Diabetes Association and the European
Association for the Study of Diabetes. Diabetes Care 2009;32(1):193-203.
4. Graffy J, Griffin S. Review of the Quality and Outcomes Framework
for Diabetes: Current Indicators 2007 - 2008. Manchester: National Primary
Care Research and Development Centre, 2008.
http://www.npcrdc.ac.uk/Publications/Diabetes_200708.pdf.
5. The Action to Control Cardiovasculr Risk in Diabetes Study Group.
Effects of Intensive Glucose Lowering in Type 2 Diabetes. New England
Journal of Medicine 2008;358(24):2545-2559.
6. The ADVANCE Collaborative Group. Intensive Blood Glucose Control
and Vascular Outcomes in Patients with Type 2 Diabetes. New England
Journal of Medicine 2008;358(24):2560-2572.
7. Holman RR, Paul SK, Bethel MA, Matthews DR, Neil HA. 10-year
follow-up of intensive glucose control in type 2 diabetes. New England
Journal of Medicine 2008;359(15):1577-89.
8. Duckworth W, Abraira C, Moritz T, Reda D, Emanuele N, Reaven PD,
et al. Glucose control and vascular complications in veterans with type 2
diabetes. New England Journal of Medicine 2009;360(2):129-39.
9. Khaw KT, Wareham N, Luben R, Bingham S, Oakes S, Welch A, et al.
Glycated haemoglobin, diabetes, and mortality in men in Norfolk cohort of
european prospective investigation of cancer and nutrition (EPIC-
Norfolk). British Medical Journal 2001;322(7277):15-18.
10. Stratton I, Adler AG, Neil HA, Matthews DR, Manley SE, Cull C, et
al. Association of glycaemia with macrovascular and microvascular
complications of type 2 diabetes (UKPDS 35): prospective observational
study. British Medical Journal 2000;321:405-412.
11. Gaede P, Lund-Andersen H, Parving H-H, Pedersen O. Effect of a
Multifactorial Intervention on Mortality in Type 2 Diabetes. New England
Journal of Medicine 2008;358(6):580-591.
12. Nathan DM, Cleary PA, Backlund JY, Genuth SM, Lachin JM, Orchard
TJ, et al. Intensive diabetes treatment and cardiovascular disease in
patients with type 1 diabetes. New England Journal of Medicine
2005;353(25):2643-53.
13. Campbell S, Reeves D, Kontopantelis E, Middleton E, Sibbald B,
Roland M. Quality of primary care in England with the introduction of pay
for performance. New England Journal of Medicine 2007;357(2):181-90.
Competing interests:
Simon Griffin and Jonathan Graffy were members of the expert reference group providing advice on the QOF diabetes targets
Competing interests: No competing interests