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Rapid Responses: Rapid Responses published:
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Glycaemic control is not a myth
- J T George, Kavitha S Rozario (17 June 2007)
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There are more important interventions than glycaemic control.
- Peter D Burrill (19 June 2007)
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J T George, Specialist Registrar in Diabetes, Endocrinology and General (Internal) Medicine York Hospital, York, YO31 8HE, Kavitha S Rozario
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We would like to disagree with the author’s observation that glycaemic control is a myth. The tone and context of the letter suggests the author’s concerns are perhaps limited to Type 2 diabetes. However, the letter fails to differentiate Type 1 and Type 2 diabetes, two different pathological conditions. The advantages of good glycaemic control in Type 1 diabetes is well established with the Diabetes Control and Complications Trial1. It is intriguing to see findings from the United Kingdom Prospective Diabetes Study (UKPDS) being referenced to question the significance of glycaemic control. The UKPDS study group concluded that in patients with type 2 diabetes the risk of diabetic complications was strongly associated with glycaemic control2. Any reduction in HbA1c was shown to reduce the risk of complications, with the lowest risk being in those with HbA1c values in the normal range (<6.0%).2 UKPDS authors have also robustly defended their findings in debate3 following the publication of their data. The author also raises questions about the clinical significance of 1-3% absolute reductions in risk. Diabetes is presently diagnosed in over two million people in the UK4 and millions more across the world. Therefore, such apparently modest reductions in absolute risk translate to large reductions in complications across the population. The suggestion that Metformin should be the only drug used for diabetes contrasts sharply with evidence-based guidelines.5-6 People with diabetes and professionals caring for them face many challenges and re-igniting the post- UKPDS debate3 with little new data is unlikely to help. It is disappointing to see the author raise fundamental questions about the validity of glycaemic control without a thorough review of existing data and literature. References 1. Lasker RD. The Diabetes Control and Complications Trial -- Implications for Policy and Practice. N Engl J Med 1993; September 30;329(14):1035-6. 2. Stratton IM, Adler AI, Neil HAW, Matthews DR, Manley SE, Cull CA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ 2000; August 12;321(7258):405-12. 3. Budenholzer B, Cruickshank JK, Jarrett RJ, Stratton IM, Cull CA, Manley SE, et al. Glycaemia and vascular effects of type 2 diabetes. BMJ 2001; May 19;322(7296):1245b. 4. Diabetes: State of the Nations 2006. Available at: http://www.diabetes.org.uk/Documents/Reports/SOTN2006_full.pdf. Accessed 06/06, 2007. 5. Heine RJ, Diamant M, Mbanya J, Nathan DM. Management of hyperglycaemia in type 2 diabetes: the end of recurrent failure?. BMJ 2006; December 9;333(7580):1200-4. 6. Global Guideline for Type 2 Diabetes. Available at: http://www.idf.org/webdata/docs/IDF%20GGT2D.pdf. Accessed 06/15, 2007. Competing interests: None declared |
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Peter D Burrill, Specialist Pharmaceutical Adviser for Public Health Derbyshire County PCT, Chesterfield, S41 7PF
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Drs George and Rozario correctly point out that the DCCT provides evidence for glycaemic control in type 1 diabetes. However, Dr Thomas's letter is clearly referring to type 2 diabetes and makes some valid points. Drs George and Rozario choose to use an observational study to support their point of view. In the hierarchy of evidence, an observational study comes below a randomised controlled trial. An observational study cannot prove cause and effect but only set a hypothesis. If at all possible, this hypothesis should be tested in a randomised controlled trial. This has been done in this case. We have UKPDS 33 and UKPDS 34. Metformin was shown to be an effective intervention, reducing the risk of several patient-orientated outcomes by a mechanism that seems to be at least partially not related to blood glucose lowering. In contrast, sulphonylurea and insulin had limited benefit despite somewhat better glycaemic control. Overall, there was a reduction in the need for retinal photocoagulation with a 10-year NNT of 37. This benefit was not apparent in obese patients. Tightly controlling blood pressure (1) and providing simvastatin 40mg (2) have the greatest impact on reducing the microvascular and macrovascular risks in type 2 diabetes. Unfortunately, presumably because diabetes is diagnosed based on blood glucose levels, many health professionals are glucocentric. This is then passed on to the patients who seem not to be aware of the prioities for lowering their risk of nasty things happening to them. Consider the law of diminishing returns. If the patient has stopped smoking, has their BP tightly controlled, and is taking metformin, simvastatin and aspirin, can their risk be realistically reduced to a clinically significant degree by tightly controlling their blood glucose? Do the patients want more intervention? Are the targets realistic? UKPDS 33 would suggest not. As Dr Daggett points out (3) "the pursuit of perfection is leading to progressive weight gain and recurrent hypoglycaemia". Dr Thomas is correct - after metformin anything else should be considered in the context of symptom control. All our interventions need to be effective, cost-effective and affordable. Tight blood glucose control in type 2 diabetes does not fit these criteria. 1) UKPDS 38. BMJ 1998; 317: 703-13 2) Heart Protection Study. Lancet 2003; 361: 2005-16 3) Achieving the new JBS2 targets - or not. Pract Diab Int 2006; 23: 280-81 Competing interests: None declared |
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