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Screening for diabetes and prediabetes COMMENTARY
 
 
  The Lancet Dec 8, 2007
 
Tim Kenealy a, C Raina Elley a and Bruce Arroll a a. Department of General Practice and Primary Health Care, University of Auckland, Auckland 1142, New Zealand
 
The Health Technology Assessment report by Norman Waugh and colleagues,1 on screening for type 2 diabetes challenges the health sector, and primary care in particular, to be more proactive in the detection and treatment of both diabetes and prediabetes. The conclusions are firmer than those of the UK National Screening Committee after a previous review.2 Waugh comes to this new view mainly as a result of the increasing prevalence of obesity and consequent type 2 diabetes, and the potential to reduce cardiovascular risk, especially with cheap generic statins. We welcome the attention given to prediabetes (impaired glucose tolerance and impaired fasting glucose).
 
We suspect that an absence of clear guidelines or acceptability for screening for diabetes has kept prediabetes in the shadows. Impaired glucose tolerance increases the risk of cardiovascular disease by about 60%, and impaired fasting glucose does the same by around 30%.3,4 Furthermore, for every person with diabetes, there are four with prediabetes.5 Although almost half of those with prediabetes progress to diabetes, this process can be prevented or slowed by diet, exercise, and several drugs that are used to treat diabetes.6 Waugh and colleagues' modelling predicts that screening for and treating impaired glucose tolerance would be cost effective, particularly when lifestyle interventions are used to treat identified cases.
 
Waugh and colleagues note that three of the National Screening Committee criteria are still not met. First, current management of diabetes is still less than optimal. Second, current staffing levels might not meet an increased workload from new diagnoses. Third, there is no evidence from randomised trials that screening for diabetes results in benefits in terms of cardiovascular disease or mortality, although a trial currently underway will have results in about 7 years. We suggest that efforts to improve diabetes care will always continue and that staffing levels often follow rather than precede new diagnoses. If we wait until diabetes management is perfect, until staff levels are ahead of requirements, and for a trial to be reported in 7 years, we could rightly be accused of fiddling while β-cell function burns.
 
We also suspect that screening for both diabetes and prediabetes has been inhibited by uncertainty over which test to use. Waugh and colleagues state that there is no perfect test. A fasting plasma-glucose test will detect diabetes and impaired fasting glucose but will miss impaired glucose tolerance. A random plasma-glucose test lacks sensitivity and specificity. An oral glucose-tolerance test is widely presented as a burden for patients and has poor reproducibility. Glycosylated haemoglobin (HbA1c) is not part of the formal diagnostic criteria for impaired fasting tolerance, impaired glucose tolerance, or diabetes, but correlates with all three and is used to monitor management of glycaemia in diabetes. Previous lack of standardisation of the HbA1c test has now largely been resolved, although some conditions such as haemoglobinopathies might still affect the result.7
 
Increasing concentrations of blood glucose, starting well below the diabetic range, measured by fasting glucose8 or HbA1c,9 are linearly related to cardiovascular disease outcomes and mortality (and also related to microvascular outcomes10). Avoidance of such outcomes is largely the purpose of diagnosis. Waugh and colleagues suggest that more people would be tested and identified at risk if HbA1c was used rather than glucose tests, and suggest a cut-off HbA1c of 5¥9% to identify diabetes and most prediabetes. The gain from this more convenient test and consequent increased uptake by patients could outweigh any disadvantages of the HbA1c test.
 
Waugh and colleagues suggest that screening be in two stages. The first step is selection of people at increased risk on the basis of age, body-mass index, or waist circumference, and other cardiovascular risk factors such as hypertension. We would add ethnic origin, family history of diabetes, and increased lipid concentrations. Various risk scores have been developed. The second step would be the blood test, such as HbA1c.
 
Admittedly some uncertainties remain. How often should screening be done if the initial screen is negative? The number of intensive lifestyle programmes that would be needed to treat large numbers of people with prediabetes are not yet in place. The alternative is to use drugs, which are less effective but might be the preferred choice for many patients.
 
Primary-care providers need a strong message that the detection and treatment of prediabetes is in their domain of activity. Ideally, risk scores would be relevant to local populations and supported by computerised calculators and reminders. Health planners might view these steps as a further strategy to reduce the health inequalities seen in most countries, because the rate of prediabetes, diabetes, and cardiovascular disease tends to disproportionately affect socially and economically disadvantaged groups in society, including indigenous peoples and minorities. It is time for prediabetes to come out of the primary-care closet.
 
BA is on the advisory board for Pharmac educational seminars; Pharmac is the Government-funded pharmaceutical-purchasing agency in New Zealand. BA is also on the primary care committee of the Future Forum and educational foundation funded by Astra Zeneca (UK). TK and CRE declare that they have no conflict of interest.
 
References
 
1. Waugh N, Scotland G, McNamee P, et al. Screening for type 2 diabetes: literature review and economic modelling. Health Technol Assess 2007; 11: http://www.hta.ac.uk/fullmono/mon1117.pdf (accessed on Sept 14, 2007)..
 
2. Wareham NJ, Griffin SJ. Should we screen for type 2 diabetes? Evaluation against National Screening Committee criteria. BMJ 2001; 322: 986-988.
 
3. The DECODE Study Group. Glucose tolerance and mortality: comparison of WHO and American Diabetes Association diagnostic criteria. Lancet 1999; 354: 617-621. Abstract | Full Text | Full-Text PDF (98 KB) | MEDLINE | CrossRef
 
4. Coutinho M, Gerstein HC, Wang Y, et al. The relationship between glucose and incident cardiovascular events: a metaregression analysis of published data from 20 studies of 95 783 individuals followed for 12¥4 years. Diabetes Care 1999; 22: 233-240. MEDLINE | CrossRef
 
5. Decode Study Group. Age- and sex-specific prevalences of diabetes and impaired glucose regulation in 13 European cohorts. Diabetes Care 2003; 26: 61-69. MEDLINE | CrossRef
 
6. Padwal R, Majumdar SR, Johnson JA, et al. A systematic review of drug therapy to delay or prevent type 2 diabetes. Diabetes Care 2005; 28: 736-744. MEDLINE | CrossRef
 
7. Genuth S, Alberti KGMM, Bennett P, et al. Follow-up report on the diagnosis of diabetes mellitus. Diabetes Care 2003; 26: 3160-3167. MEDLINE | CrossRef
 
8. Lawes CMM, Parag V, Bennett DA, et al. Blood glucose and risk of cardiovascular disease in the Asia Pacific region. Diabetes Care 2004; 27: 2836-2842. MEDLINE | CrossRef
 
9. Khaw KT, Wareham N, Luben R, et al. Glycated haemoglobin, diabetes, and mortality in men in Norfolk cohort of european prospective investigation of cancer and nutrition (EPIC-Norfolk). BMJ 2001; 322: 15-18.
 
10. Stratton IM, Adler AI, Neil HA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ 2000; 321: 405-412.
 
 
 
 
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