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Diabetes is a chronic systemic disorder of glucose metabolism. The World Health Organization (1999) described the condition as ‘a metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both’ (World Health Organization, 1999). Among the associated morbidities is impaired wound healing. This article reviews the possible mechanisms by which diabetes can affect wound healing.

Diabetes is a systemic disorder that affects almost all body systems, either directly or indirectly through its complications. Among the acute complications, acute metabolic derangements, urinary tract infections, skin and other infections and side effects of drugs are important. The major chronic complications are retinopathy, nephropathy, neuropathy, ischaemic heart disease, cerebrovascular disease, peripheral arterial disease and skin lesions. Among these, peripheral arterial disease is one of the major morbidities. In the US, 35-45% of all limb amputations are performed on people with diabetes (Stonebridge, 1996). Type 2 diabetes has a stronger association with these morbidities than type I diabetes does.

The effects of diabetes on healing are diverse, multifactorial, complex and inter-related (Greenhalgh, 2003). It is one of the well-known intrinsic factors which affect wound healing. In fact, diabetes affects almost all stages of wound healing to some extent. The underlying mechanisms have been extensively investigated in the past few decades.

Effects of non-enzymatic glycation

The hyperglycaemia associated with diabetes can cause tissue damage in two ways. The first pathway is the intracellular hyperglycaemia caused by increased flux through different metabolic pathways, which can adversely affect cellular functions. This is the underlying mechanism of early diabetic cataracts and peripheral neuropathy. The second, and more important, pathway for long-term complications in diabetes is the non-enzymatic glycation of proteins. In this process, glucose chemically attaches to the amino group of proteins without the involvement of enzymes. These stable products then accumulate over the surface of cell membranes, structural proteins and circulating proteins. They are called ‘Amadori products’.

Proteins with a longer half-life, such as collagen, fibrin, albumin and haemoglobin, accumulate advanced glycation end products, which form slowly from Amadori products through series of further reactions. The extent of these reactions depends on the concentration of glucose, the duration of hyperglycaemia and the half-life of these proteins. This non-enzymatic glycation can affect a number of physiological processes in the body, ranging from enzymatic activity and binding of regulatory molecules to cross-linking of proteins and susceptibility to proteolysis (Reiser, 1998).

The microtubular protein tubulin forms non-reducible aggregates during non-enzymatic glycation and contributes to the defective axoplasmic transport seen in diabetic neuropathy. Non-enzymatic glycation is also responsible for the thickening of the glomerular basement membrane seen in diabetic nephropathy (Makita et al, 1991). This results from accumulation of albumin and trapping of immunoglobulin G.

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Non-enzymatically glycated collagen binds soluble proteins to form in situ immune complexes characteristic of diabetic nephropathy (Brownlee et al, 1984). Similarly, thickening of basement membrane in the microcirculation can lead to ischaemia and decreased tissue perfusion, which in turn results in impaired wound healing (Cavallo et al, 1984). The important proteins from a wound healing perspective that are affected by non-enzymatic glycation are collagen, fibrin and keratin.

Fibronectin is the major glycoprotein secreted by fibroblasts during initial synthesis of extracellular matrix proteins. It serves important functions, being a chemo-attractant for macrophages, fibroblasts and endothelial cells. It promotes re-epithelialisation and acts as a transduction agent in wound contraction. Non-enzymatic glycation of fibronectin decreases its ability to bind to collagen, gelatin and heparin. Di Girolamo et al (1993) were unable to show significant differences in functional activities of fibronectin between people with diabetes and controls. They postulated, however, that defects in wound healing are caused by the hyperglycosylation of the locally synthesised cellular fibronectin and are not due to the effect on plasma fibronectin.

Altered metabolism of proteins, carbohydrates and fats

Insulin is an anabolic hormone which promotes protein synthesis and utilisation of glucose. Diabetes affects the metabolism of carbohydrates, proteins and fats, which play an important role in cellular activities, proliferation, and migration and wound healing (Cooper, 1990).

Despite overwhelming evidence of the benefits of statins for people with diabetes, many eligible patients either are still not receiving them or are being prescribed an inappropriate statin (not potent enough) or too low a dose to achieve recommended cholesterol target levels. Hence they remain at high risk of cardiovascular disease. Increasingly, the decision to prescribe statins is being made by a patient’s GP. This article looks at the influences on GPs’ prescribing of statins, in terms of current evidence and national guidelines.

Between 3% and 3.5% of patients in each general practice in the UK have diabetes, mostly type 2 (Harvey et al, 2002). Cardiovascular disease (CVD) accounts for the greatest proportion of mortality and morbidity in these patients. Prevention of CVD is therefore of major importance in this patient group, and the management of raised cholesterol in people with diabetes is a key issue.

Increasingly, the management of people with diabetes is provided by the primary care in-house diabetes clinic, and the decision to prescribe statins is made by a patient’s GP. This article looks at the factors that are most likely to influence this decision, in terms of current evidence and national guidelines.

Particular reference will be made to data from the Heart Protection Study (HPS; Collins, 2003) and the more recently reported Collaborative Atorvastatin Diabetes Study (CARDS; Colhoun et al, 2004) and A raNdomised, Double blind, study to compare Rosuvastatin (10 mg and 20 mg) and atOrvastatin (10 Mg and 20 mg) in patiEnts with type 2 DiAbetes (ANDROMEDA; Betteridge and Gibson, 2004).

* HPS compared the use of 40 mg simvastatin vs placebo. It included the largest subsection of people with diabetes ever studied and produced highly significant data.

* CARDS specifically investigated people with diabetes and resulted in an impressive 37% reduction in primary cardiovascular endpoints.

* ANDROMEDA and CORALL (COmpare the effects of Rosuvastatin with Atorvastatin on apo B/apo A-1 ratio in patients with type 2 diabetes meLLitus and dyslipidaemia; Wolffenbuttel et al, 2005) are comparative studies of rosuvastatin and atorvastatin.

All these trials used optimum doses of powerful statins. The National Institute for Health and Clinical Excellence (NICE) statin guidelines are currently under evaluation, and their influence in terms of people with diabetes will also be considered.

Evidence for the benefits of statins in diabetes

A number of large clinical trials have established statins as effective agents in the prevention of both primary and secondary coronary heart disease (CHD; Downs et al, 1998; Shepherd et al, 2002; Collins et al, 2003; Sever et al, 2003), with a clear association between cholesterol reduction and outcome benefits (Figure 1; Gould et al, 1998). Many of these studies included significant sub-groups of people with diabetes.

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The HPS demonstrated uniform risk reduction across a wide range of patients, including those with diabetes (Collins et al, 2003). Indeed, type 2 diabetes was an independent predictor of benefit from statin therapy, with a 1 mmol/l reduction in low-density lipoprotein (LDL)-cholesterol resulting in a 22% reduction in risk of a first vascular event, independent of baseline LDL-cholesterol levels.

These data are consistent with a recent meta-analysis of diabetes sub-groups from statins trials, which demonstrated that cholesterol reduction may reduce the risk of primary and secondary cardiovascular events by 22% and 24% respectively (Vijan and Hayward, 2004).

Relative risk reduction is similar in primary and secondary prevention trials; however, as patients with established CHD are at greater absolute risk, statin therapy achieves substantially higher absolute reduction in secondary prevention trials than in primary prevention studies (Vijan and Hayward, 2004). Similarly, patients with type 2 diabetes are at higher absolute risk than those without diabetes, therefore statin therapy results in greater absolute benefit in patients with type 2 diabetes (Vijan and Hayward, 2004).

Data from studies such as the HPS therefore suggest that all patients with type 2 diabetes should qualify for statin therapy. CARDS further illustrated the benefits of cholesterol reduction in patients with type 2 diabetes (Colhoun et al, 2004). In this study of more than 2800 people with type 2 diabetes and at least one other CHD risk factor, an LDL-cholesterol reduction of 40% and triglyceride reduction of 19% were associated with a 37% reduction in major coronary events and a 48% reduction in stroke.

A meta-analysis of lipid-lowering trials in type 2 diabetes has concluded that the number needed to treat to prevent one CHD event was 13.8/4.9 years of secondary prevention and 34.5/4.3 years for primary prevention (Vijan and Hayward, 2004). Thus, compared with commonly adopted medical interventions, cholesterol reduction appears to be cost-effective even in the absence of overt CVD.

The Primary Care Diabetes Society in association with Diabetes & Primary Care Journal presents Diabetes care delivery in a changing world: translating theory into day-to-day practice to be held at The Belfry, Warwickshire, 11-12 November 2005

… state-of-the-art lectures, clinical updates and masterclasses offering practical guidance to healthcare professionals on how best to confront present and future therapeutic and political issues that directly impact on their everyday practice.

CME ACCREDITATION SOUGHT

THIS CONFERENCE IS AIMED AT ALL HEALTHCARE PROFESSIONALS WHO WISH TO IMPROVE PRIMARY DIABETES CARE, INCLUDING GPS, PRACTICE NURSES, DIABETOLOGISTS, DSNS, DIETITIANS, PHARMACISTS, PODIATRISTS, COMMUNITY NURSES.

‘I am delighted to introduce the Inaugural conference of the new Primary
Care Diabetes Society (PCDS). Diabetes in primary care is in a period of
great upheaval as GPs and their teams actively engage with patients to
improve their care. It is important and timely that the PCDS, an
organisation dedicated to improving the treatment of people with
diabetes, has now emerged. As part of our plans to promote interaction
and learning among the whole range of healthcare professionals working
within diabetes care, our first annual conference will focus on the
impact of clinical, political and educational developments on the future
of primary care diabetes. This is YOUR Society and YOUR conference. I
invite you to have YOUR say.’
Colin Kenny, GP and Acting Chair of the PRIMARY CARE DIABETES SOCIETY

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CME sought

DIABETES CARE DELIVERY IN A CHANGING WORLD
The Belfry, 11-12 November 2005

DAY ONE PROGRAMME (FRIDAY 11 NOVEMBER 2005)

09.45        Registration and coffee

Session 1: The changing face of diabetes care delivery
10.45        Chair’s introduction — Colin Kenny
10.50        Conference opening — Sue Roberts
11.05        A practical approach to what you need to know about:
Emerging Therapies 1: Glycaemic Management–Cliff Bailey
* Insulin options available
* Present & future oral agents
* A place for pumps?
11.50        Emerging Therapies 2: Cardiovascular Risk–Miles Fisher
* Current management strategies
* What next?
12.35        Lunch and exhibition viewing

Session 2: Addressing the multifaceted nature of diabetes
13.45        Masterclasses (1st rotation)
1. Initiating insulin–Debbie Hicks
*  Implications for primary care
*  Which insulin for whom?
2. Supporting patients to adjust their own insulin–Heather
Daly
*  Should insulin self-adjustment be encouraged?
*  How can we support patients to take this on?
3. Encouraging concordance–are we simply whistling in the
wind?–Chas Skinner
*  Why ‘education’ does not always lead to behaviour change
*  How to promote self-management
4. Management nightmares–Neil Munro
*  Case study examples
*  When to refer
5. Patient education modules–where are we?–Mary MacKinnon
*  Which modules are relevant?
*  How and for whom do they work?
6. How to spot the at-risk foot–Roger Gadsby
*  Step one is to identify the at-risk foot
*  Step two is to decide what to do about it
14.45        Masterclasses (2nd rotation)
15.45        Tea

Session 3: Keynote Lecture–’The global challenge’
16.20        Obesity–a practical approach to a difficult problem–Omar
Ali
* Pharmacology, diet and exercise, psychology–but in what
combination?

Session 4: Sponsored satellite symposium
17.15-18.45  ‘The statins debate’–satellite symposium supported by an
unrestricted educational grant from Pfizer
20.00        Pre-dinner drinks followed by Conference Dinner

DAY TWO PROGRAMME (SATURDAY 12 NOVEMBER 2005)

08.30-09.30  Breakfast and satellite symposium supported by an
unrestricted educational grant from GlaxoSmithKline
09.30        Coffee and exhibition viewing

Session 5: Consensus or conflict in the future of primary diabetes care?
10.00        GMS2 Contract–where to next?–Peter Holden
* Likely effects on our patients, our profession and our
pockets
10.30        HEAD-TO-HEAD DEBATE: (Rory McCrea vs Clive Marchi)
‘General practice is not fit to look after people with
diabetes’
* An impassioned review of what general practice can and
cannot hope to offer the person with diabetes
11.30        Coffee
12.00        How to find the missing million–a practical approach–
Melanie Davies
* Who should be screened?
* How and where should this happen?
12.30        Primary Care Diabetes Society business–AGM, election,
soapbox, GPwSIs
13.30        Finish

There are more than 1.75 million people with type 2 diabetes in the UK, and the number of people diagnosed with type 2 diabetes is set to rise dramatically over the next decade. The UK Prospective Diabetes Study (UKPDS) provided evidence to support early active treatment of type 2 diabetes in order to reduce the risk of future complications (UKPDS Group, 1998). This article assesses the feasibility of screening for type 2 diabetes at the GP practice level.

Standard 2 of the National Service Framework (NSF) for diabetes (Department of Health [DoH], 2001) relates to the development and implementation of strategies to identify people with diabetes. The aim is to ensure that people with diabetes are identified as early as possible. Moreover, the NSF concludes that population-wide screening would not be cost-effective, and instead recommends screening sub-groups with multiple risk factors. Diabetes UK also supports the introduction of a screening programme, recommending systematic and opportunistic screening of people with two or more risk factors every 3 years (Diabetes UK, 2002).

It would seem to be a sensible step forward, then, to actively screen for diabetes, but how practical is this in primary care? The National Screening Committee (http://www.nsc.nhs.uk/[accessed 23.09.2005]) has been asked to research the feasibility of a screening programme and is due to report later this year.

The UK Prospective Diabetes Study (UKPDS; UKPDS Group 1998a) provided convincing proof of the value of good glycaemic control in type 2 diabetes. This article summarises the options for managing glycaemia in the primary care setting–from nutritional and exercise approaches to the use of oral agents and insulin therapy.

There is high quality evidence from randomised controlled trials in both type 1 and type 2 diabetes to show that intensive control of blood glucose (giving Hb[A.sub.1c] measurements of 7% or less) reduces the risk of adverse outcomes. The evidence in type 1 diabetes comes from the Diabetes Control and Complications Trial (DCCT; DCCT Research Group, 1993), in which an intensively controlled group with an average Hb[A.sub.1c] of 7% had a 47% reduced risk of severe retinopathy, a 54% reduced risk of developing microalbuminuria and a 60% reduced risk of neuropathy compared with a standard treatment group who had an Hb[A.sub.1c] of 9%.

In type 2 diabetes, the United Kingdom Prospective Diabetes Study (UKPDS) provided convincing proof of the value of good glycaemic control (UKPDS Group, 1998a). In the study, 5102 people with newly diagnosed type 2 diabetes were initially managed with 3 months’ diet treatment. Then 4209 of these who were asymptomatic and had fasting plasma glucose levels between 6 and 15 mmol/l were randomised into an intensively treated group, who had an average Hb[A.sub.1c] of 7.9%, and a conventionally treated group, who had an average Hb[A.sub.1c] of 7%. Follow up was for 12 years on average. The intensive group had 12% less risk of any diabetes-related adverse endpoints, 25% fewer adverse microvascular endpoints and 16% fewer myocardial infarctions (this figure for major macrovascular outcomes did not reach statistical significance). Neither sulphonylurea nor insulin therapy showed any advantage over the other, but a group of obese patients randomised to metformin had substantially better macrovascular outcomes (UKPDS Group, 1998b).

This UKPDS glycaemic data has also been published in an epidemiological form in which it can be shown that adverse outcomes are reduced given any reduction in Hb[A.sub.1c] level even if a target of 7% is not reached, and thus a reduction of Hb[A.sub.1c] from 10% to 9% is of benefit (Stratton et al, 2000).

The diabetes section of the Quality and Outcomes Framework of the new General Medical Services (nGMS) contract for general practitioners recognises the importance of glycaemic control in diabetes by giving 30 points for glycaemic control: 3 for Hb[A.sub.1c] process measurements and 27 for reaching Hb[A.sub.1c] quality targets (British Medical Association, 2003).

Achieving good glycaemic control: The role of nutrition and exercise

The emphasis today in diabetes is away from the concept of diet, towards the concept of healthy eating. This concept of healthy eating is important for all people and its adoption by all members of the family will help in management.

A simple written guide can be used to reinforce healthy eating messages. A full assessment can be given by a dietitian for those who need more detailed advice.

Weight reduction in those who are overweight is a vital part of type 2 diabetes management. There is clear evidence that weight reduction and exercise can prevent the onset of diabetes in people who are especially at risk (i.e. those with impaired glucose tolerance; Tuomilehto et al, 2001). Regular weighing and encouragement of weight loss (in those who are overweight) at each practice diabetes visit can help in this difficult area. Some people also benefit from attendance at peer-support groups such as ‘Weight Watchers’ and similar groups.

Encouraging exercise in diabetes is another vital part of good glycaemic control, and has been shown to help prevent the onset of diabetes in susceptible individuals (Tuomilehto et al, 2001).

It is important that advice about exercise should be realistic, simple, individualised, and enjoyable. Gentle walking for 20 minutes a day is a realistic goal in self-management for many people with diabetes. In parts of the UK ‘walking for exercise’ schemes have been established where people are invited to join in set walks which are organised and led by local volunteers.

It is usual to give most overweight people newly diagnosed with type 2 diabetes initial nutrition and exercise advice and to review them at 3 months to see if it has been successful at reducing Hb[A.sub.1c] levels to target.

If nutrition and exercise alone are not successful in giving good glycaemic control, oral agents need to be added.

Initial oral agent monotherapy NICE guidance on initial monotherapy choice

For those overweight: Metformin as initial monotherapy

The National Institute for Health and Clinical Excellence (NICE; formerly the National Institute of Clincal Excellence) guideline on glycaemic control in type 2 diabetes (NICE, 2002) recommends that metformin be the initial monotherapy of choice in all people who are overweight (defined as a body mass index [BMI] greater than 25 kg/[m.sup.2]).

Scientists have found a way to produce large amounts of a type of pancreas cell that doctors have already successfully transplanted into people with type 1 diabetes. The cells, collected from donors, have been in such short supply (SN: 6/19//04, p. 398) that only 1 percent of people in need have received transplants.

Establishing a lab-grown line of beta cells could overcome this shortage, says Ji-Won Yoon of Chicago Medical School in North Chicago, Ill. In type 1 diabetes, the immune system kills beta cells, eliminating the body’s source of insulin. Without that hormone, tissues can’t process sugar, so people with diabetes rely on insulin injections.

In the October Nature Biotechnology, Yoon and an international team of researchers report a beta cell-production technique that could, in principle, solve the supply problem. Central to their technique is what the researchers call a “reversibly immortalized” line of human beta cells.

First, the researchers extracted beta cells from pancreases collected from human cadavers. Then, because these cells tend to die quickly outside the body, the team supplied them with genes that perpetuate cell replication.

Such immortalizing of cells comes with a risk: The cells may grow into tumors. To counter that, the researchers included a mechanism to shut off the replication. They incorporated a molecular marker that guides a DNA-excising enzyme to the site of the added genes. The excision is timed to take place after large amounts of beta cells have been produced but before the cells are transplanted.

Next, the researchers screened 271 of their altered beta cell lines to find the ones most suitable for transplants. They eliminated lines that produced tumors despite the removal of the immortalization genes, and they disregarded the lines that didn’t produce insulin and other beta cell proteins. In the end, only one line passed both tests.

Using the winning beta cell line, the researchers cultured enough cells to transplant 3 million into each of 10 diabetic mice lacking immune activity. The team reports that these mice maintained normal blood-glucose concentrations for more than 30 weeks.

“What they’re selling is an impressive proof of principle,” according to Christopher Newgard of Duke University Medical Center in Durham, N.C. The lab-grown beta cells produce only 40 percent as much insulin as normal beta cells do, he notes. Therefore, more than 1 billion cells would be needed for a human transplant. This number “clearly requires large-scale cell growth,” says Newgard. It might be difficult to keep tumor-causing mutations out of such a large number of cultured cells, he cautions.

Yoon’s current goal is to mass-produce reversibly immortalized cells that are safe and effective enough to gain Food and Drug Administration approval for use in people.

He notes that his team’s beta cells would still be at risk from immunological attack when transplanted. The researchers aim to eventually develop beta cell lines that can withstand such an attack.

The Annual General Meeting and Conference of the Irish Diabetes Nurse Specialist Association was held on 30 September and 1 October 2005. It took place in the Four Seasons Hotel, Dublin. Novo Nordisk supported the conference. Over 100 delegates attended.

Dr James O’Neill, a Cardiologist, gave the first lecture of Friday’s programme on heart failure and diabetes. It was a very informative talk. Dr O’Neill highlighted the need for closer co-operation between our two specialities for the benefit of the patients attending both our services.

Ms Mary O’Scannaill, a Diabetes Nurse Specialist, and Ms Cathy Breen, a Dietitian (both based at St Columcille’s Hospital, Loughlinstown), gave the next lecture. They outlined their experience of setting up and running a Dose Adjustment For Normal Eating (DAFNE) programme. The benefits to the patients and the resources needed to run such a programme were discussed. It was a very thought-provoking lecture and prompted a lot of discussion.

The final lecture was an update on the PREDICTIVE study, given by Dr Donna Sexton. It was interesting to hear the experiences of the use of insulin detemir (Levemir; Novo Nordisk) in other countries.

On Saturday morning, Ms Nell McDowell, a Paediatric Diabetes Nurse Specialist, and Dr Colm Costigan, an Endocrinologist (both based at Our Lady’s Hospital, Crumlin), gave a comprehensive session on the paediatric management of diabetes. Particular emphasis was given to the need to individualise care based on the child’s stage of development and the needs of the family as a whole.

This session was followed by the Annual General Meeting. Rita Forde (Chairperson) and Pat Keenan (Secretary) stepped down from the executive this year. Sonia Browne and Jennifer Clarke were elected and welcomed onto the executive. I would like to thank both Rita and Pat for all the hard work they have done for the association. Finally, as the new Chairperson, I will endeavour to live up to the high standards set by my predecessors.

Carotenoids are a wide range of compounds derived solely from plants. The major ones include r-carotene, a-carotene, a-cryptoxanthin, lutein/zeaxanthin, and lycopene. Considerable epidemiologic evidence exists that some carotenoids are potent antioxidants and may play a protective role against the development of chronic disease such as atherosclerosis, stroke, certain cancers and inflammatory diseases. Although obesity and physical inactivity are known to be major risk factors for type 2 diabetes, evidence suggests that oxidative stress may also contribute to the pathophysiology of type 2 diabetes. In addition, serum or dietary vitamin A, E and C levels have been hypothesized to be lower in persons with IGT or with type 2 diabetes. Therefore, a recent study investigated the relationship between the major serum carotenoids and type 2 diabetes status in a cross-sectional population-based study in Queensland, Australia.

Adults aged older than 25 years from six randomly selected cities and towns in Queensland, Australia were included in the study: Fasting plasma glucose, an oral-glucose tolerance test and measurement of the serum concentrations of five carotenoid compounds were measured between October 2000 and December 2000. Demographic and lifestyle variables were collected by using standardized questionnaires.

Mean 2-hour postload plasma glucose and fasting insulin concentrations decreased significantly with increasing quintiles of the five serum carotenoids–a-carotene, a-carotene, a-cryptoxanthin, lutein/zeaxanthin, and lycopene. Fasting glucose concentrations also decreased significantly with increasing quintiles of a-carotene and a-carotene. Geometric mean concentrations for all serum carotenoids decreased with declining glucose tolerance status. a-carotene had the greatest decrease, to geometric means of 0.59, 0.50, and 0.42 gmol/L in persons with normal glucose tolerance, impaired glucose metabolism, and type 2 diabetes, respectively.

The results show that serum carotenoids are inversely associated with type 2 diabetes and impaired glucose metabolism. Randomized trials of diets high in carotenoids-rich vegetables and fruits are needed to confirm these results and those from other observational studies. Such evidence would have very important implications for the prevention of diabetes.

This year’s FEND (Federation of European Nurses in Diabetes) conference in Athens, Greece, marked the 10th anniversary of the group’s foundation. Appropriately entitled ‘The Diabetes Marathon’, the 2-day event took place on 9-10 September 2005 and was attended by more than 500 diabetes nurses from over 30 countries around the world.

Anne-Marie Felton, Chair of FEND, explained in her opening address that ‘for every person with diabetes, every day is a marathon for which is required training, endurance and the support of a team.’ Diabetes, she said, is a growing epidemic that has to be made a priority among leaders of the EU Parliament. For this reason, Anne invited delegates to sign the FEND Athens Declaration (available at www.fend.org) that will be presented to the EU Commissioner.

The conference included keynote lectures, masterclasses and posters. This issue of Dialogue summarises some of the main discussion points raised by speakers and delegates alike. Reports are also included on a satellite session to the recent EASD (European Association for the Study of Diabetes) 41st Annual Meeting in Athens, and Novo Nordisk’s National Symposium on Paediatric and Adolescent Diabetes in Nottingham, UK.

‘The pandemic of Diabetes Mellitus presents a major public health challenge for all European national health care systems. It is estimated that 30 million European citizens have diabetes today within the European Union, with a prevalence of 7.5% in member states. In addition a further 50% of EU citizens are estimated to have this incurable condition but are currently unaware. This indicates a pernicious low level of awareness and demonstrates a serious and unacceptable deficiency in diagnosis of high risk groups and a paucity of national prevention public health policies within the EU.

Diabetes continues to be a leading cause of premature death, a 3-4 times higher risk of cardio-vascular disease, a 20 fold higher risk of lower limb amputation, the commonest cause of renal failure and blindness. In recent years the emergence of type 2 diabetes in children and adolescents is a new and serious health challenge to the youth of Europe, their families and society. It is further estimated that pre-diabetes affects 100 million people of whom 50% will develop diabetes within the next 5 years.

The Federation of European Nurses in Diabetes is of the firm conviction that DG SANCO and the Commissioner have a unique responsibility to the citizens of Europe to establish in partnership with national ministries of health within member states and the relevant pan European NGOs, an EU Framework for the prevention and management of diabetes.

Such is the magnitude of the problem that micro plans are deemed inadequate to meet the challenge of the European diabetes epidemic and require a comprehensive European strategy in order to reduce the cost burden in terms of human suffering and economic loss.

The imperative to establish EU leadership, true connectiveness and relevance with its citizens is an opportunity that must be grasped urgently with generosity and sensitivity in partnership with key stakeholders.

We the undersigned urge the political leaders of the EU, members of the European parliament, national members of Parliament and Ministries of Health to respond positively and in a timely fashion to this urgent request.’