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Diabetes in the

  1. 1. Diabetes in the United Kingdom-1996 A British Diabetic Association Report ©1995 British Diabetic Association 10 Queen Anne Street, London, W1G 9LH Tel: 020 7323 1531 A charity helping people with diabetes and supporting diabetes research Registered Charity No. 215199
  2. 2. Acknowledgements We would like to acknowledge the help of the following in commenting upon draft text of this report: Professor H. Keen and Professor K.G.M.M. Alberti Dr W.D. Alexander Dr P. Betts Dr A.C. Burden Dr M.E. Edmonds Dr J.H. Fuller Professor P.D. Home Professor R.J. Jarrett Professor A.L. Kinmonth Professor E.M. Kohner Dr R.D.G. Leslie Dr M. Nattrass Dr. A. Neil Dr K.R. Paterson Professor R.B. Tattersall Dr R.C. Turner Professor G.C. Viberti Professor D.R.R. Williams We would also like to thank the following for allowing us to use unpublished or reworked data: Dr P, Betts (Wessex Paediatric Diabetes Audit) Dr J.K. Cruickshank (African-Caribbean prevalence data) Dr A.J. Swerdlow (BDA cohort mortality data) 2
  3. 3. Foreword The growth in size and complexity in this new version of 'Diabetes in the United Kingdom' testifies to the remarkable rate at which knowledge has increased since Sir John Nabarro produced the first edition in 1988. Perhaps the single most important factor since then has been the landmark Saint Vincent Declaration (see Appendix 1) which was very largely the voice of people with diabetes calling for a better deal. Knowledge must be turned into action. If it is, much of the burden of diabetes and its complications can be reduced. There are still important gaps in our knowledge and it is crucial that we fill them. We know for example that many older people already have some of the blood vessel problems at the time they are first diagnosed. They have had diabetes, probably for years, without being aware of it. In our efforts at prevention, we must think again about screening for unsuspected diabetes, particularly after age 40. Early diagnosis is really in the hands of the family doctor and better methods need to be developed. In the United Kingdom, the BDA/Department of Health St Vincent Joint Task Force has clarified the way ahead and it is now largely up to people in the localities, patients and professionals together, to get the recommendations put into practice, without delay. This report summarises much of what we know of diabetes in the UK today. With the right investment of imagination, determination and organisation (and money), the next edition could paint a dramatically improved picture. Professor Harry Keen Chairman, Board of Trustees British Diabetic Association 3
  4. 4. Contents page 1. What is diabetes? 5 2. How common is diabetes? 7 3. What causes diabetes? 15 4. Treatment of diabetes 17 5. The complications of diabetes 22 6. Care of the person with diabetes 42 7. The costs of diabetes 45 8. What does the future hold? 48 Appendix 1 Diabetes care and research in Europe Saint Vincent Declaration 52 Appendix 2 BDA reports 53 4
  5. 5. 1. What is diabetes? Diabetes mellitus is a condition in which the amount of glucose in the blood is abnormally high because the body is no longer able to use it adequately as a fuel. Glucose is a simple sugar, which is an essential fuel for the brain and muscles. It is obtained from certain types of food: sugar and other sweet foods, and starchy foods such as bread and potatoes, which are broken down to glucose by the digestive system. It may also be produced from the liver which stores glucose that is not immediately required. The use of glucose as a fuel requires the hormone insulin. When the amount of glucose in the blood rises, for example after a meal, insulin is released from the pancreas, enabling the glucose to enter individual cells and there be converted to energy. Insulin therefore plays a key role in the body's use of glucose. When there is a shortage of insulin, or if the available insulin does not function correctly, glucose will accumulate and diabetes will develop. There are two main types of diabetes: 1. Insulin dependent diabetes (IDDM) - sometimes known as Type 1 diabetes This occurs when there is a severe lack of insulin due to the destruction of most or all of the islet cells in the pancreas which produce it. Regular insulin injections are essential for the person's survival. This type of diabetes usually appears before the age of 40 but may occur at any age, and usually develops fairly rapidly. 2. Non insulin dependent diabetes (NIDDM) - sometimes known as Type 2 diabetes This occurs when the body is still producing some insulin, but in inadequate amounts, and/or when the insulin that is produced is not able to work properly. In most cases, glucose levels in the blood can be improved by diet, or diet and tablets, though sometimes insulin injections may be needed. This type of diabetes usually appears in people over the age of 40, tends to have a more gradual onset, and may be found incidentally The main symptoms of untreated diabetes are the passage of increased amounts of urine, increased thirst, itching of the genitals, weight loss, extreme tiredness and blurred vision. These symptoms are usually much worse in IDDM. 5
  6. 6. When the glucose level in the blood rises above a certain threshold level, it spills over into the urine. In order to get rid of this excess glucose, the kidneys excrete more water, resulting in the frequent passing of large amounts of urine. This loss of water contributes to the thirst. Urine containing a large amount of sugar may irritate the genital area, and irritating thrush infections may develop. This frequently causes itching of the vulva in women and less often, itching under the foreskin in men. When the body fails to utilize glucose, it turns to alternative sources of energy; consequently, the body's fat and protein stores are broken down. This results in weight loss, which may sometimes be rapid and severe. Tiredness and weakness result from the reduced availability of energy. Temporary blurring of vision may result when abnormally high blood glucose levels affect the light conducting pathways of the eye. 6
  7. 7. 2. How common is diabetes? Definitions of terms used: Prevalence is the number of cases at a given point in time, usually expressed as a proportion of the population. Incidence is the number of new cases occurring during a given time period, usually expressed as new cases per 100,000 of the population per year. For certain infectious diseases and other new diagnoses which are notifiable to the health authorities, or for which registers are actively kept, data on prevalence and incidence can be fairly easily obtained. Diabetes does not however fall into either of these categories at present, and estimates are based upon samples taken from various parts of the country, from the few diabetes registers that exist or from population surveys. A further problem is that diabetes may be present, but undiagnosed, sometimes for several years, in many people. A number of studies have attempted to identify all people known to have diabetes within a certain defined area by various means including analysis of medical records, prescription requests and postal questionnaires. Estimates from these studies range between 0.95 per cent and 1.36 per cent of the population. However, more recent findings from a survey of almost 17,000 adults in England suggest that the true figure may be considerably higher (see section on Adults). Although it is clear that the great majority of people with diabetes are non-insulin dependent, estimates of the exact proportion vary from 75 per cent to 90 per cent. At least part of this discrepancy is due to the fact that it can be difficult to differentiate in some people between IDDM and NIDDM; for example, people with NIDDM who are treated with insulin may be wrongly classified as having IDDM. Adults The 1993 Health Survey for England carried out by the Office of Population Censuses and Surveys, interviewed a sample of 16,569 adults (aged 16 and over). The prevalence of self-reported diabetes over the whole age range was three per cent. If this figure of three per cent is extrapolated to the whole UK population, and given that the total adult (aged 16 and over) population is approximately 46 million (1993 estimate based on 1991 census results), this means that there are about 1,380,000 adults with known diabetes in the UK. On the basis that between 75 per cent and 90 per cent of these people have NIDDM, this will mean that between 1,035,000 and 1,242,000 adults in the UK have NIDDM, and between 138,000 and 345,000 have IDDM. 7
  8. 8. The prevalence of diabetes is clearly seen to increase with age. In those aged 65 and over, it has been shown to be as high as six per cent. This is almost entirely accounted for by a higher incidence and prevalence of NIDDM. Figure 1: The age-specific prevalence of diagnosed diabetes in the Oxford Community Diabetes Study Prevalence now appears to be higher in men than in women, reversing the clear female excess of the 1950's and 60's. The 1993 Health Survey for England reported prevalence of diabetes as 3 per cent in men compared with two per cent in women. Similarly, in the UK Prospective Diabetes Study (a large study of people newly diagnosed with NIDDM, aged 25 to 65), the overall ratio of men to women was approximately 3:2. Figure 2: The age and sex distribution of people entering the UK Prospective Diabetes Study 8
  9. 9. The total number of people newly diagnosed as having diabetes each year in the UK (incidence) is very difficult to ascertain. Reports based on the number of patients newly attending diabetic clinics may also include many previously diagnosed patients referred later to the clinic. On the other hand, they would omit those diagnosed and treated solely in the primary health care setting. A survey of the number of people with newly diagnosed diabetes referred to hospitals carried out in nine British towns during 1977-8 reported annual incidence ranging between 16 per 100,000 in York and 40 per 100,000 in Preston (average for all nine towns was 24 per 100,000). A much higher figure of 100.3 per 100,000 was derived in 1978 from new attenders at a diabetes clinic in a district in Wolverhampton where the majority of new diabetic patients were seen at least once in the hospital clinic. Children and young adults It has been estimated that in the UK there are at least 20,000 people under the age of 20 with diabetes (prevalence in this age group 0.14 per cent). Almost all are insulin dependent, NIDDM being relatively rare under the age of 40. The numbers and proportions of this 20,000 in each age band are shown in Table 1 below: Table 1: The estimated number of young people with diabetes in the UK 0- <5 5- <10 10- <15 15- <20 years 1000 3200 7200 8600 (5%) (16%) (36%) (43%) This means that in the average health district, there will be about 100 people under the age of 20 with diabetes. In 1988, a study was carried out to estimate the incidence of IDDM in children under the age of 15 years in Britain. In the UK, a total of 1,529 children had a confirmed diagnosis of IDDM, giving a national incidence of 14.2 per 100,000 per year. Rates varied between regions, ranging from 8.0 per 100,000 per year in the North West Thames region to 19.8 per 100,000 per year in Scotland. Incidence of diabetes in this age group appears to be increasing; a study carried out in Leicester indicated that the number of new cases diagnosed each year in the 1970s was approximately three times higher than that in the 1950s. Data from registers kept in other UK regions also indicate a rising trend. Ethnic groups The prevalence of diabetes, NIDDM in particular, in communities of Asian and African-Caribbean origin, is higher than in those of European origin. In Southall, London, rates of known diabetes were three to four times higher in South Asians than other resident adults. A similar high prevalence was found in people of Asian background in Coventry (see Table 2). 9
  10. 10. Table 2: The prevalence of diabetes (known and previously undiagnosed) in people of Asian and European origin in the Coventry study.** Age Men Women Asian European Asian European 20-39 2.5% 0.5% 1.5% 0.5% 40-59 12.5% 3.5% 9.5% 6.0% 60-79 25.5% 6.5% 20.0% 8.0% If data from four different studies that have included people from different ethnic backgrounds are pooled, a higher prevalence in people of African-Caribbean origin is evident as well (see Table 3). Table 3: The prevalence of diabetes (known and previously undiagnosed) in people of African-Caribbean and European origin (pooled data from four UK studies).** Age Men Women African- European African- European Caribbean Caribbean 40+ 16.7% 5.0% 17.7% 3.1% **In these studies, people were classified as having diabetes or not after a glucose tolerance test, so these data include known and new or previously undiagnosed cases. Undiagnosed diabetes Most of the rates of prevalence and incidence quoted above refer to the number of people with known or clinically diagnosed diabetes. The data shown on prevalence in different ethnic groups show that in addition, a substantial number of people have diabetes which has not been diagnosed. They will be almost exclusively of the NIDDM type. In this type of diabetes, symptoms are less prominent, and sometimes absent altogether; it may be years before diabetes is recognized, sometimes only coming to light because of the development of complications. The number of people whose condition is undiagnosed can only be estimated accurately by screening population samples using oral glucose tolerance tests. In the absence of any recent, large-scale national data of this type, the results of smaller scale surveys can give some sort of picture of the situation. Surveys carried out in Bedford in 1962, and more recently in Islington and Coventry; suggest that the ratio of undiagnosed to diagnosed may be as high as 1:1. 10
  11. 11. Sources used Overall prevalence Bennett, N., Dodd, T., Flatley, J., Freeth, S. and Bolling, K. Health Survey for England 1993. Social Survey Division of the Office of Population Censuses and Surveys, London: HMSO, 1995 Burnett, S.D., Woolf, C.M. and Yudkin, J.S. Developing a district diabetic register. British Medical Journal 1992, 305: 627-630 Gatling, W., Houston, A.C. and Hill, R.D. The prevalence of diabetes mellitus in a typical English community. Journal of the Royal College of Physicians 1985, 19: 248-250 Gibbins, R.L., Rowlands, C.J. and Saunders, J. A management system for diabetes in general practice. Diabetic Medicine 1986, 3: 477-479 Howitt, A.J. and Cheales, N.A. Diabetes registers: a grassroots approach. British Medical Journal 1993, 307: 1046-1048 Nabarro, J.D.N. Diabetes in the United Kingdom: some facts and figures. Diabetic Medicine 1988, 5: 816-822 Neil, H.A.W., Gatling, W., Mather, H.M., Thompson, A.V., Thorogood, M., Fowler, G.H., Hill, R.D. and Mann, JI The Oxford Community Diabetes Study: evidence for an increase in the prevalence of known diabetes in Great Britain. Diabetic Medicine 1987, 4: 539-543 Williams, D.R.R. Hospital admissions of diabetic patients: information from hospital activity analysis. Diabetic Medicine 1985, 2: 27-32 Williams, D.R.R. Epidemiologically based needs assessment. Report 1. Diabetes mellitus. 2nd edition. DHA Project Research Programme, October 1992. 11
  12. 12. Prevalence of IDDM and NIDDM Gatling, W., Houston, A.C. and Hill, R.D. The prevalence of diabetes mellitus in a typical English community. Journal of the Royal College of Physicians 1985, 19: 248-250 Simmons, D. Prevalence and age of onset of Type 1 diabetes in adult Asians in the Coventry Diabetes Study. Diabetic Medicine 1990, 7: 238-241 Waugh, N.R., Jung, R.T. and Newton, R.W. The Dundee Prevalence Study of Insulin-Treated Diabetes: intervals between diagnosis and start of insulin therapy. Diabetic Medicine 1989, 6: 346-350 Adults Prevalence Croxson, S.C.M., Burden, A.C., Bodington, M. and Botha, J.L. The prevalence of diabetes in elderly people. Diabetic Medicine 1991, 8: 28-31 Neil, H.A.W., Gatling, W., Mather, H.W., Thompson, A.V., Thorogood, M., Fowler, G.H., Hill, R.D. and Mann, J.1. The Oxford Community Diabetes Study: evidence for an increase in the prevalence of known diabetes in Great Britain. Diabetic Medicine 1987, 4: 539-543 Neil, H.A.W., Thompson, AN., Thorogood, M., Fowler, G.H. and Mann, J.1. Diabetes in the elderly: the Oxford Community Diabetes Study. Diabetic Medicine 1989, 6: 608-613 UK Prospective Diabetes Study. IV. Characteristics of newly presenting type 2 diabetic patients: male preponderance and obesity at different ages. Diabetic Medicine 1988, 5: 154-159 Incidence Barker, D.J.P., Gardner, M.J. and Power, C. Incidence of diabetes amongst people aged 18-50 years in nine British towns: a collaborative study. Diabetologia 1982, 22: 421-425 12
  13. 13. Thorn, P.A. Care for diabetics in the United Kingdom. Diabetes in Epidemiological Perspective. Mann, J.I., Pyorala, K. and Teuscher, A. (eds), Churchill Livingstone, 1983, 305-314 Children and young people Betts, P., Wessex Paediatric Diabetes Audit. Personal Communication Burden, A.C., Hearnshaw, J.R. and Swift, P.G.F. Childhood diabetes mellitus: an increasing incidence. Diabetic Medicine 1989, 6: 334-336 Metcalfe, M.A. and Baum, J.D. Incidence of insulin dependent diabetes in children aged under 15 years in the British Isles during 1988. British Medical Journal 1991, 302: 443-447 Staines, A., Bodansky, H.J., Lilley, H.E.B., Stephenson, C., McNally, R.J.Q. and Cartwright, R.A. The epidemiology of diabetes mellitus in the United Kingdom: the Yorkshire Regional Childhood Diabetes Register. Diabetologia 1993, 36: 1282-1287 Ethnic groups Asian Mather, H.M. and Keen, H. The Southall Diabetes Survey: prevalence of known diabetes in Asians and Europeans. British Medical Journal 1985, 291: 1081-1084 Simmons, D., Williams, D.R.R. and Powell, M.J. The Coventry Diabetes Study: prevalence of diabetes and impaired glucose tolerance in Europids and Asians. Quarterly Journal of Medicine 1991, New Series 81(296): 1021-1030 African-Caribbean Chaturvedi, N., McKeigue, P.M. and Marmot, M.G. Resting and ambulatory blood pressure differences in Afro-Caribbeans and Europeans. Hypertension 1993, 22: 90-96 13
  14. 14. Cruickshank, J.K., Cooper, J., Burnett, M., MacDuff, J. and Drubra, U. Ethnic differences in fasting plasma C-peptide and insulin in relation to glucose tolerance and blood pressure. Lancet 1991, 338: 842-847 Forrest, R.D., Jackson, C.A., and Yudkin, J.S. Glucose intolerance and hypertension in North London: the Islington Diabetes Survey Diabetic Medicine 1986, 3: 338-342 McKeigue, P.M., Shah, B., and Marmot, M.G. Relation of central obesity and insulin resistance with high diabetes prevalence and cardiovascular risk in South Asians. Lancet 1991, 337: 382-386 Undiagnosed diabetes Forrest, R.D., Jackson, C.A. and Yudkin, J.S. Glucose intolerance and hypertension in North London: the Islington Diabetes Survey. Diabetic Medicine 1986, 3: 338-342 Sharp, C.L., Butterfield, W.J.H. and Keen, H. Diabetes survey in Bedford, 1962. Proceedings of the Royal Society of Medicine 1964, 57: 193-204 Simmons, D., Williams, D.R.R. and Powell, M.J. The Coventry Diabetes Study: prevalence of diabetes and impaired glucose tolerance in Europids and Asians. Quarterly Journal of Medicine 1991, New Series 81(296): 1021-1030 14
  15. 15. 3. What causes diabetes? Insulin Dependent Diabetes (IDDM) In this type of diabetes, there is a complete or near complete absence of insulin, due to destruction of the insulin-producing islet cells of the pancreas. It is currently believed that the islet cells are destroyed by an autoimmune process, whereby the body's immune system (its defence mechanism against disease) for some reason recognises the cells as being 'foreign' rather than 'self', and therefore attacks them. It is thought that this autoimmune process is triggered off in susceptible individuals by one or more environmental factors. These factors are as yet unidentified, but possible candidates include viruses and certain chemicals. Susceptibility to this type of diabetes is genetical IV determined; that is, an individual is at risk of developing IDDM if they have inherited certain genes from their parents. Again, the identity of all the genes responsible for putting an individual at risk has not been established, but it is thought that up to as many as six may be involved. It should be remembered that if a person possesses these genes, it does not necessarily mean that they will actually develop diabetes; it is only if they encounter the environmental 'trigger' that the autoimmune destruction of the islet cells will be initiated. Non Insulin Dependent Diabetes (NIDDM) In this type of diabetes, the body is still producing insulin, but it is either not being made in sufficient quantities or its functioning is hindered. Defects in the islet cells are thought to be responsible for the deficiency in insulin production. Some degree of impairment of insulin's ability to stimulate glucose uptake in muscles and other tissues, otherwise known as insulin resistance, is evident in virtually all individuals with NIDDM. The cause of this insulin resistance has not yet been fully established, but may involve defects in the action of insulin after it has bound to the insulin receptor on the surface of cells. It is not clear at present what causes the defects in the insulin-producing cells and the inability of insulin to act in the muscle, liver and other tissues. There is a genetic influence, as NIDDM tends to run in families even more strongly than IDDM. As in IDDM, it is likely that several genes are involved. Increasing age, becoming obese and having a sedentary lifestyle are important contributory factors, and probably account for the rising prevalence of NIDDM in developed countries. Other types of diabetes In a small number of cases, diabetes can be caused by other factors: • various diseases of the pancreas, such as pancreatitis, or surgery to the pancreas • other hormonal conditions, such as Cushing's disease (over-production of cortisol by the adrenal gland) and acromegaly (over-production of growth hormone by the pituitary gland) • some medications, such as steroids and some diuretics (water tablets) in large doses. 15
  16. 16. Major accidents or illnesses are not thought to cause diabetes, but, by causing a temporary increase in blood glucose, they may reveal pre-existing diabetes, or disrupt the control of established diabetes. Occasionally, during very severe illnesses such as a heart attack, or after a serious injury or major operation, the blood glucose may rise temporarily. Psychological stress is not believed to cause diabetes, but may worsen it. 16
  17. 17. 4. Treatment of diabetes The goal of treatment in all types of diabetes is to keep the blood glucose level as near normal as possible. By this means, it is hoped to eliminate symptoms and reduce the risk of development of long term complications, which are associated with sustained high blood glucose levels. The effect of good control of blood glucose levels on the development of complications is discussed in more detail in the next section. In IDDM, control is achieved with diet and insulin; since the body is no longer capable of producing the insulin it requires, insulin injections are essential for survival. In NIDDM, the body is still producing some insulin, and it is often treated at first by diet alone. If blood glucose levels are not controlled sufficiently in this way, tablets which lower the blood glucose (oral hypoglycaemic drugs) may be added to treatment. If control is still inadequate, insulin injections may then be required. Occasionally, treatment with the oral hypoglycaemic drug may be continued, with insulin being given as a supplement. Usually the tablets are stopped and replaced by insulin injections. Surveys carried out in various different parts of the country have shown that approximately 20 per cent of people with diabetes are treated by diet alone, 50 per cent with diet and tablets, and 30 per cent with diet and insulin. Diet The main aim of treatment in diabetes is to maintain blood glucose levels as near to the normal range as possible. Dietary treatment has other aims as well; these include promoting weight loss in people with NIDDM who are obese, and lowering the risk of cardiovascular disease developing, as this is particularly common in people with diabetes. No 'special' diet is required to achieve these aims; the general advice for people with diabetes is to eat a healthy diet as recommended for everyone. In broad terms, this means a diet that is low in sugar, low in fat, and high in fibre. Reducing and controlling sugar intake has obvious benefits in controlling blood glucose levels. Increased intake of fibre slows the rate of absorption of sugars from foods and helps to maintain a more even level of blood glucose, as well as promoting healthy bowel function. Restricting fat in the diet reduces calorie intake, and helps weight loss. In addition, it reduces the risk of cardiovascular disease. Since a high salt intake may be linked to high blood pressure, a reduction in salt consumption is also recommended. Special diabetic foods are not recommended as they are expensive and confer no particular nutritional advantage. 17
  18. 18. Insulin At present, the only method by which insulin can be given is by injection. It cannot be given by mouth, as it is a protein and would be quickly digested in the stomach. Until about 10 years ago, virtually all insulin for therapeutic use was extracted from pig and beef pancreas; these species were used as their insulins are very similar to human insulin in structure. Now about 80 per cent of the insulin in use is 'human insulin', not extracted from the human pancreas, but produced by genetic engineering, whereby bacteria are induced to produce insulin identical to the human variety by modifying their genetic material. Although most people do well with human insulin, some may prefer to use animal insulin, and the latter is available if prescribed. There are many different types of insulin preparation available, each with different characteristics and varying durations of action. They can be classified simply into three different groups as shown in Table 4 below: Table 4: Classification of insulin preparations Appearance 'Usual' pattern of use Short-acting Clear With meals, twice or more daily Soluble* (used in conjunction with medium or long-acting preparations) Medium-acting Cloudy Twice (or once) daily Isophane** Semilente Lente Long-acting Cloudy Once (or twice) daily Ultralente Protamine Zinc Pre-mixed/ biphasic Cloudy Twice (or once) daily (combination of short and medium acting) *Also known as crystalline or regular insulin **Also known as NPH 18
  19. 19. Short-acting soluble preparations are absorbed quickly. They therefore have a quicker onset and shorter duration of action. The longer-acting preparations are absorbed more slowly, due to the addition of substances such as protamine (a certain type of protein) in isophane, or zinc in lente preparations. These reduce the solubility of the insulin (hence their cloudy appearance); their action is therefore slower in onset, but more prolonged in duration. The goals of insulin treatment are to supply the insulin the body is lacking, and in doing so, to mimic as closely as possible the pattern of insulin release that normally occurs ie a steep rise in insulin levels in line with the rise in blood glucose levels after each meal, together with a steady background level in the blood between meals. The type(s) of insulin used, the number of injections a day, and the timing of these injections vary from one individual to another. Each person with diabetes is different in terms of, for example, how long the action of a particular type of insulin will last, the level of their own residual insulin secretion, and their levels of activity and body weight. The more commonly used regimens are: 1. a single daily dose of a long-acting insulin, only really used in older people, or as a supplement to other treatments 2. twice daily injection of a combination of short and medium acting insulins, either individually or as a pre-mixed preparation 3. four times daily injection, with short-acting insulin taken before each of the three main meals, and a medium or long-acting insulin taken at bedtime. Injections are given subcutaneously (under the skin where there is a layer of body fat), the best sites being the abdomen, outer thighs, buttocks and upper arms. Disposable plastic syringes and needles are available on prescription. Insulin 'pens', fountain-pen like devices containing prefilled cartridges of insulin, are increasingly being used, particularly in multiple injection regimens; their main advantages relate to convenience, speed and ease of injection. Oral hypoglycaemic drugs In NIDDM, when dietary measures do not lower blood glucose levels sufficiently, oral hypoglycaemic drugs may be prescribed in addition. The two main types of oral hypoglycaemic drugs used are the sulphonylureas and the biguanides. Both types work only if the pancreas is still producing some insulin. There are a number of different sulphonylureas available, all with slightly different characteristics, such as duration of action: • glibenclamide • gliclazide 19
  20. 20. • glipizide • tolbutamide • chlorpropamide • gliquidone • tolazamide The sulphonylureas work principally by stimulating the islet cells of the pancreas to produce more insulin; they may also have a beneficial effect on insulin sensitivity, enabling the insulin to work more effectively on cells. The only biguanide now used in the UK is metformin. It is thought to act by enhancing uptake of glucose by individual cells and reducing the release of glucose by the liver. It can be used either in combination with a sulphonylurea when the latter has failed to lower blood glucose levels sufficiently, or on its own if the individual is overweight. Acarbose Acarbose, the first of a new group of drugs called alpha-glucosidase inhibitors, was introduced for the treatment of NIDDM in 1993. Alpha glucosidase is an enzyme present in the intestine which helps digest complex sugars and starch. By inhibiting the activity of this enzyme, these drugs delay the increase in blood glucose levels following a meal. Monitoring control To ensure that blood glucose levels are consistently kept as near to normal as possible, they must be checked at frequent intervals; if levels are shown to be consistently too high or too low, treatment can then be adjusted accordingly without delay. People with diabetes can check their own blood glucose levels, either directly by means of a simple blood test, or indirectly by testing their urine. The blood test involves pricking a finger with a sterile lancet, and placing the drop of blood on a special testing strip; with the majority of testing systems that are currently available, these strips are impregnated with the enzyme glucose oxidase, which reacts with any glucose in the drop of blood, causing a change in colour according to the amount present. The blood glucose level can then be determined either by visually comparing the test strip with a colour scale provided, or by reading its numerical value in a special meter. When the level of glucose in the blood rises above a certain threshold, it will spill over into the urine; the amount of glucose in the urine may therefore be taken as a rough measure of how high the level in the blood has risen above the threshold. A number of different urine testing kits are available, several of which involve the use of strips similar to those used in blood testing. Urine testing has limitations, but is effective enough for many people with NIDDM. 20
  21. 21. With such tests, a blood glucose profile during the day (and night) can be obtained. Additional tests often carried out during a visit to the clinic include measurement of glycated haernoglobin (the oxygen carrying pigment of red blood cells which has glucose attached to it). This test reflects the average blood glucose level over the preceding 6-8 weeks. Glycated albumin (a protein in the blood, measured by the fructosamine assay) reflects levels over the preceding 7-14 days. These are very useful guides to overall control. Sources used Surveys of treatments Howitt, A.J. and Cheales, A.J. Diabetes registers: a grassroots approach. British Medical Journal 1993, 307: 1046-1048 21
  22. 22. 5. The complications of diabetes The aim of the treatment of diabetes is to keep the blood glucose level as near normal as possible. The level of glucose in the blood is influenced by the amounts of food eaten, exercise taken and insulin available; keeping the blood glucose at the right level is therefore a question of balance. Good control aims for blood glucose levels that do not drop too low (hypoglycaemia) or remain too high (hyperglycaemia). There are problems associated with both situations. Hypoglycaemia Hypoglycaemia often results from excessive doses of insulin or sulphonylureas, inadequate or delayed intake of food, or sudden or sustained exercise. Sometimes however, it can occur without any apparent cause. Common early warning symptoms include shakiness, sweating, irritability and palpitations, progressing to confusion, faintness, headache, and disturbances of vision. If corrective steps are not taken, loss of consciousness and, occasionally, convulsions may follow. When the blood glucose level falls, various mechanisms, which reverse the metabolic effects of insulin are automatically activated to ensure that the brain is protected against glucose deprivation. This process is known as glucose counterregulation; it is mediated principally by release of the hormones glucagon and adrenaline, both of which promote the release of glucose from stores in the liver, leading to a rise in blood glucose levels. Because of this process, a person suffering from a hypoglycaemic episode or hypo, will eventually recover by themselves. However it is vital that treatment is begun when symptoms are first noticed, to prevent the person losing consciousness. The best emergency treatment for a low blood glucose is glucose itself, either in the form of a drink or tablets; these generally act within minutes. Alternatively, food or drink rich in sugar also work fairly quickly. Where the person is unable to take corrective action, the help of a friend or colleague is vital. Giving food or drink may be hazardous if the person is semi-conscious and cannot swallow; in such cases, jam or a glucose gel (Hypostop) smeared on the inside of the cheeks may be effective. If such measures are impracticable, an injection of glucagon may be given. If the person is unconscious, medical help should be sought. This may require admission to hospital, where intravenous glucose will be given. It is very difficult to assess the frequency of hypoglycaemia with accuracy because of the wide variation in severity and outcome, the common occurrence of low glucose without symptoms, and the failure to recognize or record many mild episodes. The frequency of severe hypoglycaemia requiring the assistance of another person can be more reliably assessed. In a major European multicentre study of people with IDDM, 34 per cent of the 172 patients in the English cohort reported at least one episode of severe hypoglycaemia during the previous year. In a retrospective survey carried out in 600 insulin-treated 22
  23. 23. patients at a diabetes clinic in Edinburgh, 175 (29.2 per cent) reported a total of 964 episodes of severe hypoglycaemia in the preceding year, giving an overall frequency for the group of 1.6 episodes per patient per year. Hypoglycaemia is less common with sulphonylurea therapy than with insulin. In the UK Prospective Diabetes Study, at least 35 per cent of those treated with insulin reported at least one hypoglycaemic episode, compared to 12 per cent of those treated with chlorpropamide and 29 per cent of those taking glibenclamide. Attacks severe enough to require assistance occurred in 6.6 per cent of those on insulin, 2.0 per cent of those on chlorpropamide and 3.7 per cent of those on glibenclamide. The risk of hypoglycaemia occurring with sulphonylurea treatment does however increase with age, as it does with insulin therapy; it can be a serious hazard for the very elderly. Hyperglycaemia Ketoacidosis Ketoacidosis is an acute complication of severe insulin deficiency, which can occur when insulin dependent diabetes is untreated or very poorly controlled, if insulin injections are inadvertently or deliberately omitted, or at times when the body's need for insulin is increased, such as during an infection. In such circumstances, blood glucose levels are very high, and fat is broken down as an alternative source of energy. The resulting breakdown products include ketone bodies. Although not harmful in small quantities, if they accumulate, they can lead to the serious condition of ketoacidosis or diabetic coma, which can be fatal if untreated. Symptoms of this condition include the acute symptoms of diabetes, thirst, increased urine, weakness, progressing to nausea and vomiting, breathlessness, confusion, and rarely, coma. In the European multicentre study of people with IDDM mentioned previously, of the 172 people in the English cohort, 8.1 per cent reported one or more hospital admissions for ketoacidosis in the previous year. A centre in Birmingham treated 740 episodes over a 15 year period between 1971 and 1985; these occurred in 505 patients, 113 patients experiencing more than one episode, indicating that recurrent ketoacidosis is a significant problem for a few patients. If ketoacidosis develops, prompt hospital treatment is essential. While treatment is generally very successful, it is not uniformly so. A survey of deaths in people with diabetes under the age of 50 in 1979 indicated that ketoacidosis was the commonest cause in those under the age of 20, and it is likely that this is still the case. The current mortality rate for ketoacidosis is approximately seven per cent in specialised units. Mortality is generally higher in the elderly, and when treatment is given in less specialised centres. The commonest causes of severe ketoacidosis remain delay in diagnosing IDDM and the misplaced advice sometimes given to people to stop their insulin during intercurrent illness, when they are vomiting or not eating. 23
  24. 24. 'Late' Complications There are a number of other problems associated with diabetes, which develop over the longer term. These can be classified as follows: 1. Microvascular - due to damage to the small blood vessels in particular parts of the body • retinopathy (eyes) • nephropathy (kidneys) • neuropathy (nerves) 2. Macrovascular - where the large arteries to the heart, brain, legs and feet become narrow or blocked (cardiovascular disease) • ischaemic or coronary heart disease affecting the blood supply to the heart, manifested as angina and myocardial infarction (heart attack) • cerebrovascular disease affecting blood vessels in the brain, leading to strokes • peripheral vascular disease affecting blood supply to the legs, causing intermittent claudication (pain in the legs on walking) and gangrene if severe. 3. Other complications may affect: • feet • skin • joints and tendons • gastrointestinal tract • sexual function There is not room here to discuss all of the above in detail; a brief description of the more significant ones follows. Retinopathy Retinopathy refers to damage to the retina, the light sensitive part of the back of the eye that is responsible for transmitting visual images to the brain. It is a condition which tends to progress slowly at first, without causing any visual symptoms. This stage is often referred to as background retinopathy. It is characterized by occlusion or blockage of small blood vessels. Initially, other vessels dilate to compensate for this. However, the dilated vessels tend to become leaky, and fluid accumulates at the macula, the centre of vision, causing visual impairment (diabetic maculopathy). This is the commonest cause of visual loss in older people with diabetes. 24
  25. 25. When there are large areas in which small blood vessels are blocked, the response is growth of new blood vessels; this stage is known as proliferative retinopathy, and is another major cause of visual loss. The new vessels tend to grow forward into the vitreous, a clear jelly in front of the retina. They are fragile, and if they bleed, blood may obstruct the passage of light through the eye to the retina. In addition, these vessels develop a scar tissue covering which tends to shrink, and can drag the retina off its support structure (retinal detachment). In the European multicentre study of 3,250 people with IDDM attending hospital clinics, background retinopathy was found in 35.9 per cent and proliferative retinopathy in 10.3 per cent. Its prevalence increased with duration of diabetes. Background retinopathy was found in about seven per cent of those who had had diabetes for less than five years, but rose steeply between five and 15 years duration, reaching a plateau of 82 per cent after 20 years. Proliferative retinopathy was virtually absent before ten years duration, after which it rose steadily to reach a prevalence of 37 per cent after 30 or more years of diabetes. Higher prevalences were found in a widely quoted community study carried out in Wisconsin, in the USA. After 15 years of diabetes, 98 per cent of people with IDDM had some degree of retinopathy. Proliferative retinopathy was present in 56 per cent of those with IDDM for 20 years or more. As many as 18 per cent of people with NIDDM have diabetic retinopathy at the time of diagnosis, according to the UK Prospective Diabetes Study. Many people with this type of diabetes may well have had the condition for several years before it was actually diagnosed. Further data from the Wisconsin study indicate that, as in IDDM, prevalence of retinopathy increases with duration of NIDDM: 23 per cent of those taking insulin and 20 per cent of those not taking insulin had some degree of retinopathy during the first two years after diagnosis, rising to about 87 per cent and 53 per cent respectively after 20 years of diabetes. Proliferative retinopathy was again rare in the first few years, rising to a prevalence of 25 per cent in those taking insulin and 10 per cent in those not after 20 years of diabetes. These data relate to the USA, and absolute figures for the UK may differ, since the European multicentre study of people with IDDM suggests that the prevalence of retinopathy in people with IDDM is lower in European countries than in the USA USA Analysis of data from new registrations of blindness and visual handicap in England and Wales show that diabetes is the single most common cause of blindness among adults aged 16 to 64. The most recent data available for 1990/1 show that diabetic retinopathy was the cause in 11.9 per cent of new registrations of blindness and 8.2 per cent of those for partial sight. These figures do however suggest a steady decline when compared to figures for previous years. It is now possible to prevent much of the visual loss in diabetes by regular screening and treatment. Proliferative retinopathy and maculopathy can be treated using laser photocoagulation. This technique can be used to treat either specific target areas (new vessels) or the whole retina (pan-retinal photocoagulation) which reduces the stimulus to new vessel formation. Pan-retinal photocoagulation reduces by over 50 per cent the 25
  26. 26. likelihood of severe visual loss developing in eyes with high-risk proliferative retinopathy. In maculopathy, the leaky vessels are destroyed and fluid is allowed to drain into vessels behind the retina. In order that sight-threatening changes can be detected and treated before vision is lost, it is essential that people with diabetes have the back of their eyes examined at regular intervals (usually annually). Once vision is lost, treatment may be difficult or impossible, and is much more time-consuming and less effective. Surgical treatment may recover some useful vision, but this is technically very difficult, and may be impossible. Nephropathy Although recent data indicate that its incidence may be declining, at least in IDDM, diabetic kidney disease or nephropathy may still develop in 20-25 per cent of people with diabetes, and is particularly serious as it can lead on to kidney failure. Oft-quoted studies from Denmark and the USA published in the mid-1980s showed that 30-40 per cent of people with IDDM develop nephropathy. A more recent study from Sweden showed a much lower cumulative incidence of nephropathy in people whose IDDM was diagnosed between 1966 and 1970 (8.9 per cent) than in those diagnosed between 1961 and 1965 (30.0 per cent). Few data are available for the UK itself, but one study in Leicestershire has shown a cumulative incidence of approximately 13 per cent after 40 years of IDDM. A number of studies point to the role of good blood glucose control in lowering the risk of nephropathy developing (see later section for further discussion of this). Traditionally, nephropathy has been thought to develop in a smaller proportion of people with NIDDM than those with IDDM. However, recent data suggest that this may not be the case. Studies again from Denmark and the USA indicate that the cumulative incidence of nephropathy in people of European origin with NIDDM is in the region of 20-25 per cent. Comparisons of different ethnic groups show a higher prevalence among people of Asian or African-Caribbean origin than those of European origin. Diabetic nephropathy is responsible for a significant proportion of cases of renal failure that develop in the UK today. At one central London hospital, 27 per cent of the 651 patients treated for kidney failure between 1980 and 1989 had diabetes. A centre serving the whole of the Leicestershire region reported a much lower proportion (6.8 per cent) over virtually the same time period; this may be due in part to the low incidence of nephropathy in people with IDDM in this area that was mentioned previously. At both centres, NIDDM accounted for more than half of the cases of renal failure due to diabetes (65 per cent in London, 83 per cent in Leicester). People of Asian or African Caribbean origin appear to be at relatively increased risk of developing renal failure, as might be expected from their higher prevalence of nephropathy; in Leicester, the relative risk of end-stage renal failure in people of Asian origin compared to those of European origin was 13.6. Nephropathy is not generally evident until after 10-15 years of IDDM, but may be detected earlier in NIDDM, even at diagnosis, probably because undiagnosed diabetes has been present for several years. 26
  27. 27. Like retinopathy, nephropathy is due to damage to the small blood vessels. The walls of the fine capillaries in the kidneys become thickened or irregular, and consequently they cannot perform their function of filtering waste products out of the blood into the urine properly. Established nephropathy usually follows after several years, during which there are small but often progressively rising levels of a protein called albumin in the urine, a condition referred to as microalburninuria. If levels of albumin in the urine rise further, the condition becomes known as albuminuria or clinical proteinuria. At this stage, it is likely that no other symptoms or clinical signs will be apparent, apart from a small rise in blood pressure. However, as the function of the kidney declines, uraemic symptoms such as tiredness, nausea, shortness of breath, and swelling of legs, ankles, face etc will appear, together with a further rise in blood pressure, as the individual enters end-stage renal failure. There is evidence that the progression of nephropathy can be delayed by restricting dietary protein and by careful control of blood pressure. Recent work has also shown that a group of drugs called angiotensin-converting enzyme (ACE) inhibitors, which are currently used in the treatment of high blood pressure and heart failure, may have a significant benefit, which is due only in part to their effects on blood pressure. The treatment of choice for end-stage renal failure is kidney transplantation. However with the present shortage of donors, continuous ambulatory peritoneal dialysis is a commonly used means of treatment. In the past, people with diabetes were not widely accepted for such 'renal replacement' treatment because it was thought that they did not fare very well. However, over recent years, in certain centres at least, results with renal replacement therapy in people with diabetes have improved and are comparable with those in non-diabetic patients. There is no reason therefore to exclude people with diabetes from renal replacement therapy. Some evidence of increased acceptance of people with diabetes on to renal replacement programmes does exist; the proportion with diabetes in the UK increased from 1.2 per cent in 1974 to 11.4 per cent in 1985. Whilst this is encouraging, the findings of a survey carried out in 1987 by the BDA, the Royal College of Physicians and the Renal Association did indicate that provision of treatment of people with diabetic renal failure was still inadequate. The survey, of 181 people identified in 1985 as having previously untreated advanced renal failure, showed that one third had died without receiving renal support treatment; in some cases, death was unavoidable (mainly from heart attacks), but half died from renal failure. Early detection of nephropathy allows treatment before there is significant loss of renal function. People with diabetes should therefore have samples of their urine checked for albumin annually. 27
  28. 28. Neuropathy The term neuropathy refers to damage to the nerves. It is commonly classified with the 'microvascular' complications, but the true role of damage to the capillaries supplying the nerves in causing this has still not been established. Chemical factors may also play an important part. There are a number of different types of neuropathy that can occur in association with diabetes. The principal ones can be classified as follows. 1. Sensorimotor peripheral neuropathy: damage to nerves carrying sensory information ie touch, heat, pain, to the brain and nerves carrying motor (movement) signals to the limbs. 2. Autonomic neuropathy: damage to nerves supplying organs like the heart, blood vessels, etc which carry out a number of 'fine adjustments' and are not under voluntary control. Until recently, satisfactory information on the prevalence of neuropathy has not been available, and a range of figures have been quoted. However, more reliable data have emerged from a large study carried out in 1990, of people with diabetes attending hospital clinics for treatment. This gave a figure of approximately 30 per cent for the overall prevalence of peripheral neuropathy Prevalence was shown to increase with both age and duration of diabetes, until it was present in more than 50 per cent of NIDDM patients aged over 60 years. These figures may however overestimate the prevalence of neuropathy in the general diabetic population, since those with active complications are more likely to be attending hospital clinics. In a survey carried out in the Poole area, prevalence of neuropathy was found to be just over 16 per cent in people with diabetes, compared to three per cent in a non-diabetic comparison group. The prevalence of autonomic neuropathy is still unclear; autonomic dysfunction (function of these nerves found to be abnormal when tested) has been demonstrated in up to 40 per cent of people with diabetes, but this usually causes no symptoms. Sensory neuropathy is the commonest form. It can affect any of the senses - touch, temperature, pain, vibration or position. Classically people with diabetes develop a /glove' or 'stocking' neuropathy in which there is sensory loss either in the hands or feet, the latter being more frequent. Symptoms include tingling, burning, cramps and frank pain. Numbness may develop, to the point that injury can occur without being noticed. Motor neuropathy is less frequent. It can affect one muscle or a group of muscles. If the nerve supply is interrupted, muscles can become weak and wasted. In diabetic amyotrophy, the thigh muscles are affected in this way. There is currently no recognised treatment for the actual nerve damage itself, although a number of therapies are under investigation, including aldose reductase inhibitors, gangliosides and gamma-linolenic acid. Some of the symptoms however can be treated; 28
  29. 29. pain for example can be treated firstly with simple analgesics like aspirin or codeine, or if these are unsuccessful, tricyclic drugs like amitryptiline. In severe cases, autonomic symptoms can cause poor control of blood pressure, leading to postural hypotension (dizziness associated with a fall in blood pressure on standing up suddenly), problems with emptying the bladder, bowel and stomach (the latter being known as gastroparesis), and sweating disturbances. Erectile impotence of varying degrees may affect as many as one man in two. As yet, no way has been found to reverse autonomic neuropathy, but the Diabetes Control and Complications Trial has shown that tight control of blood glucose reduces the risks of it developing (see section on role of blood glucose control page 27), and treatment for individual symptoms can be given. Cardiovascular disease Cardiovascular disease is a major cause of chronic ill-health and premature death in the UK population in general; in people with diabetes, it is an even greater problem. Diabetes is associated with a two to three fold increased risk of coronary heart disease in men, and a four to five fold increased risk in premenopausal women. The risk of stroke is also increased two to three fold, and disease of leg arteries greatly increases the risk of exercise pain, gangrene and amputation. In a group of 497 people with diabetes aged 35 to 54 who were included in the UK part of a major multinational study coordinated through the WHO, the overall prevalence of cardiovascular disease at the end of a eight year follow-up period was 45 per cent; 43 per cent had evidence of coronary heart disease, 4.5 per cent of cerebrovascular disease and 4.2 per cent of peripheral vascular disease. Analysis of the cause of death in this group over the period 1975 to 1987 showed that heart attacks were the most common cause, accounting for 39.1 per cent of all deaths. Cardiovascular disease as a whole caused 55.4 per cent of the deaths. It was responsible for a higher proportion of deaths in people with NIDDM than in people with IDDM (62.0 per cent versus 47.6 per cent), though greater age was a factor in this. Data from death certificates mentioning diabetes from 1975-6 and 1985-6 have recently been compared. Deaths in which coronary heart disease was the underlying cause rose by 14.4 per cent in men and did not change significantly in women of all ages. However in those below the age of 45, there was a drop of 18.4 per cent in men and 23.5 per cent in women. This was less favourable than the trend in the general population, where mortality from coronary heart disease fell by 9.7 per cent in men and 8.3 per cent in women of all ages, and by 31.1 per cent in men and 40.5 per cent in women under 45 years. The major risk factors for cardiovascular disease in the population in general - high blood pressure (hypertension), high blood cholesterol, smoking, obesity and physical inactivity - also apply in people with diabetes. However, their excess risk of coronary heart disease and stroke is only partly explained by higher levels of these risk factors; diabetes appears to be an additional, perhaps amplifying risk factor. 29
  30. 30. The 'diabetic foot' People with diabetes are prone to ulceration and gangrene of the lower limb, which may greatly increase the risk of amputation. In a survey carried out in the Poole area, the prevalence of past or present foot ulceration was found to be 7.4 per cent in people with diabetes compared to 2.5 per cent in a non-diabetic comparison group. Foot ulceration was present in 3.3 per cent at the time of the survey. In a study in Oxford, overall prevalence of foot ulceration was five per cent, and seven per cent in those aged 60 or more. Foot problems can require amputation. The frequency of amputations in people with diabetes has been estimated in three different parts of the country summarised in Table 5 below: Table 5: The incidence of lower extremity amputations in people with diabetes in Leicester, Newcastle and Tayside Population Study Period Rate/10,000 people with diabetes/year Leicester - European origin 1980-85 14.2 - Asian origin 3.4 Newcastle 1989-91 57.0 Tayside 1980-82 101.0 (A number of factors may contribute to the apparent large differences between amputation rates. These include differing prevalence of diabetes, age structures of the populations, and resources available for care.) In 1989 (the last year for which comprehensive data are available), a total of 3,378 major amputations were performed in England, Wales and Northern Ireland; diabetes was recorded as being the underlying cause in 763 cases (22.6 per cent). The chief factors responsible for foot problems in diabetes are neuropathy and ischaernia, often a combination of the two, with infection as both a provoking and complicating factor. Ulcers can develop as a result of mechanical trauma to the foot. Repetitive mechanical forces generated by walking can lead to callus formation at sites of high pressure on the sole of the foot, and subsequent breakdown of these calluses leads to the formation of ulcers. Other mechanical traumas include pressure from ill-fitting shoes, direct injuries caused by nails or stones, or burns from heaters or hot-water bottles. Wounds may become infected and progress to an advanced stage before they are noted. Reduced blood supply will impair healing, and sepsis can spread rapidly through the foot, destroying bone and soft tissues. Neuropathy can also lead to fluid accumulation (oedema) of the feet and to Charcot joint, resulting from severe bone and joint destruction. 30
  31. 31. Many foot problems can be prevented by good foot care, involving both the person with diabetes and their professional carers, in particular the chiropodist. The establishment of special foot clinics has been shown to lead to significant reductions in foot problems. In the two years before the foot clinic at Kings College Hospital was set up, there were 11 and 12 major amputations yearly; this was reduced in the three following years to seven, seven and five amputations respectively. Mortality Routine mortality statistics are based on a single underlying cause of death as specified on a death certificate. In many cases therefore death is attributed to one of the complications rather than to diabetes itself. For the majority of deaths in older people with diabetes, the condition is not even mentioned on the certificate. The contribution of diabetes to mortality is therefore clearly underestimated, probably greatly so. Even without allowing for such under-representation, it is clear that mortality is higher in people with diabetes than in people of a similar age and sex without diabetes. A study in Poole showed that after eleven years follow-up, in the age range 45 to 64, the number of people with diabetes who had died was nearly twice that in the non-diabetic group. As mentioned previously, data have been collected on deaths occurring over a 12 year period between 1975 and 1987 in a group of 497 people with diabetes aged 35 to 54, when recruited to the UK arm of the WHO Multinational Study of Vascular Disease in Diabetes. A total of 92 people died over this period. Data on the underlying causes of death are shown in Figure 3 below: Figure 3: Underlying causes of death in the London cohort of the WHO Multinational Study of Vascular Disease in Diabetics 31
  32. 32. Cardiovascular disease as a whole caused 55.4 per cent of the deaths, 62 per cent of those with NIDDM and 47.6 per cent of those with IDDM. A follow-up study of a cohort of about 6,000 members of the BDA showed that under the age of 50, men with diabetes were about 3.5 times and women 11 times more likely to die from cardiovascular diseases than comparable people without diabetes. In 1979, a survey was carried out of all deaths under the age of 50 in people with diabetes mentioned on the death certificate. After cardiovascular disease (41 per cent), the next most common cause was renal disease (19 per cent). The figure today for deaths due to renal failure is likely to be lower, due to a declining incidence of nephropathy, and improvements in care. However it is still an important factor, particularly in people with IDDM, since it greatly increases the risk of cardiovascular mortality. Ketoacidosis accounted for 16 of the 23 deaths under the age of 20. In Denmark and the USA, renal disease is the principal cause of death in people who have had IDDM for between 10 and 30 years; after this, cardiovascular disease becomes the leading cause of death. The picture is probably improving however. The rate of death certificates mentioning diabetes has fallen by 31 per cent in men and 27 per cent in women under the age of 45 between 1976 and 1986. Despite difficulties in interpreting data from death certificates, this fall in diabetes-related mortality may be real, and reflect improved survival. In Leicester the risk of death in people with IDDM fell by an estimated 93 per cent between 1940-49 and 1980-89. Role of blood glucose control There has been much debate over the years as to the degree to which the complications of diabetes result from inadequate control of blood glucose levels. Ten years ago, two large multi-centre studies were set up to investigate this issue: 1. the Diabetes Control and Complications Trial (DCCT) This study was carried out in 29 centres across the USA and Canada, and involved 1,441 people with IDDM. It compared the effects of 'conventional' insulin treatment (one or two injections a day) with an intensified regimen (three or more injections a day or the use of an insulin infusion pump) on the development of and progression of retinopathy principally, but also of the other complications. This study was scheduled to finish in 1994, but was stopped a year early because the results showed conclusively that tight blood glucose control reduced the risk of complications: • a 76 per cent reduction in the risk of new retinopathy developing • a 54 per cent reduction in the risk of progression of existing retinopathy • a 39 per cent reduction in the risk of microalburninuria developing • a 54 per cent reduction in the risk of clinical alburninuria developing • a 60 per cent reduction in the risk of neuropathy 32
  33. 33. These results were achieved at the cost of a threefold increase in the risk of severe hypoglycaemia with intensive therapy. 2. the UK Prospective Diabetes Study (UKPDS) This study is being carried out in 23 centres in the UK, looking at the effects of differing forms and intensity of diabetic control, in 5,100 volunteers newly diagnosed with NIDDM. Treatment is randomised. in suitable patients between diet alone, diet and oral hypoglycaemic drugs, or insulin injections. It has already shown that one or more complications are present in 50 per cent of people with NIDDM at diagnosis. When it finally reports back, it will show the effect of tight blood glucose control on the development and progression of complications. At the same time, it will provide new evidence on the benefits and risks of tight versus less tight blood pressure control. Pregnancy Fifty years ago about 30 per cent of pregnancies in women with diabetes ended in stillbirth, or death of the baby within a week or two of birth. The situation has vastly improved over the intervening period, due to major developments in obstetric, diabetic and paediatric care. In 1980, a survey was carried out by the BDA, the Royal College of Physicians and the Royal College of Obstetricians and Gynaecologists, of 773 pregnancies in women with established diabetes. This showed that the perinatal mortality rate (the number of stillbirths or neonatal deaths, expressed as a proportion of total number of births) had fallen dramatically but was still 56 per 1,000 births (5.6 per cent), compared to the rate in the general population of 14 per 1,000 births 0.4 per cent). Major congenital malformations were responsible for about one third of these deaths. The overall incidence of congenital malformations (fatal and non-fatal) in this survey was 7.1 per cent. They may result from poor control of blood glucose levels in the early weeks of pregnancy, when critical stages of development are taking place. Whenever possible therefore good control must be achieved before conception, and pre-pregnancy clinics held for women with diabetes seeking to conceive are highly desirable. Babies of mothers with diabetes tend to be larger than normal at birth, a condition referred to as macrosomia. These offspring are at increased risk of certain neonatal complications, such as respiratory distress syndrome and hypoglycaemia. The occurrence of such problems can however be much reduced with the appropriate management of blood glucose control. Pregnancy also holds certain risks for the mother. Maternal mortality rate, currently two deaths per 10,000 pregnancies overall in the UK, is probably higher in women with diabetes, although precise figures are not known. Of the 773 women registered in the 1980 survey, two died, one from ketoacidosis and one from heart failure. Retinopathy tends to 33
  34. 34. worsen and should be carefully followed and promptly treated if necessary. Kidney disease and high blood pressure pose a much more serious threat, and special management is needed. A number of women are found to have diabetes during pregnancy; this form is known as gestational diabetes (GDM), and it may disappear at least for a few years after the pregnancy. Estimates of its incidence in the UK vary considerably (0.2-5.0 per cent), due in part to differences in the populations screened and the diagnostic criteria employed; the diagnosis and management of gestational diabetes are the subject of much debate. It may be found at any time during pregnancy, most commonly after the middle of the second trimester. Long-term follow-up studies suggest that as many as 50 per cent of women with GDM will subsequently develop established diabetes, usually NIDDM. The impact of GDM on the pregnancy is similar to that of established diabetes, although its complications are generally fewer and less severe; nonetheless, the condition should be identified and treated effectively in order to reduce the hazards to both mother and child. Women with gestational diabetes are seldom symptomatic, and screening is therefore necessary if they are to be identified. Currently, however, there is no national policy on screening for GDM, and there are considerable regional differences in terms of which women are screened, how and when. 34
  35. 35. Sources used Hypoglycaemia EURODIAB IDDM Complications Study Group. Microvascular and acute complications in IDDM patients: the EURODIAB IDDM Complications Study. Diabetologia 1994, 37: 278-285 Fox, C., Cull, C.A. and Holman, R.R. Three year response to randomly allocated therapy with diet, sulphonylurea or insulin in 1592 Type 2 diabetic patients. Diabetic Medicine 1991, 8(Suppl. 1): 8A Frier, B.M. Hypoglycaemia in the diabetic adult. Balliere's Clinical Endocrinology and Metabolism 1993, 7(3): 757-777 MacLeod, K.M., Hepburn, D.A. and Frier, B.M. Frequency and morbidity of severe hypoglycaemia in insulin-treated patients. Diabetic Medicine 1993, 10: 238-245 Ketoacidosis Basu, A., Close, C.F., Jenkins, D., Krentz, A.J., Nattrass, M. and Wright, A.D. Persisting mortality in diabetic ketoacidosis. Diabetic Medicine 1993, 10: 282-284 Chapman, J., Wright, A.D., Nattrass, M. and Fitzgerald, M.G. Recurrent diabetic ketoacidosis. Diabetic Medicine 1988, 5: 659-661 EURODIAB IDDM Complications Study Group. Microvascular and acute complications in IDDM patients: the EURODIAB IDDM Complications Study. Diabetologia 1994, 37: 278-285 Krentz, A.J. and Nattrass, M. Diabetic ketoacidosis, non-ketotic hyperosmolar coma and lactic acidosis. Textbook of Diabetes. Pickup, J.C. and Williams, G. (eds), Blackwell Scientific Publications, 1991, 479-494 Tunbridge, W.M.G. Factors contributing to deaths of diabetics under fifty years of age. Lancet 1981, 2: 569-572 35
  36. 36. Retinopathy Aldington, S.J., Stratton, I.S., Kohner, E.M., Matthews, D.R. and Turner, R.C. Prevalence of retinopathy at diagnosis of Type 2 diabetes in the UK Prospective Diabetes Study. Diabetic Medicine 1994, 11(Suppl. 2): S43-44 Diabetic Retinopathy Study Research Group. Photocoagulation treatment of proliferative diabetic retinopathy. Clinical application of DRS findings. Report no. 8. Ophthalmology 1981, 88: 583-600 EURODIAB IDDM Complications Study Group. Microvascular and acute complications in IDDM patients: the EURODIAB IDDM Complications Study. Diabetologia 1994,37: 278-285 Evans, J. Causes of blindness and partial sight in England and Wales, 1990-1991. Office of Population Censuses and Surveys. Studies on Medical and Population Subjects No. 57, HMSO, London: 1995 Klein, R., Klein, B.E., Moss, S.E., Davis, M.D. and DeMets, D.L. The Wisconsin Epiderniologic Study of Diabetic Retinopathy. II. Prevalence and risk of diabetic retinopathy when age at diagnosis is less than 30 years. Archives of Ophthalmology 1984, 102: 520-526 Klein, R., Klein, B.E., Moss, S.E., Davis, M.D. and DeMets, D.L. The Wisconsin Epiderniologic Study of Diabetic Retinopathy. III. Prevalence and risk of diabetic retinopathy when age at diagnosis is 30 or more years. Archives of Ophthalmology 1984, 102: 527-532 Nephropathy Allawi, J., Rao, P.V., Gilbert, R., Scott, G., Jarrett, R.J., Keen, H., Viberti, G.C. and Mather, H.M. Microalbuminuria in non-insulin dependent diabetes: its prevalence in Indian compared with Europid patients. British Medical Journal 1988, 296: 462-464 Ballard, D.J., Humphrey, L.L., Melton, L.J., Frohnert, P.P., Chu, C-P., O'Fallon, W.M. and Palumbo, P.J. Epidemiology of persistent proteinuria in Type II diabetes mellitus. Population-based study in Rochester, Minnesota. Diabetes 1988, 37: 405-412 36
  37. 37. Bojestig, M., Arnqvist,, H.J., Hermansson, G., Karlberg, B.E. and Ludvigsson, J. Declining incidence of nephropathy in insulin-dependent diabetes mellitus. New England Journal of Medicine 1994, 330: 15-18 Brunner, F.P., Brynger, H., Challah, S., Fassbinder, W., Geerlings, W., Selwood, N.H., Tufveson, G. and Wing, A.J. Renal replacement therapy in patients with diabetic nephropathy, 1980-1985. Report from the European Dialysis and Transplant Association Registry. Nephr. Dial. Transplant. 1988, 3: 585-595 Burden, A.C., McNally, P.G., Feehally, J. and Walls, J. Increased incidence of end-stage renal failure secondary to diabetes mellitus in Asian ethnic groups in the United Kingdom. Diabetic Medicine 1992, 9: 641-645 Grenfell, A., Bewick, M., Snowden, S., Watkins, P.J. and Parsons, V. Renal replacement for diabetic patients: experience at King's College Hospital, 19801989. Quarterly Journal of Medicine 1992, 85(307-308): 861-874 Hasslacher, C., Ritz, E., Wahl, P. and Michael, C. Similar risks of nephropathy in patients with Type 1 or Type 2 diabetes mellitus. Nephr. Dial. Transplant. 1989, 4: 859-863 Joint Working Party on Diabetic Renal Failure of the British Diabetic Association, Renal Association and the Research Unit of the Royal College of Physicians. Treatment of and mortality from diabetic renal failure in patients identified in the 1985 United Kingdom survey. British Medical Journal 1989, 299: 1135-1136 Kofoed-Enevoldsen, A., Borch-Johnsen, K., Kreiner, S., Nerup, J. and Deckert, T. Declining incidence of persistent proteinuria in Type 1 (insulin-dependent) diabetic patients in Denmark. Diabetes 1987, 36: 205-209 Krolewski, A.S., Warram, J.H., Christlieb, A.R., Busick, E.J. and Kahn, C.R. The changing natural history of nephropathy in Type 1 diabetes. American Journal of Medicine 1985, 78: 785-794 Mather, H.M. and Keen, H. The Southall Diabetes Survey: prevalence of known diabetes in Asians and Europeans. British Medical Journal 1985, 291: 1081-1084 McNally, P.G., Raymond, N.T., Botha, J.L., Swift, P.G.E., Burden, A.C. and Hearnshaw, J.R. Low incidence of microvascular complications in type 1 diabetics diagnosed and treated in one centre in the UK. Hormone Research 1991, 35: 60 37
  38. 38. McNally, P.G., Burden, A.C., Swift, P.G.F., Walls, J. and Hearnshaw, J.R. The prevalence and risk factors associated with the onset of diabetic nephropathy in juvenile-onset (insulin-dependent) diabetics diagnosed under the age of 17 years in Leicestershire 1930-1985. Quarterly Journal of Medicine 1990, 76(280): 831-844 Mogensen, C.E. Microalburninuria predicts clinical proteinuria and early mortality in maturity-onset diabetes. New England Journal of Medicine 1984, 310: 356-360 Samanta, A., Burden, A.C. and Jagger, C. A comparison of the clinical features and vascular complications of diabetes between migrant Asians and Caucasians in Leicester, U.K. Diabetes Research and Clinical Practice 1991, 14: 205-214 Neuropathy Ewing, D.J. and Clarke, B.F. Diabetic autonomic neuropathy: present insights and future prospects. Diabetes Care 1986, 9: 648-665 Ewing, D.J. Autonomic neuropathy. Chronic Complications of Diabetes. Pickup, J.C. and Williams, G. (eds), Blackwell Scientific Publications, 1994, 124-136 Walters, D.P., Gatling, W.,Mullee, M.A. and Hill, R.D. The prevalence of diabetic distal sensory neuropathy in an English community. Diabetic Medicine 1992, 9: 349-353 Young, M.J., Boulton, A.J.M., Macleod, A.F., Williams, D.R.R. and Sonksen, PH. A multicentre study of the prevalence of diabetic peripheral neuropathy in the United Kingdom hospital clinic population. Diabetologia 1993, 36: 150-154 Cardiovascular disease Bell, D.S.H. Stroke in the diabetic patient. Diabetes Care 1994,17: 213-219 Fuller, J.H., Shipley, M.J., Rose, G. et al Coronary heart disease risk and impaired glucose tolerance: the Whitehall Study. Lancet 1980, 1: 1373-1376 38
  39. 39. Morrish, N.J., Stevens, L.K., Head, J., Fuller, J.H., Jarrett, R.J. and Keen, H. A prospective study of mortality among middle-aged diabetic patients (the London cohort of the WHO Multinational Study of Vascular Disease in Diabetics) I: causes and death rates. Diabetologia 1990, 33: 538-541 Morrish, N.J., Stevens, L.K., Fuller, J.H., Keen, H. and Jarrett, R.J. Incidence of macrovascular disease in diabetes mellitus: the London cohort of the WHO Multinational Study of Vascular Disease in Diabetics. Diabetologia 1991, 34: 584-589 89 Morrish, N.J., Stevens, L.K., Fuller, J.H., Jarrett, R.J. and Keen, H. Risk factors for macrovascular disease in diabetes mellitus: the London follow-up to the WHO Multinational Study of Vascular Disease in Diabetics. Diabetologia 1991, 34: 590-594 Rosengran, A., Welin, L., Tsipogianni, A. and Wilhelmsen, L. Impact of cardiovascular risk factors on coronary heart disease and mortality among middle-aged diabetic men: a general population study. British Medical Journal 1989, 299: 1127-1131 Stephenson, J., Swerdlow, A.J., Devis, T. and Fuller, J.H. Recent trends in diabetes mortality in England and Wales. Diabetic Medicine 1992, 9: 417-421 The 'diabetic foot' Deerochanawong, C., Home, RD. and Alberti, K.G.M.M. A survey of lower limb amputation in diabetic patients. Diabetic Medicine 1992, 9: 942-946 Department of Health. Statistics and Management Information Division. Amputation statistics for England, Wales and N. Ireland, 1989. Edmonds, M.E., Blundell, M.P., Morris, M.E., Maelor Thomas, E., Cotton, L.T. and Watkins, P.J. Improved survival of the diabetic foot: the role of a specialised foot clinic. Quarterly Journal of Medicine 1986, New Series 60(232): 763-771 Gujral, J.S., McNally, P.G., O'Malley, B.P. and Burden, A.C. Ethnic differences in the incidence of lower extremity amputation secondary to diabetes mellitus. Diabetic Medicine 1993, 10: 271-274 Neil, H.A.W., Thompson, A.V, Thorogood, M., Fowler, G.H. and Mann, J.I. Diabetes in the elderly: the Oxford Community Diabetes Study. Diabetic Medicine 1989, 6: 608-613 39
  40. 40. Walters, D.P., Gatling, W., Mullee, M.A. and Hill, R.D. The distribution and severity of diabetic foot disease: a community study with comparison to a non-diabetic group. Diabetic Medicine 1992, 9: 354-358 Waugh, N.R. Amputations in diabetic patients: a review of rates, relative risks and resource use. Community Medicine 1989, 10: 279-288 Mortality Fuller, J.H., Elford, J., Goldblatt, P. and Adelstein, A.M. Diabetes mortality: new light on an underestimated public health problem. Diabetologia 1983, 24: 336-341 Marks, H.H. and Krall, L.P. Onset, course, prognosis and mortality in diabetes mellitus. Joslin's Diabetes Mellitus. Marble, A., White, P., Bradley, R.F., Krall, L.P. (eds), Lea and Febiger: 1971, 11th edition, 209-254 McNally, P.G., Raymond, N.T., Burton, P.R., Botha, J.L., Swift, P.G.F., Burden, A.C. and Hearnshaw, J.R. Mortality experience of juvenile-onset (<17 years) type 1 diabetes from 1949 to 1991. Diabetic Medicine 1992, 9(Suppl. 1): 44A Morrish, N.J., Stevens, L.K., Head, J., Fuller, J.H., Jarrett, R.J. and Keen, H. A prospective study of mortality among middle-aged diabetic patients (the London cohort of the WHO Multinational Study of Vascular Disease in Diabetics). I. Causes and death rates. Diabetologia 1990, 33: 538-541 Stephenson, J., Swerdlow, A.J., Devis, T and Fuller, J.H. Recent trends in diabetes mortality in England and Wales. Diabetic Medicine 1992, 9: 417-421 Swerdlow, A.J. and Jones, M.E. Mortality during 25 years of follow-up in a cohort of over 5000 English and Welsh patients with diabetes. Personal communication. Tunbridge, W.M.G. Factors contributing to deaths of diabetics under fifty years of age. Lancet 1981, 2: 569-572 40
  41. 41. Walters, D.P., Gatling, W., Houston, A.C., Mullee, M.A., Julious, S.A. and Hill, R.D. Mortality in diabetic subjects: an eleven year follow-up of a community-based population. Diabetic Medicine 1994,11: 968-973 Role of blood glucose control Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. New England Journal of Medicine 1993, 329: 977-986 UK Prospective Diabetes Study. VI. Complications in newly diagnosed type 2 diabetic patients and their association with different clinical biochemical risk factors. Diabetes Research 1990, 13: 1 -11 UK Prospective Diabetes Study VIII. Study design, progress and performance. Diabetologia 1991, 34: 877-890 Pregnancy Lowy, C., Beard, R.W. and Goldschmidt, J. The UK diabetic pregnancy survey. Acta Endocrinologica 1986, (Suppl. 277): 86-89 Lowy, C. Pregnancy and diabetes mellitus. Textbook of Diabetes. Pickup, J.C. and Williams, G. (eds), Blackwell Scientific Publications, 1991, 835-850 Williams, D.R.R. Epidemiologically based needs assessment. Report 1. Diabetes mellitus. 2nd edition. DHA Project Research Programme. October 1992. 41
  42. 42. 6. Care of the person with diabetes The long-term care required by people with diabetes is organised in different ways from district to district. Traditional means of providing care are based upon attendance at a hospital diabetes clinic. Increasingly however the concept of 'shared care', care shared between the hospital and the general practice team, is being employed. In 1992, the Chronic Disease Management programme for diabetes care was set up. GPs are paid a fee for providing a programme of care, often in the form of a 'mini-clinic', approved by the local Family Health Services Authority. With this system, many people with diabetes can be cared for principally by the primary health care team. Certain groups such as children, adolescents, insulin dependent patients, pregnant women and those with specific complications or difficulties in management will often require the specialised care of the hospital clinic or diabetes centre. The limitations of the traditional diabetes clinic have encouraged the establishment of district diabetes centres. Though often based in or near the district general hospital, the centres are devoted to the provision of diabetes care throughout the district, and are a major and greatly valued resource for primary health care teams, patients and carers. These centres act as a focus for local organisation of diabetes services and coordination with general practitioners, and as a centre for education resources and programmes for people with diabetes, their carers and health care professionals. Expert advice and help is available throughout the week (not just in clinic hours) for anyone with diabetes. With specialist facilities and experienced staff dedicated to diabetes care, the centre environment appears more conducive to treatment, teaching and learning. Whether an individual with diabetes is cared for principally by their general practice team or by the hospital diabetes specialist team, it is now widely recognized that care is best provided by groups of health care professionals, each with their own particular skills, working closely together. The teams include a consultant physician, diabetes specialist nurse, dietitian, chiropodist, general practitioner and practice nurse. They will also need to call upon the skills of a clinical psychologist, ophthalmologist, nephrologist, neurologist, vascular and orthopaedic surgeon, obstetrician, midwife and other specialists as necessary. The consultant physician responsible for diabetes services has a special interest in diabetes; such specialists are often referred to as diabetologists. In some districts, however the clinic is run by a general physician. One paediatrician in each district should have a specialist interest and knowledge of diabetes in children, and be part of a named and experienced paediatric diabetes team. One of the most important innovations in diabetes care over recent years has been the increasing involvement of diabetes specialist nurses in providing care. Their main function involves educating, advising and counselling people with diabetes about all aspects of living with diabetes. They can play a pivotal role in coordinating the care provided by the entire team. They are usually based at the hospital clinic or diabetes centre, but will also liaise with general practices, and visit people in their own homes. 42
  43. 43. The dietitians are also essential members of the diabetes team. They assess eating patterns, and advise on all aspects of healthy eating. The chiropodist plays an essential role in preventing the development of foot problems by providing education on foot-care, and by assessing and treating any early problems that do arise. The general practitioner has overall responsibility for routine clinical care. S/he ensures that each person with diabetes receives effective surveillance of eyes, kidneys, feet and cardiovascular status in order that modifiable risk factors are picked up and treated early. The GP may have responsibility for identification and management of diabetic complications, and for identifying those individuals who require specialist hospital services. The practice nurse is responsible for providing education and advice, and co-ordinating care with other members of the team, and can also provide local social and psychological support for the person with diabetes and their family. Education of the individual with diabetes is an integral part of diabetes care. Each individual is responsible for how their diabetes is controlled, so the more they understand the condition itself and how to treat it, the more effective they will be. All members of the professional team play a role in education, and teaching may take place either on a one-to-one basis, in group sessions, or both. Every contact between the person with diabetes and their health professional should be regarded as an opportunity for the education of both. "The diabetic patient must be his own doctor, dietitian and laboratory technician. Hence, education is the single most important aspect of treatment." R.D. Lawrence When diabetes is first diagnosed, support from the professional team is essential. Instruction about the condition and its treatment, advice about adapting lifestyle, and counselling about the implications are all vital. Continuing education, ready access to any member of the team as necessary and a full formal annual medical review to assess control and check for the development of complications should always be available. In 1984 the Royal College of Physicians and the BDA issued a joint report on the provision of medical care for adults with diabetes in the UK. Based on the results of a survey of different centres around the UK, it highlighted a number of deficiencies in the facilities available, and made a number of recommendations concerning what was required to ensure adequate care was provided. In 1990, the BDA carried out a second survey; this showed that levels of provision of care and the use of existing facilities had in general improved over the intervening period, but that several important deficiencies still remained. Although the proportion of respondents reporting no specialist diabetes nursing assistance fell from 53 per cent to 14 per cent, this 43
  44. 44. still left 29 reporting none at all. Chiropodial care was less readily available in 1990 than in 1984 with 17 per cent of respondents (compared with 11 per cent) reporting a complete lack in the clinic. A recommendation that no locality should be without at least one physician with a special interest in diabetes was fulfilled in 81.8 per cent of localities, but some were still relatively poorly staffed. A list of reports giving the BDA's full recommendations and guidelines on the provision of care to people with diabetes can be found in Appendix 2. Sources used Royal College of Physicians of London Committee on Endocrinology and Diabetes Mellitus, and the British Diabetic Association. The provision of medical care for adult diabetic patients in the United Kingdom, 1984. Spathis, G.S. Facilities in diabetic clinics in the UK: shortcomings and recommendations. Diabetic Medicine 1986, 3: 131-136 Williams, D.R.R. and Spathis, G.S. Facilities in diabetic clinics in the UK: how much have they changed? Diabetic Medicine 1992, 9: 592-596 44
  45. 45. 7. The costs of diabetes The nature of diabetes, with all that is required for its control, together with its attendant complications, means that it imposes considerable costs on both the individual and the nation as a whole. The costs fall into three different categories: 1. Direct costs The costs to the NHS of preventing, detecting and treating diabetes and its complications come under this heading. These include the costs of in-patient and out-patient care provided by the hospital, services provided in the community by GPs and district nurses, and the costs of supplies such as insulin, tablets, syringes and-blood and urine testing equipment. In addition, there are the major costs generated by the complications of diabetes, such as those incurred in the detection and treatment of retinopathy, the treatment of end-stage renal failure (dialysis and transplantation), the diagnosis, treatment and long-term support of the high rates of heart disease, stroke and peripheral vascular disease attributable to diabetes, and the costs of amputations. 2. Indirect costs These relate to the loss of productive output caused by sickness absence, early retirement and premature mortality. 3. Intangible or psychological costs These include the costs of anxiety, pain, suffering and other non-financial outcomes of the condition, and the effects of diabetes and its complications on quality of life. Psychological costs have rarely been considered in economic analyses because of the difficulties involved in assigning costs to such factors. There are also a number of difficulties inherent in calculating indirect costs. The few studies that have been carried out in the UK have therefore concentrated on the direct costs. Table 6 overleaf shows the direct costs of diabetes and its complications calculated for England and Wales in 1986-7. With an estimated NFIS budget for 1993/4 of £36 billion, if 4-5 per cent of this budget is spent on the costs of the care of people with diabetes, the cost of such care for the entire UK works out at £1.4-1.8 billion. It should be emphasised that this is only an estimate, and is likely to be an underestimate. 45
  46. 46. There is increasing evidence that substantial benefits can be derived from investing resources in 'anticipatory' care. Implementation of a number of relatively simple (and therefore relatively inexpensive) measures can have a significant impact on the health of people with diabetes, and thereby reduce subsequent treatment needs. Severe visual loss due to retinopathy can be avoided if those at risk can be identified and treated early enough. This can be achieved through systematic screening programmes. Similarly, with early detection and management, progression of nephropathy can be adequately slowed and renal function maintained; screening for microalburninuria should therefore make it possible to reduce the number of people entering end-stage renal failure. Current estimates of the total cost of providing renal replacement therapy for end-stage renal failure in people with diabetes are of the order of £70 million per year. In 1987/8, it was estimated that the cost to the NHS of major amputations in people with diabetes was £15 million a year, or £9,400 per amputation. Studies have shown that enhanced levels of foot care provided by specialised foot clinics can reduce the annual rate of lower limb amputation by 50 per cent or more. Educational programmes, with nurse specialists playing a central role, have been shown to provide significant benefits with savings in net costs; various studies have shown that the introduction of such programmes has led to a reduction in the number of hospital admissions due to ketoacidosis and other problems related to poor control of blood glucose. Table 6: Direct costs of diabetes and its complications, 1986-7, for England and Wales Diabetes cost All causes cost Diabetes as % £ million £ million of total NHS In-patient (diabetes primary 81 6,375 1.3 diagnosis) In-patient (diabetes subsidiary 217 - 3.4 diagnosis) Out-patient (diabetic clinics only) 29 1,057 2.7 GP consultations (diabetes as a 17 1,204 1.4 primary diagnosis only) GP prescriptions (diabetes as 35 1,960 1.8 primary diagnosis only) Long-term residential and 105 2,100 5.0 nursing care outside NHS hospitals (all residents reporting disability from diabetes) Total (where data available) 484 12,696 3.8* 46
  47. 47. * If the costs of complications are added in for prescriptions and GP visits, and if the cost of treating people with diabetes in ordinary out-patient clinics are included, it is estimated that the percentage of resources absorbed by people with diabetes would rise from 3.8 per cent to between four and five per cent. Sources used Alexander, W.D. and South East Thames Diabetes Physicians Group. Diabetes care in a UK health region: activity, facilities and costs. Diabetic Medicine 1988, 5: 577-581 Boulton, A.J.M. and Connor, H. The diabetic foot 1988. Diabetic Medicine 1988, 5: 796-798 Connor, H. Diabetic management and education: costs and benefits. Diabetes Education. Baksi, A.K., Hide, D.W. and Giles, G. (eds), John Wiley and Sons, 1984,3-10 Connor, H. The economic impact of diabetic foot disease. The Foot in Diabetes. Connor, H., Boulton, A.J.M. and Ward, J.D. (eds), John Wiley and Sons, 1987,145-149 Gerard, K., Donaldson, C. and Maynard, A.K. The cost of diabetes. Diabetic Medicine 1989, 6:164-170 Laing, W. and Williams, D.R.R. Diabetes: a model for healthcare management. Office of Health Economics, 1989, No. 92 47
  48. 48. 8. What does the future hold? Since the discovery of insulin back in 1921, tremendous advances have been made in our understanding of the causes and management of diabetes and its complications. Much still requires clarification; both prevention and cure, while now firmly on the agenda, remain some way off. The personal and financial arguments for intensification of research are compelling. One of the principal aims of the British Diabetic Association is to fund research in the diabetes field. The BDA is one of the largest funders of diabetes research in the UK, and is planning to spend over £4 million on research in 1996. Other organisations providing support for diabetes research include the NHS, the Medical Research Council, charities such as the Wellcome Trust and the juvenile Diabetes Foundation, and the pharmaceutical industry. Figures are not readily available for the expenditure of these other organisations on diabetes research at present, although in the future they may be so. Many different avenues are being explored by different research groups in the UK and around the world; it would be impossible to describe them all here. A few areas however are worthy of particular attention as they have an enormous potential impact on the lives of people with diabetes and those at risk of developing the condition. Prediction and prevention of insulin dependent diabetes Insulin dependent diabetes is believed to be an autoimmune disease triggered by some as yet unknown environmental factor in genetically susceptible individuals. Research teams are engaged in trying to identify which genes are responsible for this susceptibility; as many as six genes may be involved. Their identification would enable simple screening programmes to identify people at risk for insulin dependent diabetes. Screening for susceptibility will be practically useful only when the means of preventing diabetes are developed. A variety of approaches to secondary prevention are already being investigated. These include the use of drugs to suppress the activity of the immune system and in doing so blunt the attack on the insulin-producing cells; the administration of insulin injections before these are needed for survival to lighten the workload of surviving cells, thus enabling them to fight off the immune attack; and the use of nicotinamide, one of the B group of vitamins, which has been shown to protect insulin-producing cells from certain sorts of damage. Pancreas and islet transplantation The world's first human pancreas transplant was carried out in 1966 by a team at the University of Minnesota in the USA; the dramatic improvement seen initially in the recipient's condition (she was able to dispense with insulin injections almost immediately) led to real hopes of a breakthrough in the search for a cure to diabetes. Unfortunately however, a number of problems have been encountered and progress in the development of this technique has been disappointingly slow. 48