Biggest changes will be in Africa, followed very closely by MENA. NAC and Europe will change the least.
New in this edition: China takes the top spot, with India close behind. This is heavily influenced by the new study published in 2010. Our estimates are just under theirs at 90 million (compared to 91 million) and can be attributed to different age groups and a somewhat more conservative approach. Increases and changes in the position of countries relative to each other can be explained mostly by an ageing population and changes in urbanisation. Note, the BRIC countries are all in the top 10. Only the US is a high-income country.
The Pacific Islands and MENA dominate this category. The rates are more than twice the global average. Changes again only take into account changes in the population structure and urbanisation. For Pacific Islands, urbanisation is 100% so it is just age changes that can be expected. New for this edition: IMPORTANT: Nauru is no longer number 1 This is due not only to new data from the region, but may also reflect the effects of mortality due to diabetes. The emergence of MENA – 6 out of the 10 countries are in MENA
We used reports coming from the original population-based studies that tell us what proportion of the prevalence from the study were found to have diabetes at the time of the survey. The vast majority of these are people with type 2 diabetes, but undiagnosed type 1 diabetes is not unheard of, although it is of short duration, generally. In order to provide more accurate estimates for regions, and especially where data were lacking, we decided to create estimates of the proportion of undiagnosed (%) for each region and income group. For all the studies that provided data and had a sufficient quality, we took the median value of all studies within that region and income group. This allowed us to control for the skew of the data rather than if we took the mean. So if one study reported a number that was very different from all the others, it wouldn’t pull our estimate in that direction. Low-income countries in Africa have the highest estimated proportion of undiagnosed diabetes (77.9%) However, for any one region and income group, the proportion of undiagnosed diabetes was at least 27%. This is very high and likely an underestimate. Globally, half of all cases of diabetes are undiagnosed. Over 60% of all people with undiagnosed diabetes are in the Western Pacific and South-East Asia Regions.
The maps show us countries were there is high spending per person with diabetes, and high total spending on diabetes. The healthcare expenditures measure includes medical spending on diabetes by the health system as well as by people with diabetes. It does not include the indirect costs to society from lost productivity, absences from work, and the associated costs of care. In other words, this is a big underestimate of the true cost of diabetes. It is also important to note that some of this spending is necessary as part of care. However, some studies show that families pay 40-60% of medical care expenditures out of their own pockets for diabetes, which shows a disproportionate amount of the cost is borne by people with diabetes and their caregivers.
The differences in spending are almost the exact reverse of the mortality and prevalence data. High-income countries have a much higher total spending that any of the middle- or low-income countries. This additional spending is probably contributing to the lower mortality rate, prevalence, and total deaths. In addition, mean spending on diabetes per case is much higher in high-income than in any of the other groups. In low-income, it is almost non-existent.
Diabetes increases the chances of developing tuberculosis by 2.5 times at least. A person with diabetes and tuberculosis is more likely to fail tuberculosis treatment and more likely to die from tuberculosis than a person without diabetes.
Using the fact that we know that a person with diabetes has 2.5 times the chances of developing tuberculosis, we can calculate how much tuberculosis in a country may be due to diabetes. We see that for countries with a high burden of diabetes and a relatively low burden of tuberculosis, a large proportion of tuberculosis cases may be attributable to diabetes. Conversely, countries with a low diabetes burden will have fewer tuberculosis cases related to diabetes.
There is a temporal relationship between insulin resistance, insulin secretion and the development of diabetes. In the early stages of pathogenesis, as insulin resistance rises, there is a compensatory increase in insulin secretion and the individual remains normoglycaemic. 1 In the long term, if the -cells begin to fail, insulin secretion falls , impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) develop, and hyperglycaemia reaches levels defined as type 2 diabetes mellitus. 1 However, diabetes may not be diagnosed until many years later. Development of diabetes is associated with the development of serious complications that begin before type 2 diabetes is diagnosed. 2 The risk of complications increases as the disease progresses. 3 There are two potential approaches to delaying the progression of the disease and its associated complications : firstly, prevention interventions at the stage of IGT/IFG, and secondly, treatment interventions to delay disease progression following diagnosis . DeFronzo RA. Med Clin N Am 2004;88:787–835. Hu FB, et al . Diabetes Care 2002;25:1129–1134. Stratton IM, et al . BMJ 2000;32:405–412.
Copy of diabetes mellitus
DIABETES MELLITUS Prof. ADEL A EL-SAYED MD Chairman ElectMiddle East and North Africa )MENA( Region )International Diabetes Federation )IDF Professor of Internal Medicine Sohag Faculty of Medicine Sohag-EGYPT
The Problem• Diabetes occurs world-wide and the incidence of both type 1 and type 2 diabetes are rising; it is estimated that, in the year 2000, 171 million people had diabetes, and this is expected to double by 2030.• This global pandemic principally involves type 2 diabetes, to which several factors contribute, including greater longevity, obesity, unsatisfactory diet, sedentary lifestyle and increasing urbanizations.
The IDF Diabetes Atlas 5th Edition December 2011A summary of the figures and key findings
The global burden 366 million people have diabetes in 2011; by 2030 this will have risen to 552 million The number of people with type 2 diabetes is increasing in every country 80% of people with diabetes live in low-and middle-income countries The greatest number of people with diabetes are between 40 to 59 years of age 183 million people (50%) with diabetes are undiagnosed Diabetes caused 4.6 million deaths in 2011 Diabetes caused at least USD 465 billion dollars in healthcare expenditures in 2011; 11% of total healthcare expenditures in adults (20-79 years) 78,000 children develop type 1 diabetes every year
Healthcare expenditures• USD 465 billion spent on healthcare for diabetes• 11% of all healthcare spending is for diabetes• USD 1,274 is spent on diabetes care per person with diabetes in 2011
Diabetes and Tuberculosis• Focused on the linkages between the two diseases and a review of the evidence• Calculated the attributable cases of tuberculosis to diabetes• Highlights areas where there is a high double burden
Key Messages1. Diabetes is a huge and growing problem, and the costs to society are high and escalating2. Diabetes is a neglected development issue, affecting all countries3. There are cost-effective solutions to reverse the global diabetes epidemic4. Diabetes is not only a health issue, its causes are multi-sectoral and it requires a multi-sectoral response5. The UN High-level Meeting is not the end of international commitments on diabetes; it is the start of concerted and coordinated action
AETIOLOGICAL CLASSIFICATION OF DIABETES MELLITUS• Type 1 diabetes• Type 2 diabetes• Gestational diabetes• Other forms endocrine diseases such as acromegaly or Cushings syndrome unusual genetic diseases
AETIOLOGY AND PATHOGENESIS OF DIABETES• In both of the common types of diabetes, environmental factors interact with genetic susceptibility to determine which people develop the clinical syndrome.• However, the underlying genes, precipitating environmental factors and pathophysiology differ substantially between type 1 and type 2 diabetes.• Type 1 diabetes (previously IDDM) is invariably associated with profound insulin deficiency requiring replacement therapy.• Type 2 diabetes (previously NIDDM) patients retain the capacity to secrete some insulin but exhibit impaired sensitivity to insulin (insulin resistance) and can usually be treated without insulin replacement therapy.
TYPE 1 DIABETES PathologyType 1 diabetes is a slowly progressive T cell-mediated autoimmune disease. Family studies have produced evidence that destruction of the insulin-secreting cells in the pancreatic islets takes place over many years. Hyperglycaemia accompanied by the classical symptoms of diabetes occurs only when 70-90% of ß cells have been destroyed.The pathological picture in the pre-diabetic pancreas in type 1 diabetes is characterised by: insulitisIslet cell antibodies can be detected before the clinical development of type 1 diabetesType 1 diabetes is associated with other autoimmune disorders, including thyroid disease, coeliac disease, Addisons disease, pernicious anaemia and vitiligo.
Environmental factors• Although genetic susceptibility appears to be a prerequisite for the development of type 1 diabetes, the concordance rate between monozygotic twins is less than 40%and environmental factors have an important role in promoting clinical expression of the disease.• The evidence that viral infection might cause some forms of type 1 diabetes is derived from studies where virus particles known to cause cytopathic or autoimmune damage to ß cells have been isolated from the pancreas.• Several viruses have been implicated, including mumps, Coxsackie B4, retroviruses, rubella (in utero), cytomegalovirus and Epstein-Barr virus.
Environmental factors• Circumstantial evidence supports the proposition that dietary factors may influence the development of type 1 diabetes.• Bovine serum albumin (BSA), a major constituent of cows milk, has been implicated in triggering type 1 diabetes, since children who are given cows milk early in infancy are more likely to develop type 1 diabetes than those who are breastfed.• Other factors.
Metabolic disturbances in type 1 diabetes• Profound insulin deficiency is associated with metabolic sequelae.• Hyperglycaemia leads to glycosuria and dehydration.• Unrestrained lipolysis and proteolysis result in weight loss, increased gluconeogenesis and ketogenesis.• When generation of ketone bodies exceeds the capacity for their metabolism, ketoacidosis results.
TYPE 2 DIABETES Pathology• Type 2 diabetes is a more complex condition than type 1 diabetes because there is a combination of resistance to the actions of insulin in liver and muscle together with impaired pancreatic ß-cell function leading to relative insulin deficiency• Insulin resistance appears to come first, and leads to elevated insulin secretion in order to maintain normal blood glucose levels.• However, in susceptible individuals the pancreatic ß cells are unable to sustain the increased demand for insulin and a slowly progressive insulin deficiency develops.
22Type 2 diabetes is a progressive disease: early intervention is critical Macrovascular complications Microvascular complications β-cell function Insulin resistance Blood glucose –10 Prevention 0 Treatment 10+ Years Diagnosis IFG/IGT Type 2 diabetesIFG: impaired fasting glucoseIGT: impaired glucose tolerance Adapted from DeFronzo RA. Med Clin N Am 2004;88:787–835.
UKPDS: progressive decline of β-cell function over time 100 80 Start of treatment β-cell function )%( 60 40 20 P < 0.0001 0 –10 –9 –8 –7 –6 –5 –4 –3 –2 –1 1 2 3 4 5 6 Time from diagnosis )years(HOMA model, diet-treated (n = 376) Adapted from Holman RR. Diabetes Res Clin Pract 1998; 40 (Suppl.):S21–S25.
Metabolic disturbances in type 2 diabetes• Patients with type 2 diabetes have a slow onset of relative insulin deficiency.• Ketoacidosis are rare.• Glycosuria occurs when the blood glucose concentration exceeds the renal threshold.• The severity of the classical osmotic symptoms of polyuria and polydipsia is related to the degree of glycosuria.• Thus, patients are often asymptomatic, but usually present with a long history (typically many months) of fatigue, with or without osmotic symptoms.
INVESTIGATIONS• URINE TESTING: Glucose, Ketones Protein.• BLOOD TESTING: Glucose, Glycated haemoglobin, Blood lipids.• The diagnostic criteria for diabetes mellitus
Clinical assessment• Hyperglycaemia causes a wide variety of symptoms.• The classical symptoms of thirst, polyuria, nocturia and rapid weight loss are prominent in type 1 diabetes, but are often mild or absent in patients with type 2 diabetes.• fatigue and malaise.• increased susceptibility to infection.
Clinical assessment• The physical signs in patients with type 2 diabetes at diagnosis depend on the mode of presentation:• More than 70% are overweight, and obesity may be central (truncal or abdominal).• Hypertension is present in at least 50% of patients with type 2 diabetes.• Although hyperlipidaemia is also common, skin lesions such as xanthelasma and eruptive xanthomas are rare.
Patient Education• Outpatient education: achieved by a multidisciplinary team (doctor, dietitian, specialist nurse and podiatris).• Inpatient education: when insulin injections are needed.• Self-assessment of glycaemic control: urine, SMBG.• Education of treatment targets: BG, BP, Serum lipids.
Advice to patients with IGT• Lifestyle advice.• Monitoring of blood glucose level.• Other cardiovascular risk factors should be treated aggressively.
Management• dietary/lifestyle modification (diet and excercise).• oral anti-diabetic agents.• insulin injections.• In parallel with treatment of hyperglycaemia, other risk factors for complications of diabetes need to be addressed (hypertension, dyslipidaemia and advice on smoking cessation).
ORAL ANTI-DIABETIC DRUGS• Although their mechanisms of action are different, most depend upon a supply of endogenous insulin. No role in treatment of type 1 DM.• The sulphonylureas and the biguanides have been the mainstay of treatment for many years and have the strongest evidence of preventing complications of diabetes.• Newer agents include the insulin sensitizers the thiazolidinediones, the a-glucosidase inhibitors and incretins.• Primary and secondary failure.
SULPHONYLUREAS• Mechanism of action: The principal effect of sulphonylureas is to stimulate the release of insulin from the pancreatic ß cell (insulin secretagogue).• Indications for use: valuable in the treatment of non- obese patients with type 2 diabetes who fail to respond to dietary measures alone.• The main differences between the individual compounds lie in their potency, duration of action and cost.• Tolbutamide and chlorpropamide are now rarely used.• gliclazide and glipizide, glibenclamide and glimepride are used more often now.• Side effects.
BIGUANIDES• Metformin is the only biguanide available.• Indications for use.• Advantages.• Side effects and contraindications.• Dose and method of administration.
ALPHA-GLUCOSIDASE INHIBITORS• The a-glucosidase inhibitors delay carbohydrate absorption in the gut.• Acarbose or miglitol is available and is taken with each meal.• Lower post-prandial blood glucose and modestly improve overall glycaemic control.• The main side-effects are flatulence, abdominal bloating and diarrhoea.
THIAZOLIDINEDIONES• These drugs (also called TZD drugs, glitazones or PPAR? agonists) bind and activate peroxisome proliferator-activated receptor.• A nuclear receptor present mainly in adipose tissue that regulates the expression of several genes involved in metabolism, and work by enhancing the actions of endogenous insulin.• Plasma insulin concentrations are not increased and hypoglycaemia is not a problem.• Types, price, indications, and side effects.
INCRETIN MIMETICS• A new class of therapeutic agents is being developed for treatment of type 2 diabetes.• The secretion of insulin in response to a rise in blood glucose is greater when glucose is given by mouth, rather than by intravenous infusion.• In part this is caused by secretion of gut hormones, or incretins, which potentiate glucose-induced insulin secretion.• Glucagon-like peptide (GLP-1) is an incretin hormone which stimulates insulin secretion in a glucose-dependent manner, thus hypoglycaemia is unlikely.
INCRETIN MIMETICS• In addition, GLP-1 suppresses glucagon secretion, delays gastric emptying, reduces appetite and encourages weight loss.• It has to be given by injection.• As GLP-1 is rapidly degraded by the enzyme, dipeptidyl peptidase IV, inhibitors of this enzyme will have to be given to prolong its biological effect.• Alternatively, long-acting GLP-1 analogues are being developed. These include liraglutide and exenatide (synthetic exendin-4).• DPP4 inhibitors.
INSULIN• History, manufacture and formulation.• Regular insulin.• The duration of action of short-acting, unmodified insulin (soluble or regular insulin), which is a clear solution, can be extended by the addition of protamine and zinc at neutral pH (isophane or NPH insulin) or excess zinc ions (lente insulins).• Pre-mixed formulations.• Insulin analogues.