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Diabetes and Thalassaemia

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1 Diabetes and Thalassaemia
3rd Pan-European Conference on Haemoglobinopathies & Rare Anaemias Limassol, 24 – 26 October 2012 Dr Maria Barnard & Dr Ploutarchos Tzoulis Romilla Jones, Emma Prescott, Dr Farrukh Shah The Whittington Hospital NHS Trust, London

2 The Diabetes Epidemic Diabetes affects 366 million people worldwide
Predicted to affect 552 million people by 2030 Diabetes caused 4.6 million deaths in 2011 Every 10 seconds a person dies from diabetes-related causes Every 10 seconds two people develop diabetes Greatest number of people with diabetes are between to 59 years of age 78,000 children develop type 1 diabetes each year International Diabetes Federation. IDF Atlas, 5th edn. Brussels, Belgium: IDF, 2

3 The Top 10 International Diabetes Federation. IDF Atlas, 5th edn. Brussels, Belgium: IDF, 3

4 Diabetes Prevalence International Diabetes Federation. IDF Atlas, 5th edn. Brussels, Belgium: IDF, 4

5 The Top 10 by Prevalence International Diabetes Federation. IDF Atlas, 5th edn. Brussels, Belgium: IDF, 5

6 Healthcare Expenditure (2011)
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 International Diabetes Federation. IDF Atlas, 5th edn. Brussels, Belgium: IDF, 6

7 Diabetes in β-Thalassaemia Major
Diabetes prevalence ~20% (age, chelation therapy) Aetiology and risk factors: Transfusional iron overload Poor chelation therapy, poor compliance, advanced age of onset Altered β-cell insulin secretion Autoimmunity Insulin resistance secondary to liver disease HCV infection Global epidemic – type 1/type 2 diabetes 7

8 Early Diagnosis of Diabetes
Annual oral glucose tolerance tests (OGTT) from puberty or from age 10 years if there is a positive family history Prompt treatment of hyperglycaemia Intensification of iron chelation therapy Thalassaemia International Federation. Guidelines for the Clinical Management of Thalassaemia. 2nd Revised Edition Available at: United Kingdom Thalassaemia Society. Standards for the Clinical Care of Children and Adults with Thalassaemia in the UK. 2nd Edition Available at: 8

9 Plasma Glucose (mmol/l) Plasma Glucose (mg/dl)
Diagnosis of Diabetes Category Plasma Glucose (mmol/l) Fasting 2h Post-Glucose Load Diabetes mellitus ≥ 7.0 ≥ 11.1 Impaired glucose tolerance (IGT) < 7.0 7.8 – 11.0 Impaired fasting glycaemia (IFG) 6.1 – 6.9 (WHO) 5.6 – 6.9 (ADA) < 7.8 Not diabetic or glucose intolerant ≤ 6.0 (WHO) ≤ 5.6 (ADA) Category Plasma Glucose (mg/dl) Fasting 2h Post-Glucose Load Diabetes mellitus ≥ 126 ≥ 200 Impaired glucose tolerance (IGT) < 126 140 – 199 Impaired fasting glycaemia (IFG) 110 – 125 (WHO) 100 – 125 (ADA) < 140 Not diabetic or glucose intolerant < 110 (WHO) < 100 (ADA) 9

10 Aim of Treatment Prevention, detection and management of complications
Microvascular & Macrovascular Background retinopathy Kidney glomerulus Neuropathic foot ulcer Proliferative retinopathy Glomerular sclerosis Ischaemia 10

11 Mortality in Diabetes Risk for death among people with diabetes twice that of people of similar age but without diabetes In 2004, heart disease noted on 68% of diabetes-related death certificates among people aged 65 years or older (USA) In 2004, stroke noted on 16% of diabetes related death certificates among people aged 65 years or older (USA) Centers for Disease Control and Prevention. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention, 2011 11

12 Antidiabetic Drugs Acarbose I GLP-1 Sulphonylureas Meglitinides
Glucose (G) Carbohydrate Glucose DIGESTIVE ENZYMES Insulin (I) I G Sulphonylureas Meglitinides GLP-1 analogues DPP-IV inhibitors Metformin Acarbose Glitazone GLP-1 Liver Pancreas Adipose tissue Muscle

13 Stepwise Management of Diabetes
Insulin ± oral agents Oral combination Oral monotherapy Diet & exercise Sulphonylureas Gliptins GLP-1 analogues Metformin Type 2 diabetes is traditionally treated in a stepwise manner. Initial therapy is usually diet and increased exercise. However, lifestyle measures generally fail to control glycaemia and, therefore, pharmacological treatment is instigated. Initial therapy is with a single oral drug although monotherapy often fails over a period of time and a combination of two or more oral therapies is used. Subsequently, failure of all oral combination therapy may occur when -cell failure has progressed to such a degree that additional, exogenous insulin is required.

14 Insulin Therapy Physiological insulin regimen
24 hour insulin and glucose profile in non-diabetic persons Genetic risk factors alone cannot explain the increasing incidence of type 1 diabetes throughout the world or other temporal changes in incidence. Various environmental factors appear important and this raises the possibility of identifying factors which could prevent the onset of type 1 diabetes. Viruses may initiate autoimmunity and perhaps also precipitate diabetes in subjects with autoimmunity. Enteroviruses have been most strongly linked to type 1 diabetes, but though multiple cohort studies support an association between enteroviruses and the onset of type 1 diabetes, convincing proof of causality remains elusive. Enterovirus infection could initial B-cell autoimmunity through molecular mimicry between CBV P2-C protein and GAD, or limited capacity of B-cells to neutralise free radicals released in the infectious process could initiate B-cell autoimmunity. Rotavirus contains peptide sequences highly similar to islet autoantigens and could trigger islet autoimmunity by molecular mimicry. There is evidence of a relationship between rotavirus infection and the first appearance or an increase in islet autoantibodies during follow-up of babies with a first degree relative with type 1 diabetes. Dietary factors – cow’s milk or wheat introduced at weaning triggers insulinitis and diabetes in animal models, perhaps through molecular mimicry. Human studies have suggested an association between short duration of breast feeding and increase in type 1 diabetes, but other cohort studies have failed to find an association between cow’s milk and B-cell autoimmunity. There is also evidence that the introduction of gluten before age of 3 months increases the risk of development of B-cell autoimmunity. Vitamins – In vitro studies have shown that Vit D3 is immunosuppressive or immunomodulating. European studies have shown a protective effect of vitamin D supplementation in infancy against type 1 diabetes. Vitamin D possibly might protect or arrest an ongoing immune process initiated in susceptible people by environmental exposures. Social mixing – Early infectious exposure may play a role in the development of immunoregulatory mechanisms that protect against diabetes. There are variable results but social mixing through attendance at day care in early infancy appears to confer protection against the development of childhood diabetes. Improvement in hygiene – Hypothesis that increased hygiene in the Western World has led to a decline in immunity among women of childbearing age. These women are more likely to develop viraemia during pregnancy, resulting in congenital persistent infection of B-cells and early onset type 1 diabetes in the offspring. 14

15 Basal-Bolus Insulin Regimen
e.g. Insulin aspart (Novorapid) + insulin glargine (Lantus) Breakfast Lunch Dinner Bedtime Insulin (Rapid) Insulin (Rapid) Insulin (Rapid) Insulin (Basal)

16 Insulin Dose Adjusting
To calculate rapid insulin dose given with a meal: Take capillary blood glucose before eating If >7 mmol/l, calculate insulin correction dose Estimate carbohydrate content of food 10g carbohydrate = 1 Carbohydrate Portion (CP) Calculate food insulin using 1 – 3 units for each CP Remember to adjust for all other factors that may affect glycaemic control (exercise, illness, alcohol etc) Give insulin (correction dose + food insulin) 16

17 Whittington Joint Diabetes Thalassaemia Clinic
Aims: Provide high quality diabetes, endocrine and haematology care Optimise metabolic control Support patient self-management Support partnership working between specialist teams and between patients and clinicians Provide education, training and research opportunities 17

18 Whittington Joint Diabetes Thalassaemia Clinic
Patients seen jointly: Consultant Diabetologist (Dr Maria Barnard) Consultant Haematologist (Dr Farrukh Shah) Diabetes Specialist Nurse (Romilla Jones) Haematology Specialist Nurse (Emma Prescott) Senior Diabetes Dietitian Clinical Psychologist Access to Whittington type 1 diabetes structured education courses (WINDFAL) 18

19 Whittington Joint Diabetes Thalassaemia Clinic
Complete full diabetes annual review once a year Address the 9 Key Care Processes for diabetes: [1] Glycaemic control [2] Blood pressure [3] Serum cholesterol [4] Serum creatinine [5] Urinary albumin [6] Weight [7] Diabetic foot examination [8] Smoking status assessment [9] Retinal screening 19

20 Whittington Joint Diabetes Thalassaemia Clinic
Measure Target Fructosamine (umol/l) HbA1c (%) < 322 (< 299) < 7.0 (< 6.5) Capillary blood glucose (mmol/l) Pre-prandial Post-prandial (2 h) 4 – 7 5 – 8 Blood pressure (mmHg) - with nephropathy < 130 / 80 < 125 / 75 Total cholesterol (mmol/l) < 4.0 LDL cholesterol (mmol/l) < 2.0 Triglycerides (mmol/l) < 1.7 Smoking status Non-smoker Body mass index (kg/m2) 20 – 25 Exercise Daily Aspirin (75 mg) if > 50 y of age or CV risk 20

21 Whittington Joint Diabetes Thalassaemia Clinic
Clinic Population Description Gender - Female Male 59% 41% Age* 39 years (28 – 59y) Ethnic origin Greek Cypriot / Greek South Asian (Indian, Pakistani, Bangladeshi) 36% 64% Ferritin at first appointment* 1827 ug/l ( ug/l) Diabetes duration* 13 years (<1 – 29y) Age at diagnosis* 21 years (10 – 40y) BMI* 24.8 kg/m2 Treatment – insulin 73% Treatment – oral antidiabetic drugs only 14% Treatment – diet control only *median values 21

22 Performance: Joint Clinic vs. National Audit for England
Care Process Performance of Key Care Processes Joint Clinic ( ) National Diabetes Audit ( ) Fructosamine (HbA1c) 97.5% 91.1% Serum cholesterol 89.9% Serum creatinine 100% 91.2% Urinary albuminuria 62.7% Weight / Body mass index 88.8% Blood pressure (BP) 80.4% 93.7% Foot assessment 89.2% 77.1% Smoking status 86.5% 22

23 Target achievement: Joint Clinic vs. National Audit for England
Percentage of patients achieving treatment target Joint Clinic ( ) National Diabetes Audit ( ) Fructosamine < 345 umol/l (HbA1c < 7.5%) 72.7% 62.9% BP < 135/75 mmHg 57.9% 30.1% Total cholesterol < 5.0 mmol/l 82.1% 78.0% 23

24 Metabolic improvement in Joint Clinic
Parameter First appointment 1 year follow-up Change Fructosamine 344 umol/l 319 umol/l -25 umol/l BP 122/70 mmHg 124/77 mmHg +2/7 mmHg Total cholesterol 3.8 mmol/l 3.5 mmol/l -0.3 mmol/l 33% of patients achieved reduction in ferritin of >10% 23% were on antihypertensive agents 23% were on lipid lowering agents 32% on antiplatelet/anticoagulant agents 24

25 Diabetic Complications in Patients Attending Joint Clinic
Prevalence in patients attending Joint Clinic Microalbuminuria 13.6% Diabetic retinopathy ≥1 microvascular complication 22.7% Charcot neuroarthropathy 4.5% Cataracts 9.1% Macrovascular complications Diabetic emergencies 25

26 Endocrinopathies in Patients Attending Joint Clinic
Endocrinopathy Prevalence in patients attending Joint Clinic Hypogonadism - Hypogonadotrophic hypogonadism - Primary hypogonadism 86% 59% 27% Hypothyroidism 18% Hypoparathyroidism 23% Osteopenia 14% Osteoporosis 55% Glucocorticoid deficiency Growth hormone deficiency 26

27 Whittington Joint Diabetes Thalassaemia Clinic - Discussion
Joint Diabetes Thalassaemia Clinic effective at providing high quality care in the most complex patients 41% patients diagnosed with diabetes <19 years of age Early effective iron chelation is critical Be aware of diabetic complications (microvascular) Optimise glycaemic control Modify cardiovascular risk 27

28 Diabetes and Thalassaemia -Conclusions
Patients with diabetes and thalassaemia have complex medical care needs Psychological impact – treatment burden, impact on daily life, feeling of difference, dependence and anxiety Partnership working of the Joint Diabetes Thalassaemia Clinic: Patients have easy access to senior specialist clinicians Continuity of care Supported by multidisciplinary team Working together with the patient and each other Supporting self-management 28

29 Diabetes and Thalassaemia -Conclusions
Patients receive training in carbohydrate counting and insulin dose adjustment Patients access type 1 diabetes structured education Significant educational opportunities for healthcare professionals and staff in training Managing diabetes is one of the greatest challenges a person with thalassaemia can face. Joint Diabetes Thalassaemia Clinic enables our patients to effectively manage their physical and psychological long-term health 29


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