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اپيدميولوژي و كليات ديابت

اپيدميولوژي و كليات ديابت. دکتر فريدون عزيزي پژوهشكده علوم غدد درون ريز و متابوليسم دانشگاه علوم پزشکي شهيد بهشتي. Diabetes: A significant threat to public health. WHO has described diabetes as a “a silent epidemic” 1 Trends revealed over the 1995-2025 period 2 :

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اپيدميولوژي و كليات ديابت

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  1. اپيدميولوژي و كليات ديابت دکتر فريدون عزيزي پژوهشكده علوم غدد درون ريز و متابوليسم دانشگاه علوم پزشکي شهيد بهشتي

  2. Diabetes: A significant threat to public health • WHO has described diabetes as a “a silent epidemic”1 • Trends revealed over the 1995-2025 period2: • Adult population will rise by 64% • Accompanied by rise in diabetes prevalence of 35% and increase in number of cases by 122% • Major impact will be in developing countries: • 1995: 62% of people with diabetes lived in developing countries (84 million cases) • 2025: 75% of people with diabetes will be living in developing countries (228 million cases) • Estimated loss of 5-10 years in life expectancy for patients aged over 403 1. Diabetes mellitus: Report of a WHO study group. Geneva, World Health Organization, 1985 (WHO Technical Report Series, No. 727). 2. King H, Aubert RE, Herman WH. Global burden of diabetes 1995–2025: prevalence, numerical estimates and projections. Diabetes care, 1998, 21:1414–31. 3. Dobrossy L ed. Prevention in primary care: recommendations for promoting good practice. Copenhagen, WHO Regional Office for Europe, 1995. (EUR/ ICP/CIND 94 01/PB01).

  3. جدول بندي سبب شناختي ديابت نوع 2 جدول 1) 1- ديابت نوع 1 الف) با مداخله سيستم ايمني ب) ايديوپاتيك 2- ديابت نوع 3- علت هاي ديگر الف) اختلال ژنيتيكي سلول هاي بتا ب) اختلال ژنيتيكي در عمل انسولين ج) بيماريهاي لوزالمعده د) بيماريهاي غدد درون ريز ه) به علت دارو يا مواد شيميايي و) عفونت ها ز) انواع نادر تر همراه با بيماريهاي ژنيتيكييا اشكال ايمني بدن 4- ديابت آبستني (GDM)

  4. The History of Diabetes Ebers papyrus (1550 BC): referred to symptoms Hipocratic physicians (460-370 BC): do not have a description of diabetes Celsus(roman, 25 BC-50 AD): Described a disease with polyuria and lack of pain, but weakness, the fluid output greater than fluid intake. Aretaeos (81-96 AD): The first description; melting down of the flesh and limbs into urine; life is short, disgusting and painful. Galen(130-200 AD): described DM as a “weakness of the kidneys”, “Diarrhea of the urine” and “causing thirst” Rhazes= Al-Razi (860-932 AD): described diabetes mellitus

  5. Avicenna (980-1037)(PrincepsDoctorum) Al-Qanon: * Standard description of diabetes mellitus: Abnormal appetite Breakdown of sexual function Diabetic gangrene Sweet taste of diabetic urine * Excellent description of therapeutic measures for: Hypoglycemic coma Bulimia Abnormal appetite * Beginner of clinical trials Medvel VC. The Hisoty of Clinical Endocrinology. Parthenon Pub, New York 1993; p 46. Nabipour I. Clinical Endocrinology in Islamic Civilization in Iran. Int J EndocrinolMetab 2003; 1: 43 Sajadi MM et al. Ann Intern Med 2009; 150: 640

  6. The Road to Insulin Works by Thomas Willis, Mathew Dobson, thomasCawley, John Rollo, Benedict, Adolph kussmaul, Claude Bernard, Moritz Shiff, Apollinaire, Bouchardat, … in 17-19thcentrury. Joseph von Mering, Oscar Minkowski, Hedon, Langerhans, Jean de Meyer (1889-1910): Pancreatic diabetes Elliott P. Joslin (1986-1962): Clinical diabetes. Nobel prize for the discovery of insulin: Banting and Macleod (Best & collip). The team approach of diabetes & modern endocrinology.

  7. The rise and rise of diabetes Incidence (cases/100,000/year) 1920 1940 1960 1980 2000

  8. Diabetes: A Worldwide EpidemicGlobal Projections 1995-2010 22.0 32.9 50% 62.8 132.3 111% 13.0 17.5 35% 7.3 14.1 93% 12.4 22.5 81% 0.9 1.3 44% World 1995 = 118 million 2010 = 221 million (Increase 87% ) 2025=300 million (Americas 13.8-42.8, Eastern Med. 13.8-42.8)

  9. Islets comprise mainly beta cells that produce the hormone insulin

  10. Type 1 diabetes Immune cells invade the islets and destroy the beta cells. Lack of insulin leads to an increase in the level of blood glucose, which causes the symptoms and complications of diabetes.

  11. NATURAL HISTORY OF TYPE 1 DIABETES ENVIRONMENTAL MODIFIERS 100% ANTIBODIES TO INSULIN, GAD65, IA2, ZnT8 LOSS OF FIRST PHASE INSULIN RESPONSE (iv glucose) BETA CELL FUNCTION INSULITIS BETA-CELL INJURY GENETIC PREDISPOSITION LOSS OF GLUCOSE TOLERANCE (oral glucose) PRE-DIABETES DIABETES Years

  12. خصوصيات ديابت نوع 1و نوع 2

  13. A map of the region

  14. عوامل مساعد كننده ژنتيكي عوامل محيطي تغييرات سلولي فعال كننده ايمونولوژيك صدمه سلولي

  15. Risk factors for diabetes Type 1 Both genetic and environmental influences apear to be important in the development of type I diabetes. Potential environmental triggers include viruses, toxins in the food chain and dietary components, though to date the involvement of these factors has not been proven in the majority of cases.

  16. شيوع ديابت نوع 1 در كشورهاي مختلف 30 فنلاند سوئد 20 نروژ دانمارك، اسكاتلند، هلند، آمريكا، زلاند نو 10 كانادا انگلستان 5 كويت فرانسه بحرين

  17. New cases of type 1 diabetes in children, 0-14 years (cases per 100,000 aged 0-14 years per year), 2010

  18. Temporal model for development of type 1 diabetes

  19. پاتوژنز ديابت نوع 2 • نوع معمولي ديابت نوع 2 يك بيماري پولي ژنيك • اشكال در ترشح انسولين و مقاومت به انسولين (هر دو) • انواع مونوژنتيك بسيار نادر

  20. تشخيص ديابت نوع2به سه طريق ممكن است: 1- غلظت قند پلاسماي سياهرگي دو ساعت پس از مصرف 75 گرم گلوكزمساوي يا بالاتر از mg/dl200 . 2- غلظت قند پلاسماي سياهرگي در يك نمونه اتفاقي (رندوم) مساوي ويا بالاتر از mg/dl 200همراه با علائم واضح ديابت. 3- غلظت قند پلاسماي سياهرگي در دو نوبت ناشتا مساوي يا بالاتر ازmg/dl 126

  21. انجمن ديابت آمريكا مقادير ناشنا قند خون را ترجيح مي دهد، زيرا عملي تر، مناسب تر وبيشتر قابل تكرار است و ارتباط آن را با افزايش خطر عوارض قلبي- عروقي بيشتر از ساير شاخص ها مي داند . در صورتي كه غلظت قند پلاسماي ناشتا بين 100 و 125 باشد به آن “ اختلال قند ناشتا” (IFG) مي گويند. اگر غلظت قند در دو ساعت پس از مصرف گلوكزبين 140 و mg/dl 200باشد”اختلال تحمل گلوكز” IGT)( ناميده ميشود. در اين گروه زمينه ابتلاء به ديابت بيشتر است، اگر چه ممكن است دو سوم آنان هيچگاه علائم ديابت را نشان ندهند. در اين افراد شانس ابتلاء به بروز عوارض قلبي عروقي افزايش دارد. تغيير در عادتهاي غذايي و ورزش مي تواند نيل اين گروه به ديابت نوع 2 را كاهش دهد.

  22. تعاريف اختلالات متابوليسم كربوهيدرات ها

  23. Natural history of type 2 diabetes Genetic susceptibility Early life events:Low birth weightFormula feeding Obesity Insulin resistance ↑ Compensatoryinsulin secretion Physicalinactivity Intrauterine nutritionInherited -cell defect GlucotoxicityLipotoxicity Reduced-cellfunction IGT Type 2 diabetes

  24. How has the environment changed? Infections and ‘hygiene’ Food calories, composition Physical activity Climate ambient temp UVR-vitamin D Toxins Sleep Pharmaceuticals Modifiers: culture, education, wealth, access to technology, family size, maternal age……..

  25. Food Pro-inflammatory Anti-inflammatory Total caloric load Fructose Vitamin D High glucose Marine (n-3) fat Saturated Flavonoids (trans) fat /anti-oxidants AGEs Resveratrol ER stress ROS Contaminants (PCBs, dioxin)

  26. Obesity/type 2 diabetes = low grade inflammation Macrophages -cell dysfunction Hepatic steatosis Insulin resistance Atherogenesis

  27. Sites of inflammation in obesity/T2D Adipose tissue Arterial wall Liver Pancreatic islets Blood IL-1 IL IL-8 C-reactive protein etc

  28. Risk factor for diabetes Type 2 Overweight and obesity Age Physical inactivityEthnicity High-fat and low-fibre diet Family history Low birth weight Previously identified IFG or IGT Low HDL or high triglyceride History of GDM or big baby Polycystic ovary Hypertension

  29. Excess weight is a risk factor for type 2 diabetes (Nurses Health Study) Relative risk of type 2 diabetes 100 93.2 80 60 54.0 40.3 40 27.6 20 15.8 8.1 5.0 4.3 2.9 1.0 0 <22 22.0–22.9 23.0–23.9 24.0–24.9 25.0–26.9 27.0–28.9 29.0–30.9 31.0–32.9 33.0–34.9 35 BMI (kg/m2) Colditz et al. Ann Intern Med 1995; 122: 481-6

  30. Physical inactivity is a risk factor for type 2 diabetes(Health Professionals Follow-up Study- 51,529 subjects) Relative risk of type 2 diabetes 1.0 0.8 0.6 0.4 0.2 0 0–5.9 6–13.7 13.8–24.2 24.3–40.8 >40.8 Energy expenditure (MET-hours per week) Hu et al. Arch Intern Med 2001;161:1542-1548

  31. شيوه زندگي معيوب افزايش انرژي دريافتي کم تحرکي پاسخ استرس اثر به عضله مقاومت به انسولين افزايش انسولين خون چربي اکتوپيک اثر بر کبد هيپر گليسمي انهدام سلول بتا ليپوژنر چاقي مرکزي افزايش قابليت انعقادي افزايش تجمع پلاکتها التهاب بيماري مزمن

  32. نكات عمده در اپيدميولوژي ديابت نوع 2 • اپيدمي ديابت نوع 2 با افزايش تعداد ديابتي در جهان از 150 ميليون در سال 2000 به 220 ميليون در سال 2010 و 300 ميليون در سال 2025 • افزايش ديابت نوع 2 در كودكان و نوجوانان از 2-1% به 8-45% ديابتي ها در اين سنين، در دهه اخير

  33. DM IGT Zinjan (rural) Tehran (rural) Tehran (urban) Islamshahr (city) Booshehr (urban) 0 5 10 15 20 25 Prevalence (%) Prevalence of diabetes and IGT in the Iranian population over 30 years of age Azizi F et al. Epidemiology of Common Diseases in Iran 2001 p.44-45

  34. Prevalence of diabetes and IGT in the Iranian population over 30 years of age Azizi F et al. Epidemiology of Common Diseases in Iran ; 2009, p.44-45

  35. Prevalence of diabetes and impaired fasting glucose in the adult (20-64 years) urban population of Iran Esteghamati AR, et al. Diabetes Care 2008, 31:96-8

  36. High prevalence of diabetes and abnormal glucose tolerance in adult population (≥20 years) of Tehran Hadaegh F. at al. BMC Public Health 2008. 8:176

  37. Age-specific prevalence of diabetes mellitus

  38. شيوع اختلالات تحمل گلوكز در ايران (20≥سال)

  39. Phase I Men Women Phase II Men Women IGT IFG New diabetes Old diabetes Overall diabetes 10.2* 1.3 8.8 2.5 10.9 13.6 1.6 8.2 4.3 12.0 13.0 3.5 9.1 4.5 13.0 15.7 3.1 8.8 6.9 15.1 * All numbers are in percent Azizi et al. Tehran Lipid and Glucose Study 2003. Changes in the prevalence of glucose disorders among 846 men and 1287 womenaged 20 years and over, during 3 years of follow up (TLGS)

  40. Estimation of the Prevalence IGT and Diabetes in Iran in 2007 *Millions (for 70 milion population and 65% 20 yr of age) Azizi F. Epidemiology of Common Diseases in Iran, 2007

  41. The prevalence of diabetes and impaired glucose tolerance (IGT) in Tehranian adult population, Tehran Lipid and Glucose Study.

  42. از شروع ديابت تا تشخيص آن اغلب 5-7 سال فاصله است. نيمي از بيماران ديابتي از بيماري خود بي خبرند. پيشگيري اوليه پيشگيري ثانويه پيشگيري ثالثيه بسياري از بيماران ديابتي هنگامي براي درمان مراجعه مي كنند كه عوارض وخيمي در چشم، قلب، كليه ها و سلسله اعصاب دارند.

  43. National Diabetes Programmesgoals and objectives The following themes consistently appeared in the respondents’ specification of their country’s NDP goals: • Raising public awareness: national promotion, information and education • Prevention: primary (reduce diabetes incidence), secondary (early diagnosis and behaviour change), tertiary (reduce complications, mortality, minimize impact) • Improve quality of diabetes treatment and care: accessible, community-based, multi-disciplinary teams, patient-centred approach • Ongoing professional development/training for diabetes care personnel (health workers) • Development of national clinical guidelines for diabetes • Support for research into diabetes • Establish a diabetes register (type 1 diabetes)

  44. National Diabetes Programmes (NDP)

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