1. EPIDEMIOLOGY OF DIABETES MELLITUS
Dr Faris Al-Lami
MB ChB PhD FFPH

2. Definition: It is a heterogeneous group of disorders characterized by:
Hyperglycemia,
And
Disturbances of carbohydrate, fat and protein metabolism
With
Absolute or relative deficiency of insulin action and or secretion

3. General Epidemiological Characteristics:
It affects large number of people, 366millions were affected in 2011, and expected to reach 530 million in 2030
It affects all ethnic and socioeconomic groups
Incidence and prevalence are highly varied between and within countries folds difference
Considerable impact on economic and social condition.

4. General Epidemiological Characteristics:
DM is an important cause of premature death and causes serious health consequences
It is important RF of CHD which is the leading cause of death among diabetics
In developing countries, the incidence and prevalence of Type 2 DM are rapidly increasing mostly due to modernization of life style
In developing countries, mortality from acute complications is high due to lack of basic requirements

5. CLINICAL STAGING OF DM
Clinical staging regardless of its etiology, progresses through several clinical staging during its natural history
Individual subject may move from one stage to another in either direction
Clinical staging reflects the hyperglycemia which reflects the extent of the disease process

6. CLINICAL STAGING OF DM I. DM
Regardless of underlying cause is subdivided into:
Insulin requiring for survival
Insulin requiring for control
Not Insulin requiring

7. II. Impaired Glucose Regulation
It is a metabolic state intermediate between normal glucose homeostasis and DM
IFG: Impaired fasting glycemia (fasting)
FPG: > 110 mg/dl- <126 mg/dl (>6.1- <7 mmol/L)
Whole blood : >100 mg/dl-<110mg/dl (>5.6-< 6.1 mmol/L)
IGT: Impaired glucose tolerance (postprandial)

8. II. Impaired Glucose Regulation
All those with IFG should have OGTT
Individuals with IFG or IGT may be euglycemic in their daily life as seen through HbA1C
IGT and IFG are not clinical entities, rather risk categories for future DM and or CVD
They are often associated with Metabolic Syndrome

9. III. Normoglycemia
FPG < 110/dl

10. Diagnosis:
Diagnosis is clear when symptoms are severe with gross hyperglycemia
Sever hyperglycemia under stress is not sufficient

11. Diagnosis: Asymptomatic subject:
A single abnormal test is not sufficient
At least one additional result within diabetic range , if it fails , then surveillance with periodic retesting taking in consideration ethnicity , family history , age, adiposity and concomitant risk factors
Glycated Hb had similar sensitivity and specificity for glucose test
OGTT is indicated if casual blood test is uncertain

12. Diagnostic range Fasting Plasma Glucose: 126 mg/dl (7.0 mmol/L)
Whole blood: 110mg/dl (6.1mmol/L)
In epidemiologic studies FPG is sufficient or 2hr after 75 gm oral glucose load

13. AETIOLOGICAL CLASSIFICATION I - Type 1
B-cell destruction usually leading to absolute insulin deficiency (low or undetected c-peptide level)
Insulin is usually required for survival
Risk of ketoacidosis

14. Type 1 a) Autoimmune DM Results from autoimmune destruction of B-cell
Destruction could be rapid especially in children or slow especially in adults (Latent Autoimmune Diabetes in Adults LADA)

15. Markers of Immune destruction
Islet cell auto Abs
Insulin Auto Abs
Auto Abs to glutamic acid decarboxylase (GAD)

16. Type 1 a) Autoimmune DM
Some individuals may be metabolically normal before the disease become evident, but the progress of B cell destruction can be detected
Immunological markers are present in 85-90% of those patients
Peak incidence in childhood and adolescence
Environmental factors play a role
Genetic predisposition
Patients are usually not obese
Other autoimmune diseases may be present

17. Type-1 b) Idiopathic No known etiology
Seen more in Africans and Asians

18. II – Type 2
They have relative rather than absolute insulin deficiency with resistance to insulin action
They do not require insulin for survival
They may remain undetected for long time
They have increased risk of macro and micro vascular complications
The autoimmune destruction does not occur
Ketoacidosis is infrequent
Obesity is very common
Insulin level could be normal or elevated

19. II – Type 2
Insulin sensitivity can be increased by decreasing weight, increasing physical activity and or pharmacologic treatment
Risk increases with age, obesity, lack of physical activity
More in women with GDM and individuals with HT or Dyslipidemia
Genetic predisposition is common
Prevalence showed racial / ethnic variation

20. III – Other specific types
Genetic defects of B cell function
Genetic defects of insulin action
Diseases of exocrine pancreas
Endocrinopathies
Drugs or chemical induced DM
infections
Uncommon but specific forms of immune mediated DM
Other genetic syndromes sometimes associated with DM

21. GESTATIONAL HYPERGLYCEMIA AND DIABETES
It is carbohydrate intolerance resulting in various severity of hyperglycemia with onset or first recognized during pregnancy

22. GESTATIONAL HYPERGLYCEMIA AND DIABETES
Elevated fasting or postprandial plasma glucose level in the early pregnancy (first trimester, and first half of second trimester) indicates that DM antedate pregnancy
Normal OGTT in early pregnancy does not exclude the possibility that GDM is not going to develop

23. High Risk Groups Older women
Women with previous history of large for gestational age baby
Women from certain ethnic group
Any women with elevated fasting or casual blood glucose

24. High Risk Groups
It is better to screen such groups during the first trimester to detect previous undiagnosed DM
Formal systematic testing for gestational DM is usually done between 24 and 28 weeks
After the pregnancy ends, the woman should be re-classified as having:
DM, IGT, or Normal Glucose Tolerance based on OGTT done 6 weeks or more after delivery
Women with GDM are at increased risk for subsequent DM

25. THE METABOLIC SYNDROME Working definition:
Glucose intolerance, IGT or DM and /or insulin resistance together with 2 or more of the following:
Raised arterial BP (>140/90)
Raised Pl.TG =/> 150 mg/dl and/or low HDL-C (<35mg/dl in males; < 39 mg/dl in females)
Central obesity (waist: hip ratio: Males: >0.9, Females: >0.85)
And /or BMI >30
Microalbuminurea (>/= 20 ug/ml or Albumin/creatinin ratio >/= 30 mg/gm)
Other components: hyperuricemia, coagulation disorders, raised PAI-1

26. THE METABOLIC SYNDROME
There is heterogeneity in the strength of insulin resistance
Metabolic syndrome increases risk of Macro vascular disorders
Management should include control strategies of all components and not only hyperglycemia
Metabolic syndrome may be present for up to 10 years before detection of the glycemic disorder

27. PRIMARY PREVENTION OF TYPE 1 DM
It should be done before onset of type 1 pathological process. i.e: before development of immunological markers
It is still EXPERIMENTAL
Because of the very low prevalence, it required screening test of high specificity and sensitivity, inexpensive and easy to perform

28. Screening include: Family history Genetic markers (HLA)
Immunological risk markers (ICA, IAA, Anti GAD)
Metabolic risk factors

29. Screening Screening is costly and technically difficult
Those have these factors have 10 folds excess risk
Still 95-97% of them do not develop the disease later

30. Primary Prevention Strategy
Deprivation of caw milk protein in the neonatal and early infancy
Administration of free radical scavenger, as nicotinamide
Allowing B-cell rest by administration of early insulin treatment
Encouraging the development of Antigen tolerance by administration of early insulin treatment or oral antigens
Immunosuppression or Immunomodulation

31. PRIMARY PREVENTION OF TYPE 2 DM
No population based studies on primary prevention of type 2 DM
Prevention should be based on efforts to decrease insulin resistance and promotion of insulin secretion

32. Life –style measures that decrease insulin resistance:
Correction and prevention of obesity
Avoidance of high fat diet
Encouraging using unrefined sugar and soluble fibers
Avoidance or cautious use of diabetogenic drugs
Encourage physical activity

33. SECONDARY PREVENTION OF TYPE 2 DM
Aims at retarding progression of DM, decreases risk or severity of complications and so decreases premature morbidity and mortality
Screening for undetected DM
Control of hyperglycemia, and other metabolic abnormalities
Correction of other CV RFs (smoking, dyslipidemias, obesity)

34. Screening Approaches Population approach
Selective screening: on high risk individuals
Opportunistic screening: most appropriate and highly cost effective

35. TERTIARY PREVENTION OF TYPE 2 DM
Aims at decreasing morbidity and mortality by delaying or arresting the complications
Good glycemic control (by intensive treatment, frequent monitoring of blood glucose level)
Slow or arrest development of early microvascular complications