diagnosis, classification and prevention of diabetes

Diagnosis, classification and prevention of diabetes

Diagnosis and typesCurriculum Module II-1

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Slides current until 2008

Definition of diabetes

Characterized by hyperglycaemia

• Defects in insulin production

• Autoimmune or other destruction of beta cells

• Insulin insensitivity

• Impaired action of insulin on target tissues


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Definition of diabetes

Chronic hyperglycaemia associated with long-term damage to:

• Eyes

• Kidneys

• Nerves

• Heart and blood vessels


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The diabetes epidemic

• 230 million affected in 2006

• 350 million within 20 years

• Most rapid in Indian and Asian subcontinents

IDF Diabetes Atlas


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Classification

• Type 1 diabetes

–autoimmune

–LADA

–idiopathic

• Type 2 diabetes


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Other specific types

• MODY

• Defects in insulin action

• Diseases of the pancreas

• Endocrine disorders

• Drug- or chemical-induced

• Infections

Classification


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• Uncommon forms of immune-mediated diabetes

• Other genetic syndromes

• Gestational diabetes

Classification


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Insulin

GluconeogenesisGlycogenolysisGlycogen synthesis

Glucose uptakeGlycogen synthesis

Blood glucose

Insulin and glucose disposal

Free fatty acid release


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Glucose uptake Glycogenolysis Gluconeogenesis (amino acids) Ketone production (fatty acids)

Glucose uptake Protein degradation amino acids

Blood glucose

Insulin deficiency in type 1 diabetes

Triglyceride degradation fatty acids


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Glucose uptake

Glycolysis

Gluconeogenesis (amino acids)


Blood glucose

Insulin insensitivity in ttype 2 diabetes


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Blood glucose

Glucose uptake

Insensitivity to insulin inttype 2 diabetes

Glucose uptake

Glycolysis




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Blood glucoseConverted to triglycerides

Effect of insulin resistance in ttype 2 diabetes

Glucose uptake

Glycolysis



Glucose uptake


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Pathogenesis of type 1 diabetes

• Immunological activation

• Progressive beta-cell destruction

• Insufficient beta-cell function

• Dependent on exogenous insulin

• Risk of ketoacidosis


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• Genetic susceptibility

• Immune factors– other autoimmune disease– antigen-specific antibodies

• Environmental trigger– viruses– bovine serum albumin– nitrosamines: cured meats– chemicals: vacor (rat poison),

streptozotin


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Beta-cell mass


Time (months - years)

Trigger

Genetic

Pre-diabetes ‘Honeymoon’

Chronic phase

Clinical diabetes

Immunological abnormalities


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Idiopathic type 1 diabetes

Non-autoimmune type 1 diabetes

• No autoimmune markers

• Permanent insulinopenia

• Ketoacidosis

• People of African and Asian origin


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Epidemiology of type 1 diabetes

• Increasing in recent years

• Geographic variation

• Relative affluence

• Lack of treatment

IDF Diabetes Atlas


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• Age of onset peaks

– preschool

– puberty

• Autumn/winter peaks



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Type 2 diabetes

• 90%-95% of people with diabetes

• Insulin insensitivity and relative insulin deficiency

• Obesity or overweight

• Complications often present at diagnosis


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• Multiple genes involved

• Hyperinsulinaemia

• Poor fetal nutrition beta-cell formation

• Low birth weight/weight change

• “Thrifty gene”

• 7% beta-cell loss


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Age (years)

Endogenous insulin

Insulin requirements

Beta-cell loss

The natural history of type 2 diabetes

Insulin requirements with age

Primary failure


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Age (years)

Endogenous insulin


Beta-cell loss

Insulin insensitivity

Hyper-insulinaemia




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Age (years)

Endogenous insulin


Secondary failure


Effect of oral drugs


Beta-cell loss

Hyper-insulinaemia

Insulin insensitivity


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• Dramatic increase

• Aging population

• Disturbing trends parallel obesity epidemic

• Especially in adolescents and minority groups

• Increasing in young people


Slide 25 of 48ACTIVITY


• What are the most common risk factors for type 2 diabetes for people in your country?

• Are any of these risk factors modifiable?


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Risk factors for type 2 diabetes

• Age > 40 years

• First-degree relative with diabetes

• Member of high risk population

• History of impaired glucose tolerance, impaired fasting glucose

• Vascular disease

• History of gestational diabetes

• History of delivery of macrosomic baby

CDA 2003


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• Hypertension

• Dyslipidaemia

• Abdominal obesity

• Overweight

• Polycystic ovary disease

• Acanthosis nigricans

• Schizophrenia

Risk factors for type 2 diabetes


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• Polydipsia

• Polyuria

• Nocturia

• Visual disturbance

• Fatigue

• Weight loss

• Infections

Signs and symptoms


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Diagnosing diabetes

Normal Impaired fasting glucose*

Impaired glucose tolerance**

Diabetes

FPG <6.1mmol/L

<110mg/dL

6.1 to 6.9mmol/L*

110 to 126mg/dL

≥7.0mmol/L

≥126mg/dL

2hr PG <7.8mmol/L

<126mg/dL

7.8 to 11mmol/L**

126 to 200mg/dL

≥11.1mmol/L

≥200mg/dL

CDA 2003, ADA 2004, WHO 2002


Slide 30 of 48Table 2—Criteria for the diagnosis of diabetes

1. A1C 6.5%. The test should be performed in a laboratory using a methodthat is NGSP certified and standardized to the DCCT assay.*OR2. FPG 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.OR

3. Two-hour plasma glucose 200 mg/dl (11.1 mmol/l) during an OGTT.The test should be performed as described by the World HealthOrganization, using a glucose load containing the equivalent of 75 ganhydrous glucose dissolved in water.*OR

4. In a patient with classic symptoms of hyperglycemia or hyperglycemiccrisis, a random plasma glucose 200 mg/dl (11.1 mmol/l).*In the absence of unequivocal hyperglycemia, criteria 1–3 should be confirmed by repeat testing.

ADA 2010 Guideline


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Impaired glucose toleranceImpaired fasting glucose

• Intermediate states

• Increased risk of developing diabetes

• Prevention strategies to prevent or delay progression

• Increased risk of cardiovascular disease


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Uncertain diagnosis:Oral glucose tolerance test

• 75 g glucose load after 8 hours fasting

• Readings taken in fasting state and at 1 and 2 hours

• Possible problems


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• Urinary ketones

• Antibodies

• C-peptide

Tests for differential diagnosis


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Metabolic syndrome

• Cluster of risk factors or syndrome

• Type 2 diabetes

• Different criteria

• Three-fold increase in heart disease and stroke

• Two-fold increase in cardiovascular disease deaths


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Prevention of type 1 diabetes

• Early exposure to cows milk protein

• Nicotinamide


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Insulin

• Diabetes Prevention Trial

• Diabetes Prediction and Prevention Project


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Lifestyle modification

• Da Qing Study

• Finnish Diabetes Prevention Study


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Lifestyle vs medication

• Diabetes Prevention Program

• STOP-NIDDM


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Type 2 diabetes can be delayed in people with IGT

Lifestyle modification is most effective

What do you think could be done at community level to prevent or delay diabetes?


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Summary

Type 1 diabetes

• Results from progressive beta-cell destruction

• People with type 1 diabetes need insulin therapy to live


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Type 2 diabetes

• Often characterized by insulin insensitivity and relative rather than absolute insulin deficiency

• A progressive condition

• Most people with type 2 diabetes will need insulin within 5 to 10 years of diagnosis

Summary


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Review question

1. The pathogenesis for type 2 diabetes includes:

a. Insulin deficiency and insulin insensitivity

b. Insensitivity to insulin and autoimmune beta-cell destruction

c. Autoimmune beta-cell destruction and glucagon deficiency

d. Insulin deficiency and glucagon deficiency


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Review question

2. A person with type 2 diabetes, recently started on insulin, asks if there is a way to measure if he/she is still producing any insulin. The correct response would be:

a. Islet cell antibody tests

b. C-peptide test

c. HbA1c test

d. Serum insulin test


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Review question

3. The Diabetes Prevention Program (DPP):

a. Included people with type 1 diabetes

b. Included only people with IGT

c. Tested the value of exercise

d. Included people with type 2 diabetes


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Review question

4. Type 1 diabetes is usually caused by:

a. Injury to the pancreas

b. An autoimmune reaction

c. Insulin insensitivity in the cells

d. Hypersensitivity to insulin


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Answers

1. a

2. b

3. b

4. b


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References

1. American Diabetes Association. Diagnosis and classification of diabetes mellitus. Diabetes Care 2004; 27(suppl 1): S5-S10.

2. Canadian Diabetes Association Clinical Practice Guidelines Expert Committee. Canadian Diabetes Association 2003 clinical practice guidelines for the prevention and management of diabetes in Canada. Can J Diab 2003; 27(suppl 2).

3. Chiasson JL, Josse RG, Gomis R, et al. Acarbose for prevention of type 2 diabetes mellitus: The STOP-NIDDM randomized trial. Lancet 2002; 346: 393-403.

4. Delahanty LM and Halford BN. The role of Diet Behaviours in Achieving improved glycaemic control in intensively treated patients in the Diabetes Control and Complications Trial. Diabetes Care 1993; 16(11): 1453-58.

5. Diabetes Control and Complications Trial Research Group. Effect of intensive diabetes treatment on the development and progression of long-term complications in adolescents with insulin dependent diabetes mellitus: Diabetes Control and Complications Trial. The Journal of Paediatrics 1994; 125(2): 177-88.

6. Diabetes Control and Complications Trial/epidemiology of diabetes interventions and complications research group intensive diabetes therapy and carotid intima-media thickness in type 1 diabetes mellitus. New Engl J Med 2003; 348: 2294-303.

7. Diabetes Control and Complications Trial: The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl J Med 1993; 329: 977-86.


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References

8. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey. JAMA 2002; 297: 356-59.

9. Diabetes Atlas 2006. Brussels: International Diabetes Federation, 2006.

10. Isomaa B, Almgren P, Tuomi T, et al. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care 2001; 24(4): 683-9.

11. Pan X, Li G, Hu Y, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance: The Da Qing IGT and Diabetes Study. Diabetes Care 1997; 20(4): 537-44.

12. Report of a WHO Consultation. Laboratory Diagnosis and monitoring of Diabetes Mellitus. World Health Organisation 2002. http://whqlibdoc.who.int/hq/2002/9241590483.pdf cited April 30, 2005.

13. Tuomilehto J, Lindstrom J, Eriksson JG, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Eng J Med 2001; 344: 1343-50.

14. The Diabetes Prevention Program Research Group. The diabetes prevention Program (DPP). Diabetes Care 2002; 23(12): 2165-71.

15. UK Prospective Diabetes Study Group. Intensive blood-glucose control with sulpfonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes. Lancet 1998; 352: 837-53.


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References

16. UK Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes UKPDS 38. BMJ 1998; 317: 703-13.

17. IDF Clinical Guidelines Task Force. Global Guideline for Type 2 Diabetes. Brussels: International Diabetes Federation, 2005.

18. Harris SB, Ekoe JM, Zdanowicz Y, Webster-Bogaert S. Glycemic Control and morbidity in the Canadian primary care setting (results of the diabetes in Canada evaluation study). Diab Research and Clin Pract 2005; 70: 90-7.

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