EPIDEMIOLOGY OF EPIDEMIOLOGY OF DIABETES MELLITUSDIABETES MELLITUS

Dr Salam Jassim

DefinitionDefinition: :

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

General Epidemiological General Epidemiological Characteristics:Characteristics: It affects large number of people of about 100 million

The number can increase to 230 million by 2010

It affects all ethnic and socioeconomic groups

Incidence and prevalence are highly varied between and within countries 20-60 folds difference

Considerable impact on economic and social condition, In1992 DM cost USA 90 billion $

General Epidemiological General Epidemiological Characteristics:Characteristics: DM is an important cause of premature death and

causes serious health consequences

It is important RF of CHD

CHD 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

CLINICAL STAGING OF DMCLINICAL STAGING OF DMI. DM I. DM

Regardless of underlying cause is subdivided into:

Insulin requiring for survivalInsulin requiring for controlNot Insulin requiring

II. Impaired glucose regulationII. 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)

II. Impaired glucose regulationII. 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

III. Normoglycemia III. Normoglycemia

FPG < 110/dl

CLINICAL STAGING OF DMCLINICAL STAGING OF DM

Clinical staging regardless of its etiology, progress through several clinical staging during its natural history

Individual subject may move from one stage to another in either direction

Clinical staging reflect the hyperglycemia which reflect the extent of the disease process

Diagnosis: Diagnosis:

Diagnosis is clear when symptoms are severe with gross hyperglycemia

Sever hyperglycemia under stress is not sufficient

Diagnosis: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

Diagnostic range 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

AETIOLOGICAL AETIOLOGICAL CLASSIFICATIONCLASSIFICATIONI - Type 1 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

Type 1Type 1a) Autoimmune DM 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)

Markers of Immune destructionMarkers of Immune destruction

Islet cell auto Abs

Insulin Auto Abs

Auto Abs to glutamic acid decarboxylase (GAD)

Type 1Type 1a) Autoimmune DMa) 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

Type-1Type-1b) Idiopathic b) Idiopathic No known etiology

Seen more in Africans and Asians

II – Type 2 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

II – Type 2II – Type 2

Insulin sensitivity can be increased by decreasing weight, increasing physical activity and or pharmacologic treatment

The risk of this type increases with age, obesity, lack of physical activity

It is more in women with GDM and individuals with HT or Dyslipidemia

Genetic predisposition is common

Prevalence showed racial / ethnic variation

III – Other specific types 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

GESTATIONAL GESTATIONAL HYPERGLYCEMIA AND HYPERGLYCEMIA AND DIABETESDIABETES

It is carbohydrate intolerance resulting in various severity of hyperglycemia with onset or first recognized during pregnancy

GESTATIONAL GESTATIONAL HYPERGLYCEMIA AND HYPERGLYCEMIA AND DIABETESDIABETESElevated 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

High Risk Groups 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

High Risk GroupsHigh 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

THE METABOLIC SYNDROMETHE METABOLIC SYNDROMEWorking definitionWorking 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/min or Albumin/creatinin

ratio >/= 30 mg/gm) Other components: hyperuricemia, coagulation

disorders, raised PAI-1

THE METABOLIC SYNDROMETHE 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 the components and not only hyperglycemia

Metabolic syndrome may be present for up to 10 years before detection of the glycemic disorder

PRIMARY PREVENTION OF PRIMARY PREVENTION OF TYPE 1 DMTYPE 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

Screening include: Screening include:

Family history

Genetic markers (HLA)

Immunological risk markers

(ICA, IAA, Anti GAD)

Metabolic risk factors

ScreeningScreening

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

Primary Prevention StrategyPrimary 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

PRIMARY PREVENTION OF PRIMARY PREVENTION OF TYPE 2 DMTYPE 2 DMNo 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

Life –style measures that decrease Life –style measures that decrease insulin resistance: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

SECONDARY PREVENTION OF SECONDARY PREVENTION OF TYPE 2 DMTYPE 2 DM Aims at retarding progression of DM, decrease

risk or severity of complications and so decrease premature morbidity and mortality

1. Screening for undetected DM

2. Control of hyperglycemia, and other metabolic abnormalities

3. Correction of other CV RFs (smoking, dyslipidemias, obesity)

Screening approachesScreening approaches: :

Population approach

Selective screening: on high risk individuals

Opportunistic screening: most appropriate and highly cost effective

TERTIARY PREVENTIONOF TERTIARY PREVENTIONOF TYPE 2 DMTYPE 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

COMPLICATIONS OF DM COMPLICATIONS OF DM

ACUTE COMPLICATIONS

1. Hypoglycemia 1. Hypoglycemia

Affect the brain and the heart The risk is more among:1. Hypoglycemia unawareness and

counter regulatory unresponsiveness as in autonomic neuropathy, B-blockers and alcoholism

2. Infants3. Patients with IHD or TIA

Prevention: Prevention:

health education

Cautious exercise

Glucagons for emergency

Caution and health education when changing treatment

2. Diabetic ketoacidosis 2. Diabetic ketoacidosis

10-15% mortality, 50% of them are avoidable

Precipitating factors1. Infection2. Acute illnesses3. Insufficient insulin treatment

Prevention:1. Health education2. Early control of precipitating factors

3. Infections 3. Infections

Poorly controlled diabetics are at increased risk of:

1. TB , lung and other organs

2. fungal infection of skin and mucus membrane

3. anaerobic infection of deep tissues

4. UTI ( increasing diabetic nephropathy)

CHRONIC CHRONIC COMPLICATIONSCOMPLICATIONSI. Macrovascular Complications

Atherosclerosis: CAD, CVA, PVDAtherosclerosis: CAD, CVA, PVD

The most common complication among diabetics, account for 75% of their deaths

DM increases CAD and CVA by 2-3 folds and PVD by 4 folds

Diabetic women lose their relative protection against CAD before menopause

Atherosclerosis: Atherosclerosis:

Role of hyperglycemia as CRF mediated through:

1. Glycation of LDL particles

2. Glycation of arterial wall protein 3. Stimulate insulin secretion

Atherosclerosis:Atherosclerosis:

Hyperinsulinemia is independently associated with atherosclerosis through its effect on BP, TG, PAI-1 level or arterial wall metabolism

Obesity (especially central) increases liability to atherosclerosis and DM through:

Increased insulin resistance, hyperinsulinemia, Dyslipidemia, and HT

Among diabetics the process of atherosclerosis is accelerated with smoking and nephropathy

Atherosclerosis: Atherosclerosis:

Screening for RFs of macrovascular complications: Lipid profile, BP, Ht, waist/hip ratio, smoking history, family

history, urinary albumin excretion

Presence of macro vascular complications is ascertained through:

1. Clinical history: history of MI, TIA, and intermittent claudication

2. Physical examination: bruit, peripheral pulses, evidence of ischemia on ECG

The sensitivity and specificity of these measures are moderate

CHRONIC CHRONIC COMPLICATIONSCOMPLICATIONS

II. Microvascular complications

1. Diabetic Retinopathy 1. Diabetic Retinopathy It is asymptomatic gradual process, so screening is

vital at least every 2 years

Drugs and glycemic control can not prevent it

It is responsible for 86% of blindness among Type 1diabetics, and 35% of Type 2 diabetics.

100% of Type 1 diabetics developed Diabetic retinopathy, 75% of proliferate type

60% of Type 2 diabetics developed diabetic retinopathy, 10% pf proliferative Type

Diabetic RetinopathyDiabetic Retinopathy

Timely laser photocoagulation can prevent 90% of sever visual loss

Treatment of HT and avoidance of smoking are important in its control

2. Diabetic Neuropathy 2. Diabetic Neuropathy

It is the commonest complication of DM

The prevalence is increased with:

1. Increased duration of DM

2. Increased glycated Hb level

3. Smoking

4. History of CVD

Types of Neuropathy Types of Neuropathy A. Peripheral Neuropathy

Polyneuropathy: Distal sensorimotor neuropathy, Proximal motor neuropathy Focal neuropathy: mononeuropathy,

entrapment neuropathy

Multifocal neuropathy

B. Autonomic Neuropathy

Types of NeuropathyTypes of Neuropathy

The most common is the distal sensorimotor neuropathy which is classified into:

1. Early: asymptomatic, detectable sensory loss, positive neurological tests

2. Symptomatic: sensory loss, frank numbness, parasthesia+/- pain

3. Severe: motor involvement, disabling symptoms, potential for ulceration, infection, necrosis, and gangrene

Screening Tests Screening Tests

Inspection: feet: dry skin, hair or nail abnormality, callus or infection

Vibration sensation on the dorsum of big toe: normal, reduced, absent

Ankel Reflex: normal, reduced, absent

Types of NeuropathyTypes of Neuropathy

Cardiovascular autonomic neuropathy

Serious and can precipitate death.

They have difficulty in detecting

hypoglycemia and / or spontaneous

recovery from hypoglycemia

Prevention: Prevention:

Education of patients and PHC physicians

Good glycemic control

Aldose reductase inhibitor

3. Diabetic Nephropathy 3. Diabetic Nephropathy

A major cause of premature morbidity and mortality in diabetics

DM increases risk of Renal Failure by about 17-20 folds

25% of ESRD are due to DM

Diabetic NephropathyDiabetic Nephropathy

Diabetic Nephropathy can be divided into:

1. Incipient (sub clinical) nephropathy Microalbuminuria: 30-300mg/24 hours HT may be present

2. Clinical nephropathy Persistent proteinuria >300 mg/ 24 hours Usually accompanied with HT

Diabetic NephropathyDiabetic Nephropathy

3. Advanced nephropathy

Significant reduction of GFR,Symptoms of uremia +/- nephritic

syndrome

4. ESRD

Prevention Prevention

Tight glycemic control

Yearly urinary microalbumin test

Dietary protein restriction

Vigorous control of BP

PreventionPrevention

Other supportive measures:

– Correction of lipid abnormalities, metabolic bone diseases, and anemia

– Avoidance of fluid retention

– Vigorous treatment of UTI

– Avoidance of nephrotoxic drugs

4. DIABETIC FOOT 4. DIABETIC FOOT

It is infection, ulceration, destruction, of deep tissues with neurological and peripheral vascular diseases

Diabetics have 15 folds risk of amputation than non diabetics

DIABETIC FOOTDIABETIC FOOT

Incidence of amputation is associated with:

1. Duration of DM

2. Glycemic control

3. HT

4. Smoking

DIABETIC FOOTDIABETIC FOOT

Lower limb amputation is more in developing countries:

1. Lack of proper foot wear

2. Inadequate hygiene

3. Poorly controlled DM

ScreeningScreening

1. Abnormal vibration test

2. Presence of foot deformity

3. Past history of lower extremity ulceration or amputation

Screening should be done by a trained physician

Prevention Prevention

Regular attendance to health care settings

Formal teaching sessions

Provision of appropriate written and or audiovisual materials

The patient should be advisedThe patient should be advised

– Not to walk bare-footed– Daily looking to foreign bodies in the shoes– Avoid bathroom surgery– Treat fungal disease and minor cuts– Usage of mirror to examine plantar side of

the foot– Test the degree to which pain sensation is

lost– Prevent burns

AMPUTATION IS

A PREVENTABLE

COMPLICATION

EDUCATION OF DIABETIC EDUCATION OF DIABETIC PATIENTSPATIENTS

It is the corner stone of DM management

It covers:self carechanging behavior to prevent and

control of complications encourage interaction with health care

providers

Contents of Educational ProgramContents of Educational Program

Nature of disease, types, clinical

presentation, diagnosis, complications,

types of treatment, side effects, exercise,

self monitoring , avoidance and recognition

of hypoglycemia, and hyperglycemia, foot

care , pregnancy and OC, avoidance of

smoking, CV RFs, need for follow up, self

management skills and attitudes

Active participation of the family is vital in DM management

Types of education methodsTypes of education methods

1. Individual counseling

2. Group teaching

3. Educational materials: posters, pamphlets, books…

Special educational programs are needed for special groups as children and pregnant women

Education of Health ProfessionalsEducation of Health Professionals

Basic understanding of DM and its managements

Training in educational methods

Training of dietetics and nurses

Education of the communityEducation of the community

Prevention or modification of dietary habits and other life-style characteristics that link with DM