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UPDATE ON CHILDHOOD DIABETES MELLITUS

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Title: UPDATE ON CHILDHOOD DIABETES MELLITUS


1
UPDATE ON CHILDHOOD DIABETES MELLITUS
  • Abdelaziz Elamin
  • MD, PhD, FRCPCH Professor of Child Health
  • Sultan Qaboos University

2
DEFINITION
  • The term diabetes mellitus describes
  • a metabolic disorder of multiple
  • etiologies characterized by chronic
  • hyperglycemia with disturbances of
  • carbohydrate, fat and protein
  • metabolism resulting from defects of
  • insulin secretion, insulin action or
  • both.

3
DIABETES EPIDEMIOLOGY
  • Diabetes is the most common endocrine problem
    is a major health hazard worldwide.
  • Incidence of diabetes is alarmingly increasing
    all over the globe.
  • Incidence of childhood diabetes range between
    3-50/100,000 worldwide in Oman it is estimated
    as 4/100000 per year.

4
OLD CLASSIFICATION (1985)
  • Type 1, Insulin-dependent (IDDM)
  • Type 2, Non Insulin-dependent (NIDDM)
  • obese
  • non-obese
  • MODY
  • IGT
  • Gestational Diabetes

5
WHO CLASSIFICATION 2000
  • Is based on etiology not on type of treatment or
    age of the patient.
  • Type 1 Diabetes
  • (idiopathic or autoimmune b-cell destruction)
  • Type 2 Diabetes
  • (defects in insulin secretion or action)
  • Other specific types

6
WHO CLASSIFICATION/2
  • Both type 1 type 2 can be further subdivided
    into
  • Not insulin requiring
  • Insulin requiring for control
  • Insulin requiring for survival
  • Gestational diabetes is a separate entity
  • Impaired Glucose Tolerance (IGT) indicates blood
    glucose levels between normal diabetic cut off
    points during glucose tolerance test.

7
DIAGNOSTIC CRITERIA
  • Fasting blood glucose level
  • Diabetic
  • Plasma gt7.0 mmol
  • Capillary gt6.0 mmol
  • IGT
  • Plasma 6.0-6.9 mmol
  • Capillary 5.6-6.0 mmol
  • 2 hours after glucose load
  • (Plasma or capillary BS)
  • IGT
  • 7.8-11.0
  • Diabetic level
  • gt 11.1 (200 mg)

8
Types of Diabetes in Children
  • Type 1 diabetes mellitus accounts for gt90 of
    cases.
  • Type 2 diabetes is increasingly recognized in
    children with presentation like in adults.
  • Permanent neonatal diabetes
  • Transient neonatal diabetes
  • Maturity-onset diabetes of the young
  • Secondary diabetes e.g. in cystic fibrosis or
    Cushing syndrome.

9
MODY
  • Usually affects older children adolescents
  • Not rare as previously considered
  • 5 subclasses are identified, one subclass has
    specific mode of inheritance (AD)
  • Not associated with immunologic or genetic
    markers
  • Insulin resistance is present

10
TRANSIENT NEONATAL DIABETES
  • Observed in both term preterm babies, but more
    common in preterm
  • Caused by immaturity of islet b-cells
  • Polyuria dehydration are prominent, but baby
    looks well suck vigorously
  • Highly sensitive to insulin
  • Disappears in 4-6 weeks

11
PERMANENT NEONATAL DIABETES
  • A familial form of diabetes that appear shortly
    after birth continue for life
  • The usual genetic immunologic markers of Type 1
    diabetes are absent
  • Insulin requiring, but ketosis resistant
  • Is often associated with other congenital
    anomalies syndromes e.g. Wolcott-Rallison
    syndrome.

12
TYPE 1 DIABETES ETIOLOGY
  • Type 1 diabetes mellitus is an autoimmune
    disease.
  • It is triggered by environmental factors in
    genetically susceptible individuals.
  • Both humoral cell-mediated immunity are
    stimulated.

13
GENETIC FACTORS
  • Evidence of genetics is shown in
  • Ethnic differences
  • Familial clustering
  • High concordance rate in twins
  • Specific genetic markers
  • Higher incidence with genetic syndromes or
    chromosomal defects

14
AUTOIMMUNITY
  • Circulating antibodies against b-cells and
    insulin.
  • Immunofluorescent antibodies lymphocyte
    infiltration around pancreatic islet cells.
  • Evidence of immune system activation. Circulating
    immune complexes with high IgA low interferon
    levels.
  • Association with other autoimmune diseases.

15
ENVIRONMENTAL INFLUENCE
  • Seasonal geographical variation.
  • Migrants take on risk of new home.
  • Evidence for rapid temporal changes.
  • Suspicion of environmental agents causing disease
    which is confirmed by case-control experimental
    animal studies.

16
ENVIRONMENTAL SUSPECTS
  • Viruses
  • Coxaschie B
  • Mumps
  • Rubella
  • Reoviruses
  • Nutrition dietary factors
  • Cows milk protein
  • Contaminated sea food

17
OTHER MODIFYING FACTORS
  • The counter-regulatory hormones
  • glucagon
  • cortisol,
  • catecholamines
  • thyroxin,
  • GH somatostatin
  • sex hormones
  • Emotional stress

18
ETIOLOGIC MODEL
  • The etiologic model of type 1 diabetes resembles
    that of Rheumatic fever.
  • Rheumatic fever was prevented by elimination of
    the triggering environ. factor (b-streptococci).
  • Similarly type 1 diabetes may be prevented by
    controlling the triggering factors in high risk
    persons.

19
CLINICAL PRESENTATIONS
  • Classical symptom triad
  • polyuria, polydipsia and weight loss
  • DKA
  • Accidental diagnosis
  • Anorexia nervosa like illness

20
DIAGNOSIS
  • In symptomatic children a random plasma glucose
    gt11 mmol (200 mg) is
    diagnostic.
  • A modified OGTT (fasting 2h) may be needed in
    asymptomatic children with hyperglycemia if the
    cause is not obvious.
  • Remember acute infections in young non-diabetic
    children can cause hyperglycemia without
    ketoacidosis.

21
NATURAL HISTORY
  • Diagnosis initiation of insulin
  • Period of metabolic recovery
  • Honeymoon phase
  • State of total insulin dependency

22
METABOLIC RECOVERY
  • During metabolic recovery the patient may
  • Develop one or more of the following
  • Hepatomegaly
  • Peripheral edema
  • Loss of hair
  • Problem with visual acuity
  • These are caused by deposition of
    glycogen metabolic re-balance.

23
HONEYMOON PERIOD
  • Due to b-cell reserve optimal function
    initiation of insulin therapy.
  • Leads to normal blood glucose level without
    exogenous insulin.
  • Observed in 50-60 of newly diagnosed patients
    it can last up to one year but it always ends.
  • Can confuse patients parents if not educated
    about it early.

24
COMPLICATIONS OF DIABETES
  • Acute
  • DKA
  • Hypoglycemia
  • Late-onset
  • Retinopathy
  • Neuropathy
  • Nephropathy
  • Ischemic heart disease stroke

25
TREATMENT GOALS
  • Prevent death alleviate symptoms
  • Achieve biochemical control
  • Maintain growth development
  • Prevent acute complications
  • Prevent or delay late-onset complications

26
TREATMENT ELEMENTS
  • Education
  • Insulin therapy
  • Diet and meal planning
  • Monitoring
  • HbA1c every 2-months
  • Home regular BG monitoring
  • Home urine ketones tests when indicated

27
EDUCATION
  • Educate child care givers about
  • Diabetes
  • Insulin
  • Life-saving skills
  • Recognition of Hypo DKA
  • Meal plan
  • Sick-day management

28
INSULIN
  • A polypeptide made of 2 b-chains.
  • Discovered by Bants Best in 1921.
  • Animal types (porcine bovine) were used before
    the introduction of human-like insulin
    (DNA-recombinant types).
  • Recently more potent insulin analogs are produced
    by changing aminoacid sequence.

29
FUNCTION OF INSULIN
  • Insulin being an anabolic hormone stimulates
    protein fatty acids synthesis.
  • Insulin decreases blood sugar
  • By inhibiting hepatic glycogenolysis and
    gluconeogenesis.
  • By stimulating glucose uptake, utilization
    storage by the liver, muscles adipose tissue.

30
TYPES OF INSULIN
  • Short acting (neutral, soluble, regular)
  • Peak 2-3 hours duration up to 8 hours
  • Intermediate acting
  • Isophane (peak 6-8 h duration 16-24 h)
  • Biphasic (peak 4-6 h duration 12-20 h)
  • Semilente (peak 5-7 h duration 12-18 h)
  • Long acting (lente, ultralente PZI)
  • Peak 8-14 h duration 20-36 h

31
INSULIN CONCENTRATIONS
  • Insulin is available in different concentrations
    40, 80 100 Unit/ml.
  • WHO now recommends U 100 to be the only used
    insulin to prevent confusion.
  • Special preparation for infusion pumps is soluble
    insulin 500 U/ml.

32
INSULIN REGIMENS
  • Twice daily either NPH alone or NPHSI.
  • Thrice daily SI before each meal and NPH only
    before dinner.
  • Intensive 4 times/day SI before meals NPH or
    Glargine at bed time.
  • Continuous s/c infusion using pumps loaded with
    SI.

33
INSULIN ANALOGS
  • Ultra short acting
  • Insulin Lispro
  • Insulin Aspart
  • Long acting without peak action to simulate
    normal basal insulin
  • Glargine

34
NEW INSULIN PREPARATIONS
  • Inhaled insulin proved to be effective will be
    available within 2 years.
  • Nasal insulin was not successful because of
    variable nasal absorption.
  • Oral insulin preparations are under trials.

35
ADVERSE EFFECTS OF INSULIN
  • Hypoglycemia
  • Lipoatrophy
  • Lipohypertrophy
  • Obesity
  • Insulin allergy
  • Insulin antibodies
  • Insulin induced edema

36
PRACTICAL PROBLEMS
  • Non-availability of insulin in poor countries
  • injection sites technique
  • Insulin storage transfer
  • Mixing insulin preparations
  • Insulin school hours
  • Adjusting insulin dose at home
  • Sick-day management
  • Recognition Rx of hypo at home

37
DIET REGULATION
  • Regular meal plans with calorie exchange options
    are encouraged.
  • 50-60 of required energy to be obtained from
    complex carbohydrates.
  • Distribute carbohydrate load evenly during the
    day preferably 3 meals 2 snacks with avoidance
    of simple sugars.
  • Encouraged low salt, low saturated fats and high
    fiber diet.

38
EXERCISE
  • Decreases insulin requirement in diabetic
    subjects by increasing both sensitivity of muscle
    cells to insulin glucose utilization.
  • It can precipitate hypoglycemia in the unprepared
    diabetic patient.
  • It may worsen pre-existing diabetic retinopathy.

39
MONITORING
  • Compliance (check records)
  • HBG tests
  • HbA1 every 2 months
  • Insulin meal plan
  • Growth development
  • Well being life style
  • School hobbies

40
ADVANCES IN MONITORING
  • Smaller accurate meters for intermittent BG
    monitoring
  • Glucowatch continuous monitoring using reverse
    iontophoresis to measure interstitial fluid
    glucose every 20 minutes
  • Glucosensor that measures s/c capillary BG every
    5 minutes
  • Implantable sensor with high low BG alarm

41
ADVANCES IN MANAGEMENT
  • Better understanding of diabetes allows more
    rational approach to therapy.
  • Primary prevention could be possible if the
    triggering factors are identified.
  • The DCCT studies proves beyond doubt that chronic
    diabetic complication can be controlled or
    prevented by strict glycemic control.

42
TREATMENT MADE EASY
  • Insulin pens new delivery products
  • Handy insulin pumps
  • fine micro needles
  • Simple accurate glucometers
  • Free educational material
  • computer programs for comprehensive management
    monitoring

43
TELECARE SYSTEMS
  • IT has improved diabetes care
  • Internet sites for education support
  • Web-based systems for telecare are now available.
    The patient feeds his HBGM data and get the
    physician, nurse dietician advice on the
    required modification to diet insulin treatment.

44
PITFALLS OF MANAGEMENT
  • Delayed diagnosis of IDDM
  • The honey-moon period
  • Detection treatment of NIDDY
  • Problems with diagnosis treatment of DKA
    hypoglycemia
  • Somogis effect (dawn phenomenon) may go
    unrecognized.

45
FUTURE PROMISES
  • The cure for IDDM is successful islet cell
    transplantation, which will be available in the
    near future.
  • Primary prevention by a vaccine or drug will be
    offered to at risk subjects identified by genetic
    studies.
  • Gene modulation therapy for susceptible subjects
    is a promising preventive measure.

46
Pancreas Islet Cell Transplantation
  • Pancreas transplants are usually given to
    diabetics with end stage renal disease.
  • Islet cell transplants, the ultimate treatment of
    type 1 diabetes is under trial in many centers in
    the US Europe with encouraging results but
    graft rejection recurrence of autoimmunity are
    serious limitations.

47
IMMUNE MODULATION
  • Immunosuppressive therapy for
  • Newly diagnosed
  • Prolonged the honey moon
  • For high risk children
  • Immune modulating drugs
  • Nicotinamide
  • mycophenolate

48
GENE THERAPY
  • Blocks the immunologic attack against islet-cells
    by DNA-plasmids encoding self antigen.
  • Gene encode cytokine inhibitors.
  • Modifying gene expressed islet-cell antigens like
    GAD.

49
PREDICTION OF DIABETES
  • Sensitive specific immunologic markers
  • GAD Antibodies
  • GLIMA antibodies
  • IA-2 antibodies
  • Sensitive genetic markers
  • HLA haplotypes
  • DQ molecular markers

50
PREVENTION OF DIABETES
  • Primary prevention
  • Identification of diabetes gene
  • Tampering with the immune system
  • Elimination of environmental factor
  • Secondary prevention
  • Immunosuppressive therapy
  • Tertiary prevention
  • Tight metabolic control good monitoring

51
Dreams are the seedlings of realities
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